delete extraneous refs

-@article{toncUnexpectedSuppressionTumorigenesis2021,

- title = {Unexpected Suppression of Tumorigenesis by C-{{MYC}} via {{TFAP4-dependent}} Restriction of Stemness in {{B}} Lymphocytes},

- author = {Tonc, Elena and Takeuchi, Yoshiko and Chou, Chun and Xia, Yu and Holmgren, Melanie and Fujii, Chika and Raju, Saravanan and Chang, Gue Su and Iwamoto, Masahiro and Egawa, Takeshi},

- date = {2021-12-16},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {138},

- number = {24},

- eprint = {34283887},

- eprinttype = {pmid},

- pages = {2526--2538},

- issn = {1528-0020},

- doi = {10.1182/blood.2021011711},

- abstract = {The proliferative burst of B lymphocytes is essential for antigen receptor repertoire diversification during the development and selective expansion of antigen-specific clones during immune responses. High proliferative activity inevitably promotes oncogenesis, the risk of which is further elevated in B lymphocytes by endogenous gene rearrangement and somatic mutations. However, B-cell-derived cancers are rare, perhaps owing to putative intrinsic tumor-suppressive mechanisms. We show that c-MYC facilitates B-cell proliferation as a protumorigenic driver and unexpectedly coengages counteracting tumor suppression through its downstream factor TFAP4. TFAP4 is mutated in human lymphoid malignancies, particularly in {$>$}10\% of Burkitt lymphomas, and reduced TFAP4 expression was associated with poor survival of patients with MYC-high B-cell acute lymphoblastic leukemia. In mice, insufficient TFAP4 expression accelerated c-MYC-driven transformation of B cells. Mechanistically, c-MYC suppresses the stemness of developing B cells by inducing TFAP4 and restricting self-renewal of proliferating B cells. Thus, the pursuant transcription factor cascade functions as a tumor suppressor module that safeguards against the transformation of developing B cells.},

- langid = {english},

- pmcid = {PMC8678995},

- keywords = {Animals,B-Lymphocytes,Carcinogenesis,Cell Transformation Neoplastic,DNA-Binding Proteins,Gene Expression Regulation Neoplastic,Genes Tumor Suppressor,Humans,Leukemia Lymphoid,Lymphoma B-Cell,Mice,Mice Inbred C57BL,Mutation,Proto-Oncogene Proteins c-myc,Transcription Factors,Tumor Cells Cultured}

-}

-@article{kizhakeyilDDX3XLossAdverse2021,

- title = {{{DDX3X}} Loss Is an Adverse Prognostic Marker in Diffuse Large {{B-cell}} Lymphoma and Is Associated with Chemoresistance in Aggressive Non-{{Hodgkin}} Lymphoma Subtypes},

- author = {Kizhakeyil, Atish and Zaini, Nurmahirah Binte Mohammed and Poh, Zhi Sheng and Wong, Brandon Han Siang and Loh, Xinpeng and Ng, Aik Seng and Low, Zun Siong and Prasannan, Praseetha and Gong, Chun and Tan, Michelle Guet Khim and Nagarajan, Chandramouli and Huang, Dachuan and Lu, Pang Wan and Lim, Jing Quan and Barrans, Sharon and Ong, Choon Kiat and Lim, Soon Thye and Chng, Wee Joo and Follows, George and Hodson, Daniel J. and Du, Ming Qing and Goh, Yeow Tee and Tan, Suat Hoon and Grigoropoulos, Nicholas Francis and Verma, Navin Kumar},

- date = {2021-10-16},

- journaltitle = {Molecular Cancer},

- shortjournal = {Mol Cancer},

- volume = {20},

- number = {1},

- eprint = {34654425},

- eprinttype = {pmid},

- pages = {134},

- issn = {1476-4598},

- doi = {10.1186/s12943-021-01437-0},

- langid = {english},

- pmcid = {PMC8520256},

- keywords = {Antineoplastic Agents,Biomarkers Tumor,Cell Line Tumor,Cyclin D1,DDX3X mutation,DEAD-box RNA Helicases,Disease Progression,Drug resistance,Drug Resistance Neoplasm,Exome Sequencing,Hematolymphoid malignancy,Humans,Lymphoma Large B-Cell Diffuse,Lymphoma Non-Hodgkin,Mitogen-Activated Protein Kinases,Mutation,Prognosis,STAT3 Transcription Factor,Tumour metastasis}

-}

-

-@article{campos-martinClinicalDiagnosticRelevance2017,

- title = {Clinical and Diagnostic Relevance of {{NOTCH2-and KLF2-mutations}} in Splenic Marginal Zone Lymphoma},

- author = {Campos-Martín, Yolanda and Martínez, Nerea and Martínez-López, Azahara and Cereceda, Laura and Casado, Felipe and Algara, Patrocinio and Oscier, David and Menarguez, Francisco J. and García, Juan F. and Piris, Miguel A. and Mollejo, Manuela},

- date = {2017-08-01},

- journaltitle = {Haematologica},

- volume = {102},

- number = {8},

- pages = {e310-e312},

- issn = {1592-8721},

- doi = {10.3324/haematol.2016.161711},

- issue = {8},

- langid = {english}

-}

-@article{rowhTp53DeletionLineage2011,

- title = {Tp53 Deletion in {{B}} Lineage Cells Predisposes Mice to Lymphomas with Oncogenic Translocations},

- author = {Rowh, M. a. W. and DeMicco, A. and Horowitz, J. E. and Yin, B. and Yang-Iott, K. S. and Fusello, A. M. and Hobeika, E. and Reth, M. and Bassing, C. H.},

- date = {2011-11-24},

- journaltitle = {Oncogene},

- shortjournal = {Oncogene},

- volume = {30},

- number = {47},

- eprint = {21625223},

- eprinttype = {pmid},

- pages = {4757--4764},

- issn = {1476-5594},

- doi = {10.1038/onc.2011.191},

- abstract = {Inactivating Tp53 mutations are frequent genetic lesions in human tumors that harbor genomic instability, including B lineage lymphomas with IG translocations. Antigen receptor genes are assembled and modified in developing lymphocytes by RAG/AID-initiated genomic rearrangements that involve the induction of DNA double strand breaks (DSBs). Although TP53 inhibits the persistence of DSBs and induces apoptosis to protect cells from genomic instability and transformation, the development of spontaneous tumors harboring clonal translocations has not been reported in mice that only lack wild-type Tp53 protein or express Tp53 mutants. Tp53-deficient (Tp53(-/-)) mice succumb to T lineage lymphomas lacking clonal translocations but develop B lymphoid tumors containing immunoglobulin (Ig) translocations upon combined inactivation of DSB repair factors, RAG mutation or AID overexpression; mice expressing apoptosis-defective Tp53 mutants develop B cell lymphomas that have not been characterized for potential genomic instability. As somatic rather than germline inactivating mutations of TP53 are typically associated with human cancers and Tp53 deletion has cellular context dependent effects upon lymphocyte transformation, we generated mice with conditional Tp53 deletion in lineage-committed B lymphocytes to avoid complications associated with defective Tp53 responses during embryogenesis and/or in multi-lineage potential cells and, thereby, directly evaluate the potential physiological role of Tp53 in suppressing translocations in differentiated cells. These mb1-cre:Tp53(flox/flox) mice succumbed to lymphoid tumors containing Ig gene rearrangements and immunophenotypes characteristic of B cells from various developmental stages. Most mb1-cre:Tp53(flox/flox) tumors harbored clonal translocations, including Igh/c-myc or other oncogenic translocations generated by the aberrant repair of RAG/AID-generated DSBs. Our data indicate that Tp53 serves critical functions in B lineage lymphocytes to prevent transformation caused by translocations in cell populations experiencing physiological levels of RAG/AID-initiated DSB intermediates, and provide evidence that the somatic TP53 mutations found in diffuse large B-cell lymphoma and Burkitt's lymphoma may contribute to the development of these human malignancies.},

- langid = {english},

- keywords = {Animals,B-Lymphocytes,Burkitt Lymphoma,Cell Lineage,DNA Breaks Double-Stranded,DNA End-Joining Repair,Female,Genes Immunoglobulin,Genes myc,Immunoglobulin Heavy Chains,Lymphoma B-Cell,Male,Mice,Translocation Genetic,Tumor Suppressor Protein p53}

-}

-

-@article{gongExpressionClinicalValue2021,

- title = {Expression and {{Clinical Value}} of {{Eukaryotic Translation Elongation Factor 1A1}} ({{EEF1A1}}) in {{Diffuse Large B Cell Lymphoma}}},

- author = {Gong, Tiejun and Shuang, Yuerong},

- year = {2021},

- journaltitle = {International Journal of General Medicine},

- shortjournal = {Int J Gen Med},

- volume = {14},

- eprint = {34737619},

- eprinttype = {pmid},

- pages = {7247--7258},

- issn = {1178-7074},

- doi = {10.2147/IJGM.S324645},

- abstract = {BACKGROUND: The eukaryotic translation elongation factor 1A1 (EEF1A1) participates in protein translation and has been reported to be involved in tumor progression such as hepatocellular carcinoma. Diffuse large B-cell lymphoma (DLBCL) is the most common lymphoid malignancy in adults. In the present study, we aimed to detect the expression of EEF1A1 in DLBCL and to analyze its relationship with prognosis. METHODS: We reviewed medical records of DLBCL patients in our hospital and evaluated their expression level of EEF1A1 in tumor tissues using immunohistochemical (IHC) assay. The Chi-square method was used for correlation analysis. The Kaplan-Meier method with Log rank test was used for univariate analysis. Cox proportional hazards model was used for multivariate analysis. Cellular and mice models were introduced to validate its oncogenic role. RESULTS: EEF1A1 expression in tumor cells was higher in certain DLBCL cases. Patients with higher EEF1A1 expression were more likely to have advanced tumor stage and poorer 5-year overall survival (OS) rates. EEF1A1 expression in tumor cells was an independent risk predictor for OS (P {$<$} 0.05). Cellular assays demonstrated that EEF1A1-shRNA significantly inhibited lymphoma cell proliferation. The study of xenografts further verified the effect of EEF1A1-shRNA on suppressing tumor growth in vivo. CONCLUSION: EEF1A1 positivity predicts short survival in DLBCL patients. For patients with higher EEF1A1 expression, more strategy such as anti-EEF1A1 antibody treatment should be developed.},

- langid = {english},

- pmcid = {PMC8559353},

- keywords = {diffuse large B-cell lymphoma,EEF1A1,prognosis,proliferation}

-}

-@article{merirantaDeltex1MutationsPredict2017b,

- title = {Deltex-1 Mutations Predict Poor Survival in Diffuse Large {{B-cell}} Lymphoma},

- author = {Meriranta, Leo and Pasanen, Annika and Louhimo, Riku and Cervera, Alejandra and Alkodsi, Amjad and Autio, Matias and Taskinen, Minna and Rantanen, Ville and Karjalainen-Lindsberg, Marja-Liisa and Holte, Harald and Delabie, Jan and Lehtonen, Rainer and Hautaniemi, Sampsa and Leppä, Sirpa},

- date = {2017-05},

- journaltitle = {Haematologica},

- shortjournal = {Haematologica},

- volume = {102},

- number = {5},

- eprint = {28183850},

- eprinttype = {pmid},

- pages = {e195-e198},

- issn = {1592-8721},

- doi = {10.3324/haematol.2016.157495},

- langid = {english},

- pmcid = {PMC5477623},

- keywords = {Adult,Aged,Biomarkers Tumor,DNA Mutational Analysis,Exons,Female,Humans,Lymphoma Large B-Cell Diffuse,Male,Middle Aged,Mutation,Neoplasm Grading,Neoplasm Staging,Prognosis,Proportional Hazards Models,Protein Domains,Ubiquitin-Protein Ligases}

-}

-

-@article{zhaoExpressionPrognosticValue2016,

- title = {[Expression and prognostic value of CARD11 in diffuse large B cell lymphoma]},

- author = {Zhao, Danqing and Li, Dongmei and Zhong, Dingrong and Zhang, Wei},

- date = {2016-01},

- journaltitle = {Zhonghua Xue Ye Xue Za Zhi = Zhonghua Xueyexue Zazhi},

- shortjournal = {Zhonghua Xue Ye Xue Za Zhi},

- volume = {37},

- number = {1},

- eprint = {26876250},

- eprinttype = {pmid},

- pages = {30--34},

- issn = {0253-2727},

- doi = {10.3760/cma.j.issn.0253-2727.2016.01.006},

- abstract = {OBJECTIVE: To determine the CARD11 expression and its prognostic value in diffuse large B cell lymphoma (DLBCL). METHODS: This retrospective study included previously untreated patients diagnosed with DLBCL from January 2007 to December 2012. Formalin-fixed, paraffin-embedded blocks of these patients were collected. Tissue microarray was built and expression of CARD11 was examined immunohistochemically. Subtype of DLBCL was determined by Hans algorithm (CD10, BCL6, MUM1). The pattern of CARD11 was further studied and their correlation with outcome was analyzed. RESULTS: 79 patients with DLBCL were enrolled and two reactive lymph nodes were used as control. The positive rate of high CARD11 expression in DLBCL was 65.33\%, which showed no significant associations with patients' characteristics. Positive CARD11 expression was associated with an inferior event free survival (EFS)(2- year EFS: 52.03\%vs 86.12\%,P=0.036). Even in patients with a high international prognostic index (IPI, 3-5 points), this difference still remained significant (Median EFS not reached vs 557 days,P=0.033). CONCLUSION: DLBCL patients with high CARD11 expression had a shorter EFS compared with low level of CARD11. This difference remained significant when patients were in high IPI (3-5 points), which might indicate the value of CARD11 in stratification of high-risk DLBCL patients.},

- langid = {chi},

- pmcid = {PMC7342294},

- keywords = {CARD Signaling Adaptor Proteins,Disease-Free Survival,Guanylate Cyclase,Humans,Lymphoma Large B-Cell Diffuse,Prognosis,Retrospective Studies}

-}

-

-@article{abrisquetaObservationInitialManagement2017,

- title = {Observation as the Initial Management Strategy in Patients with Mantle Cell Lymphoma},

- author = {Abrisqueta, P. and Scott, D. W. and Slack, G. W. and Steidl, C. and Mottok, A. and Gascoyne, R. D. and Connors, J. M. and Sehn, L. H. and Savage, K. J. and Gerrie, A. S. and Villa, D.},

- date = {2017-10-01},

- journaltitle = {Annals of Oncology: Official Journal of the European Society for Medical Oncology},

- shortjournal = {Ann. Oncol.},

- volume = {28},

- number = {10},

- eprint = {28961827},

- eprinttype = {pmid},

- pages = {2489--2495},

- issn = {1569-8041},

- doi = {10.1093/annonc/mdx333},

- abstract = {Background: Patients with mantle cell lymphoma (MCL) follow a heterogeneous clinical course. While they generally require treatment initiation shortly after diagnosis, it is unclear whether deferring treatment in selected patients with an indolent clinical behavior affects their overall outcome. Patients and methods: In this population-based study, all patients diagnosed with MCL during 1998-2014 were identified in the British Columbia Cancer Agency Lymphoid Cancer Database. The associations between clinico-pathologic characteristics, including the expression of Ki67, SOX11, and TP53, and time to treatment (TtT) and OS were analyzed. Results: A total of 440 patients with MCL were evaluated: 365 (83\%) received early treatment and 75 (17\%) were observed ≥3\,months. In the observation group, 54 (72\%) patients had a nodal presentation, 16 (21\%) a non-nodal presentation, and 5 (7\%) had only gastrointestinal involvement. Characteristics associated with deferred treatment included good performance status, no B symptoms, low LDH, non-bulky disease, non-blastoid morphology, and lower Ki67 values. The median TtT in the observation group was 35\,months (range 5-79), and 60 (80\%) patients were observed beyond 12\,months. The median OS was significantly longer in the observation group than in the early treatment group (72 versus 52.5\,months, respectively, P\,=\,0.041). In multivariable analysis, treatment decision was not associated with OS [HR 0.804 (95\% CI 0.529-1.221), P\,=\,0.306]. Conclusions: A subgroup of patients with MCL may be safely observed from diagnosis without negatively impacting their outcomes, including patients with non-nodal presentation as well as asymptomatic patients with low burden nodal presentation and a low proliferative rate.},

- langid = {english},

- keywords = {Adult,Aged,Aged 80 and over,British Columbia,Cohort Studies,Female,Humans,indolent,leukemic non-nodal,Lymphoma Mantle-Cell,Male,mantle cell lymphoma,Middle Aged,observation,Retrospective Studies,treatment deferral,Watchful Waiting}

-}

-@article{ahmedGeneMutationsActionable2016,

- title = {Gene Mutations and Actionable Genetic Lesions in Mantle Cell Lymphoma},

- author = {Ahmed, Makhdum and Zhang, Leo and Nomie, Krystle and Lam, Laura and Wang, Michael},

- date = {2016-07-19},

- journaltitle = {Oncotarget},

- volume = {7},

- number = {36},

- pages = {58638--58648},

- issn = {1949-2553},

- doi = {10.18632/oncotarget.10716},

- abstract = {Oncotarget | https://doi.org/10.18632/oncotarget.10716 Makhdum Ahmed, Leo Zhang, Krystle Nomie, Laura Lam, Michael Wang}

-}

-

-@article{akbariMegabasescaleMethylationPhasing2021,

- title = {Megabase-Scale Methylation Phasing Using Nanopore Long Reads and {{NanoMethPhase}}},

- author = {Akbari, Vahid and Garant, Jean-Michel and O’Neill, Kieran and Pandoh, Pawan and Moore, Richard and Marra, Marco A. and Hirst, Martin and Jones, Steven J. M.},

- date = {2021-02-22},

- journaltitle = {Genome Biology},

- shortjournal = {Genome Biology},

- volume = {22},

- number = {1},

- pages = {68},

- issn = {1474-760X},

- doi = {10.1186/s13059-021-02283-5},

- abstract = {The ability of nanopore sequencing to simultaneously detect modified nucleotides while producing long reads makes it ideal for detecting and phasing allele-specific methylation. However, there is currently no complete software for detecting SNPs, phasing haplotypes, and mapping methylation to these from nanopore sequence data. Here, we present NanoMethPhase, a software tool to phase 5-methylcytosine from nanopore sequencing. We also present SNVoter, which can post-process nanopore SNV calls to improve accuracy in low coverage regions. Together, these tools can accurately detect allele-specific methylation genome-wide using nanopore sequence data with low coverage of about ten-fold redundancy.},

- keywords = {Allele-specific methylation,NanoMethPhase,Nanopore sequencing,Phasing}

-}

-

-@article{alaggio5thEditionWorld2022,

- title = {The 5th Edition of the {{World Health Organization Classification}} of {{Haematolymphoid Tumours}}: {{Lymphoid Neoplasms}}},

- shorttitle = {The 5th Edition of the {{World Health Organization Classification}} of {{Haematolymphoid Tumours}}},

- author = {Alaggio, Rita and Amador, Catalina and Anagnostopoulos, Ioannis and Attygalle, Ayoma D. and Araujo, Iguaracyra Barreto de Oliveira and Berti, Emilio and Bhagat, Govind and Borges, Anita Maria and Boyer, Daniel and Calaminici, Mariarita and Chadburn, Amy and Chan, John K. C. and Cheuk, Wah and Chng, Wee-Joo and Choi, John K. and Chuang, Shih-Sung and Coupland, Sarah E. and Czader, Magdalena and Dave, Sandeep S. and family=Jong, given=Daphne, prefix=de, useprefix=true and Du, Ming-Qing and Elenitoba-Johnson, Kojo S. and Ferry, Judith and Geyer, Julia and Gratzinger, Dita and Guitart, Joan and Gujral, Sumeet and Harris, Marian and Harrison, Christine J. and Hartmann, Sylvia and Hochhaus, Andreas and Jansen, Patty M. and Karube, Kennosuke and Kempf, Werner and Khoury, Joseph and Kimura, Hiroshi and Klapper, Wolfram and Kovach, Alexandra E. and Kumar, Shaji and Lazar, Alexander J. and Lazzi, Stefano and Leoncini, Lorenzo and Leung, Nelson and Leventaki, Vasiliki and Li, Xiao-Qiu and Lim, Megan S. and Liu, Wei-Ping and Louissaint, Abner and Marcogliese, Andrea and Medeiros, L. Jeffrey and Michal, Michael and Miranda, Roberto N. and Mitteldorf, Christina and Montes-Moreno, Santiago and Morice, William and Nardi, Valentina and Naresh, Kikkeri N. and Natkunam, Yasodha and Ng, Siok-Bian and Oschlies, Ilske and Ott, German and Parrens, Marie and Pulitzer, Melissa and Rajkumar, S. Vincent and Rawstron, Andrew C. and Rech, Karen and Rosenwald, Andreas and Said, Jonathan and Sarkozy, Clémentine and Sayed, Shahin and Saygin, Caner and Schuh, Anna and Sewell, William and Siebert, Reiner and Sohani, Aliyah R. and Tooze, Reuben and Traverse-Glehen, Alexandra and Vega, Francisco and Vergier, Beatrice and Wechalekar, Ashutosh D. and Wood, Brent and Xerri, Luc and Xiao, Wenbin},

- date = {2022-07},

- journaltitle = {Leukemia},

- shortjournal = {Leukemia},

- volume = {36},

- number = {7},

- eprint = {35732829},

- eprinttype = {pmid},

- pages = {1720--1748},

- issn = {1476-5551},

- doi = {10.1038/s41375-022-01620-2},

- abstract = {We herein present an overview of the upcoming 5th edition of the World Health Organization Classification of Haematolymphoid Tumours focussing on lymphoid neoplasms. Myeloid and histiocytic neoplasms will be presented in a separate accompanying article. Besides listing the entities of the classification, we highlight and explain changes from the revised 4th edition. These include reorganization of entities by a hierarchical system as is adopted throughout the 5th edition of the WHO classification of tumours of all organ systems, modification of nomenclature for some entities, revision of diagnostic criteria or subtypes, deletion of certain entities, and introduction of new entities, as well as inclusion of tumour-like lesions, mesenchymal lesions specific to lymph node and spleen, and germline predisposition syndromes associated with the lymphoid neoplasms.},

- langid = {english},

- pmcid = {PMC9214472},

- keywords = {Hematologic Neoplasms,Humans,Lymphoma,World Health Organization}

-}

-

-@article{alarconHNRNPA2B1MediatorM6ADependent2015,

- title = {{{HNRNPA2B1 Is}} a {{Mediator}} of {{m6A-Dependent Nuclear RNA Processing Events}}},

- author = {Alarcón, Claudio R. and Goodarzi, Hani and Lee, Hyeseung and Liu, Xuhang and Tavazoie, Saeed and Tavazoie, Sohail F.},

- date = {2015-09-10},

- journaltitle = {Cell},

- shortjournal = {Cell},

- volume = {162},

- number = {6},

- eprint = {26321680},

- eprinttype = {pmid},

- pages = {1299--1308},

- publisher = {Elsevier},

- issn = {0092-8674, 1097-4172},

- doi = {10.1016/j.cell.2015.08.011},

- langid = {english}

-}

-@article{alcaideTargetedErrorsuppressedQuantification2017,

- title = {Targeted Error-Suppressed Quantification of Circulating Tumor {{DNA}} Using Semi-Degenerate Barcoded Adapters and Biotinylated Baits.},

- author = {Alcaide, Miguel and Yu, Stephen and Davidson, Jordan and Albuquerque, Marco and Bushell, Kevin and Fornika, Daniel and Arthur, Sarah and Grande, Bruno M and McNamara, Suzan and family=Tertre, given=Mathilde Couetoux, prefix=du, useprefix=false and Batist, Gerald and Huntsman, David G and Cavallone, Luca and Aguilar, Adriana and Basik, Mark and Johnson, Nathalie A and Deyell, Rebecca J and Rassekh, S Rod and Morin, Ryan D},

- date = {2017-09},

- journaltitle = {Scientific reports},

- volume = {7},

- number = {1},

- pages = {10574}

-}

-

-@article{alcaideUltrasensitiveDetectionCirculating2019,

- title = {Ultrasensitive {{Detection}} of {{Circulating Tumor DNA}} in {{Lymphoma}} via {{Targeted Hybridization Capture}} and {{Deep Sequencing}} of {{Barcoded Libraries}}},

- author = {Alcaide, Miguel and Rushton, Christopher and Morin, Ryan D.},

- date = {2019},

- journaltitle = {Methods in Molecular Biology (Clifton, N.J.)},

- shortjournal = {Methods Mol Biol},

- volume = {1956},

- eprint = {30779047},

- eprinttype = {pmid},

- pages = {383--435},

- issn = {1940-6029},

- doi = {10.1007/978-1-4939-9151-8_20},

- abstract = {Liquid biopsies are rapidly emerging as powerful tools for the early detection of cancer, noninvasive genomic profiling of localized or metastatic tumors, prompt detection of treatment resistance-associated mutations, and monitoring of therapeutic response and minimal residual disease in patients during clinical follow-up. Growing evidence strongly supports the utility of circulating tumor DNA (ctDNA) as a biomarker for the stratification and clinical management of lymphoma patients. However, ctDNA is diluted by variable amounts of cell-free DNA (cfDNA) shed by nonneoplastic cells causing a background signal of wild-type DNA that limits the sensitivity of methods that rely on DNA sequencing. Here, we describe an error suppression method for single-molecule counting that relies on targeted sequencing of cfDNA libraries constructed with semi-degenerate barcode adapters. Custom pools of biotinylated DNA baits for target enrichment can be designed to specifically track somatic mutations in one patient, survey mutation hotspots with diagnostic and prognostic value or be comprised of comprehensive gene panels with broad patient coverage in lymphoma. Such methods are amenable to track ctDNA levels during longitudinal liquid biopsy testing with high specificity and sensitivity and characterize, in real time, the genetic profiles of tumors without the need of standard invasive biopsies. The analysis of ultra-deep sequencing data according to the bioinformatics pipelines also described in this chapter affords to harness lower limits of detection for ctDNA below 0.1\%.},

- langid = {english},

- keywords = {Blood Specimen Collection,Cell-free DNA,Circulating Tumor DNA,DNA Barcoding Taxonomic,DNA damage,DNA Mutational Analysis,Duplex sequencing,Gene Library,High-Throughput Nucleotide Sequencing,Humans,Liquid biopsy,Liquid Biopsy,Lymphoma,Minimal residual disease,Mutation detection,Noninvasive genetic profiling,Nucleic Acid Hybridization,Targeted enrichment,Therapeutic response,Tumor burden}

-}

-

-@article{alduaijMolecularDeterminantsClinical2023,

- title = {Molecular Determinants of Clinical Outcomes in a Real-World Diffuse Large {{B-cell}} Lymphoma Population},

- author = {Alduaij, Waleed and Collinge, Brett and Ben-Neriah, Susana and Jiang, Aixiang and Hilton, Laura K. and Boyle, Merrill and Meissner, Barbara and Chong, Lauren and Miyata-Takata, Tomoko and Slack, Graham W. and Farinha, Pedro and Craig, Jeffrey W. and Lytle, Andrew and Savage, Kerry J. and Villa, Diego and Gerrie, Alina S. and Freeman, Ciara L. and Gascoyne, Randy D. and Connors, Joseph M. and Morin, Ryan D. and Sehn, Laurie H. and Mungall, Andrew J. and Steidl, Christian and Scott, David W.},

- date = {2023-05-18},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {141},

- number = {20},

- pages = {2493--2507},

- issn = {0006-4971},

- doi = {10.1182/blood.2022018248},

- abstract = {Molecular heterogeneity of diffuse large B-cell lymphoma (DLBCL) underlies the variable outcomes achieved with immunochemotherapy. However, outcomes of gene expression profiling (GEP)–defined molecular subgroups in a real-world DLBCL population remain unknown. Here we examined the prevalence and outcomes of molecular subgroups in an unselected population of 1149 patients with de novo DLBCL in British Columbia, Canada. Evaluable biopsies were profiled by fluorescence in situ hybridization (FISH), immunohistochemistry, and digital GEP to assign cell-of-origin and the so-called “double-hit signature” (DHITsig)—a signature originally described as being characteristic for high-grade B-cell lymphoma with MYC and BCL2 rearrangements (HGBCL-DH-BCL2). DHITsig was expressed in 21\% of 431 germinal center B-cell-like (GCB)–DLBCL and all 55 Burkitt lymphomas examined. Reflecting this latter finding, DHITsig has been renamed the “dark zone signature” (DZsig). DZsigpos-DLBCL, non-DZsigpos GCB-DLBCL and activated B-cell-like (ABC)–DLBCL were associated with a 2 year overall survival of 57\%, 89\%, and 71\%, respectively. 62\% of DZsigpos tumors were negative for HGBCL-DH-BCL2 by FISH, but were associated with outcomes similar to HGBCL-DH-BCL2. A small group of HGBCL-DH-BCL2 that lacked DZsig expression had different molecular features compared with DZsig-expressing HGBCL-DH-BCL2 and were associated with favorable outcomes comparable to DLBCL, not otherwise specified. DZsigpos and ABC-DLBCL had a shorter diagnosis-to-treatment interval (DTI) than GCB-DLBCL, with this metric being associated with outcome. In conclusion, DZsig expression extends beyond HGBCL-DH-BCL2 and captures a poor-prognosis DLBCL subgroup with short DTI, including patients unidentifiable by routine FISH testing, that should be considered for treatment intensification or novel therapies in prospective trials.}

-}

-

-@article{algamalGeneSelectionMicroarray2018,

- title = {Gene Selection for Microarray Gene Expression Classification Using {{Bayesian Lasso}} Quantile Regression},

- author = {Algamal, Zakariya Yahya and Alhamzawi, Rahim and Mohammad Ali, Haithem Taha},

- date = {2018-01-06},

- journaltitle = {Computers in Biology and Medicine},

- shortjournal = {Comput. Biol. Med.},

- volume = {97},

- eprint = {29729489},

- eprinttype = {pmid},

- pages = {145--152},

- issn = {1879-0534},

- doi = {10.1016/j.compbiomed.2018.04.018},

- abstract = {Gene selection has been proven to be an effective way to improve the results of many classification methods. However, existing gene selection techniques in binary classification regression are sensitive to outliers of the data, heteroskedasticity or other anomalies of the latent response. In this paper, we propose a new Bayesian hierarchical model to overcome these problems in a relatively straightforward way. In particular, we propose a new Bayesian Lasso method that employs a skewed Laplace distribution for the errors and a scaled mixture of uniform distribution for the regression parameters, together with Bayesian MCMC estimation. Comprehensive comparisons between our proposed gene selection method and other competitor methods are performed experimentally, depending on four benchmark gene expression datasets. The experimental results prove that the proposed method is very effective for selecting the most relevant genes with high classification accuracy.},

- langid = {english},

- keywords = {Algorithms,Bayes Theorem,Bayesian hierarchical model,Classification,Computational Biology,Databases Genetic,Gene Expression Profiling,Gene selection,Humans,Lasso,Models Statistical,Neoplasms,Oligonucleotide Array Sequence Analysis,Quantile regression,Regression Analysis,Transcriptome}

-}

-

-@article{alhusainNonparametricApproachesPopulation2018,

- title = {Nonparametric Approaches for Population Structure Analysis},

- author = {Alhusain, Luluah and Hafez, Alaaeldin M.},

- date = {2018-05-09},

- journaltitle = {Human Genomics},

- shortjournal = {Hum. Genomics},

- volume = {12},

- number = {1},

- eprint = {29743099},

- eprinttype = {pmid},

- pages = {25},

- issn = {1479-7364},

- doi = {10.1186/s40246-018-0156-4},

- abstract = {The analysis of population structure has many applications in medical and population genetic research. Such analysis is used to provide clear insight into the underlying genetic population substructure and is a crucial prerequisite for any analysis of genetic data. The analysis involves grouping individuals into subpopulations based on shared genetic variations. The most widely used markers to study the variation of DNA sequences between populations are single nucleotide polymorphisms. Data preprocessing is a necessary step to assess the quality of the data and to determine which markers or individuals can reasonably be included in the analysis. After preprocessing, several methods can be utilized to uncover population substructure, which can be categorized into two broad approaches: parametric and nonparametric. Parametric approaches use statistical models to infer population structure and assign individuals into subpopulations. However, these approaches suffer from many drawbacks that make them impractical for large datasets. In contrast, nonparametric approaches do not suffer from these drawbacks, making them more viable than parametric approaches for analyzing large datasets. Consequently, nonparametric approaches are increasingly used to reveal population substructure. Thus, this paper reviews and discusses the nonparametric approaches that are available for population structure analysis along with some implications to resolve challenges.},

- langid = {english},

- pmcid = {PMC5944014},

- keywords = {Allele-sharing distance,Clustering,Dimension reduction,Genetic data,Population genetics,Population structure analysis,Principal component analysis,Single nucleotide polymorphism}

-}

-

-@article{aligDistinctHodgkinLymphoma2024,

- title = {Distinct {{Hodgkin}} Lymphoma Subtypes Defined by Noninvasive Genomic Profiling},

- author = {Alig, Stefan K. and Shahrokh Esfahani, Mohammad and Garofalo, Andrea and Li, Michael Yu and Rossi, Cédric and Flerlage, Tim and Flerlage, Jamie E. and Adams, Ragini and Binkley, Michael S. and Shukla, Navika and Jin, Michael C. and Olsen, Mari and Telenius, Adèle and Mutter, Jurik A. and Schroers-Martin, Joseph G. and Sworder, Brian J. and Rai, Shinya and King, Daniel A. and Schultz, Andre and Bögeholz, Jan and Su, Shengqin and Kathuria, Karan R. and Liu, Chih Long and Kang, Xiaoman and Strohband, Maya J. and Langfitt, Deanna and Pobre-Piza, Kristine Faye and Surman, Sherri and Tian, Feng and Spina, Valeria and Tousseyn, Thomas and Buedts, Lieselot and Hoppe, Richard and Natkunam, Yasodha and Fornecker, Luc-Matthieu and Castellino, Sharon M. and Advani, Ranjana and Rossi, Davide and Lynch, Ryan and Ghesquières, Hervé and Casasnovas, Olivier and Kurtz, David M. and Marks, Lianna J. and Link, Michael P. and André, Marc and Vandenberghe, Peter and Steidl, Christian and Diehn, Maximilian and Alizadeh, Ash A.},

- date = {2024-01},

- journaltitle = {Nature},

- shortjournal = {Nature},

- volume = {625},

- number = {7996},

- eprint = {38081297},

- eprinttype = {pmid},

- pages = {778--787},

- issn = {1476-4687},

- doi = {10.1038/s41586-023-06903-x},

- abstract = {The scarcity of malignant Hodgkin and Reed-Sternberg cells hampers tissue-based comprehensive genomic profiling of classic Hodgkin lymphoma (cHL). By contrast, liquid biopsies show promise for molecular profiling of cHL due to relatively high circulating tumour DNA (ctDNA) levels1-4. Here we show that the plasma representation of mutations exceeds the bulk tumour representation in most cases, making cHL particularly amenable to noninvasive profiling. Leveraging single-cell transcriptional profiles of cHL tumours, we demonstrate Hodgkin and Reed-Sternberg ctDNA shedding to be shaped by DNASE1L3, whose increased tumour microenvironment-derived expression drives high ctDNA concentrations. Using this insight, we comprehensively profile 366 patients, revealing two distinct cHL genomic subtypes with characteristic clinical and prognostic correlates, as well as distinct transcriptional and immunological profiles. Furthermore, we identify a novel class of truncating IL4R mutations that are dependent on IL-13 signalling and therapeutically targetable with IL-4Rα-blocking antibodies. Finally, using PhasED-seq5, we demonstrate the clinical value of pretreatment and on-treatment ctDNA levels for longitudinally refining cHL risk prediction and for detection of radiographically occult minimal residual disease. Collectively, these results support the utility of noninvasive strategies for genotyping and dynamic monitoring of cHL, as well as capturing molecularly distinct subtypes with diagnostic, prognostic and therapeutic potential.},

- langid = {english},

- keywords = {Circulating Tumor DNA,Genome Human,Genomics,Hodgkin Disease,Humans,Mutation,Reed-Sternberg Cells,Single-Cell Gene Expression Analysis,Tumor Microenvironment}

-}

-

-@article{alix-panabieresCirculatingTumorCells,

- title = {Circulating Tumor Cells and Circulating Tumor {{DNA}}.},

- author = {Alix-Panabières, Catherine and Schwarzenbach, Heidi and Pantel, Klaus},

- journaltitle = {Annual review of medicine},

- volume = {63},

- pages = {199--215}

-}

-

-@article{alizadehDistinctTypesDiffuse2000,

- title = {Distinct Types of Diffuse Large {{B-cell}} Lymphoma Identified by Gene Expression Profiling.},

- author = {Alizadeh, A A and Eisen, M B and Davis, R E and Ma, C and Lossos, I S and Rosenwald, A and Boldrick, J C and Sabet, H and Tran, T and Yu, X and Powell, J I and Yang, L and Marti, G E and Moore, T and Hudson, J and Lu, L and Lewis, D B and Tibshirani, R and Sherlock, G and Chan, W C and Greiner, T C and Weisenburger, D D and Armitage, J O and Warnke, R and Levy, R and Wilson, W and Grever, M R and Byrd, J C and Botstein, D and Brown, P O and Staudt, L M},

- date = {2000-02},

- journaltitle = {Nature},

- volume = {403},

- number = {6769},

- pages = {503--511}

-}

-

-@article{alizadehLymphochipSpecializedCDNA1999,

- title = {The Lymphochip: A Specialized {{cDNA}} Microarray for the Genomic-Scale Analysis of Gene Expression in Normal and Malignant Lymphocytes},

- author = {Alizadeh, A and Eisen, M and Davis, R and Ma, C and Sabet, H and Tran, T and Powell, J and Yang, L and Marti, G and Moore, D and Hudson, J and Chan, W and Greiner, T and Weisenburger, D and Armitage, J and Lossos, I and Levy, R and Botstein, D and Brown, P and Staudt, L},

- date = {1999},

- journaltitle = {Cold Spring Harbor symposia on quantitative biology},

- volume = {64},

- pages = {71--78}

-}

-

-@article{alizadehNovelClassificationHuman2001,

- title = {Towards a Novel Classification of Human Malignancies Based on Gene Expression Patterns},

- author = {Alizadeh, A. A. and Ross, D. T. and Perou, C. M. and family=Rijn, given=M., prefix=van de, useprefix=true},

- date = {2001-09},

- journaltitle = {The Journal of Pathology},

- shortjournal = {J Pathol},

- volume = {195},

- number = {1},

- eprint = {11568890},

- eprinttype = {pmid},

- pages = {41--52},

- issn = {0022-3417},

- doi = {10.1002/path.889},

- abstract = {As a result of progress on the human genome project, approximately 19 000 genes have been identified and tens of thousands more tentatively identified as partial fragments of genes termed expressed sequence tags (ESTs). Most of these genes are only partially characterized and the functions of the vast majority are as yet unknown. It is likely that many genes that might be useful for diagnosis and/or prognostication of human malignancies have yet to be recognized. The advent of cDNA microarray technology now allows the efficient measurement of expression for almost every gene in the human genome in a single overnight hybridization experiment. This genomic scale approach has begun to reveal novel molecular-based sub-classes of tumours in breast carcinoma, colon carcinoma, lymphoma, leukaemia, and melanoma. In several instances, gene microarray analysis has already identified genes that appear to be useful for predicting clinical behaviour. This review discusses some recent findings using gene microarray technology and describes how this and related technologies are likely to contribute to the emergence of novel molecular classifications of human malignancies.},

- langid = {english},

- keywords = {Breast Neoplasms,Cluster Analysis,DNA Fingerprinting,Expressed Sequence Tags,Gene Expression Regulation Neoplastic,Genetic Markers,Genome Human,Humans,Lymphoma,Neoplasms,Oligonucleotide Array Sequence Analysis,Prognosis}

-}

-@article{alizadehPredictionSurvivalDiffuse,

- title = {Prediction of Survival in Diffuse Large {{B-cell}} Lymphoma Based on the Expression of 2 Genes Reflecting Tumor and Microenvironment},

- author = {Alizadeh, A A and Gentles, A J and Alencar, A J}

-}

-@article{AnalysisCirculatingTumor2001,

- title = {Analysis of {{Circulating Tumor DNA}} in {{Plasma}} at {{Diagnosis}} and during {{Follow-Up}} of {{Lung Cancer Patients}}},

- date = {2001-06},

- pages = {1--5}

-}

-

-@article{andersHTSeqPythonFramework2015,

- title = {{{HTSeq--a Python}} Framework to Work with High-Throughput Sequencing Data},

- author = {Anders, Simon and Pyl, Paul Theodor and Huber, Wolfgang},

- date = {2015-01-15},

- journaltitle = {Bioinformatics (Oxford, England)},

- shortjournal = {Bioinformatics},

- volume = {31},

- number = {2},

- eprint = {25260700},

- eprinttype = {pmid},

- pages = {166--169},

- issn = {1367-4811},

- doi = {10.1093/bioinformatics/btu638},

- abstract = {MOTIVATION: A large choice of tools exists for many standard tasks in the analysis of high-throughput sequencing (HTS) data. However, once a project deviates from standard workflows, custom scripts are needed. RESULTS: We present HTSeq, a Python library to facilitate the rapid development of such scripts. HTSeq offers parsers for many common data formats in HTS projects, as well as classes to represent data, such as genomic coordinates, sequences, sequencing reads, alignments, gene model information and variant calls, and provides data structures that allow for querying via genomic coordinates. We also present htseq-count, a tool developed with HTSeq that preprocesses RNA-Seq data for differential expression analysis by counting the overlap of reads with genes. AVAILABILITY AND IMPLEMENTATION: HTSeq is released as an open-source software under the GNU General Public Licence and available from http://www-huber.embl.de/HTSeq or from the Python Package Index at https://pypi.python.org/pypi/HTSeq.},

- langid = {english},

- pmcid = {PMC4287950},

- keywords = {Gene Expression Regulation,Genome Human,Genomics,High-Throughput Nucleotide Sequencing,Humans,Software}

-}

-@article{aresuPhenotypicalCharacterizationClinical2021,

- title = {Phenotypical {{Characterization}} and {{Clinical Outcome}} of {{Canine Burkitt-Like Lymphoma}}},

- author = {Aresu, Luca and Agnoli, Chiara and Nicoletti, Arturo and Fanelli, Antonella and Martini, Valeria and Bertoni, Francesco and Marconato, Laura},

- date = {2021},

- journaltitle = {Frontiers in Veterinary Science},

- shortjournal = {Front. Vet. Sci.},

- volume = {8},

- publisher = {Frontiers},

- issn = {2297-1769},

- doi = {10.3389/fvets.2021.647009},

- url = {https://www.frontiersin.org/articles/10.3389/fvets.2021.647009/full},

- urldate = {2021-05-13},

- abstract = {In dogs, Burkitt-like lymphoma (B-LL) is rare tumour and it is classified as a high-grade B-cell malignancy. The diagnosis is challenging because of the similar histologic appearance with other histotypes, no defined phenotypical criteria and poorly described clinical aspects. The aim of the study was to provide a detailed description of clinical and morphological features, as well as immunophenotypical profile of B-LL in comparison with the human counterpart. Thirteen dogs with histologically proven B-LL, for which a complete staging and follow-up were available, were retrospectively selected. Immunohistochemical expression of CD20, PAX5, CD3, CD10, BCL2, BCL6, MYC and caspase-3 was evaluated. Histologically, all B-LLs showed a diffuse architecture with medium to large-sized cells, high mitotic rate and diffuse starry sky appearance. B-phenotype of neoplastic cells was confirmed both by flow-cytometry and immunohistochemistry. Conversely, B-LLs were negative for BCL2 and MYC, whereas some cases co-expressed BCL6 and CD10, suggesting a germinal centre B-cell origin. Disease stage was advanced in the majority of cases. All dogs received CHOP-based chemotherapy with or without immunotherapy. Despite treatment, prognosis was poor, with a median time to progression and survival of 130 and 228 days, respectively. Nevertheless, approximately 30\% of dogs survived more than one year. An increased apoptotic index, a high turnover index and caspase-3 index correlated with shorter survival. In conclusion, canine B-LL shows phenotypical differences with the human counterpart along with features that might help to differentiate this entity from diffuse large B-cell lymphoma.},

- langid = {english},

- keywords = {apoptic index,Burkitt-like lymphoma,Caspase - 3,dog,MYC,prognosis}

-}

-

-@article{arnedo-pacOncodriveCLUSTLSequencebasedClustering2019,

- title = {{{OncodriveCLUSTL}}: A Sequence-Based Clustering Method to Identify Cancer Drivers},

- shorttitle = {{{OncodriveCLUSTL}}},

- author = {Arnedo-Pac, Claudia and Mularoni, Loris and Muiños, Ferran and Gonzalez-Perez, Abel and Lopez-Bigas, Nuria},

- date = {2019-11-01},

- journaltitle = {Bioinformatics (Oxford, England)},

- shortjournal = {Bioinformatics},

- volume = {35},

- number = {22},

- eprint = {31228182},

- eprinttype = {pmid},

- pages = {4788--4790},

- issn = {1367-4811},

- doi = {10.1093/bioinformatics/btz501},

- abstract = {MOTIVATION: Identification of the genomic alterations driving tumorigenesis is one of the main goals in oncogenomics research. Given the evolutionary principles of cancer development, computational methods that detect signals of positive selection in the pattern of tumor mutations have been effectively applied in the search for cancer genes. One of these signals is the abnormal clustering of mutations, which has been shown to be complementary to other signals in the detection of driver genes. RESULTS: We have developed OncodriveCLUSTL, a new sequence-based clustering algorithm to detect significant clustering signals across genomic regions. OncodriveCLUSTL is based on a local background model derived from the simulation of mutations accounting for the composition of tri- or penta-nucleotide context substitutions observed in the cohort under study. Our method can identify known clusters and bona-fide cancer drivers across cohorts of tumor whole-exomes, outperforming the existing OncodriveCLUST algorithm and complementing other methods based on different signals of positive selection. Our results indicate that OncodriveCLUSTL can be applied to the analysis of non-coding genomic elements and non-human mutations data. AVAILABILITY AND IMPLEMENTATION: OncodriveCLUSTL is available as an installable Python 3.5 package. The source code and running examples are freely available at https://bitbucket.org/bbglab/oncodriveclustl under GNU Affero General Public License. SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.},

- langid = {english},

- pmcid = {PMC6853674},

- keywords = {Cluster Analysis,Genomics,Humans,Neoplasms,Software}

-}

-@article{ashrafuzzamanAptamersBothDrugs2014,

- title = {Aptamers as {{Both Drugs}} and {{Drug-Carriers}}},

- author = {family=Ashrafuzzaman, given=Md., given-i={{Md}}},

- date = {2014},

- journaltitle = {BioMed Research International},

- shortjournal = {Biomed Res Int},

- volume = {2014},

- eprint = {25295268},

- eprinttype = {pmid},

- pages = {697923},

- issn = {2314-6133},

- doi = {10.1155/2014/697923},

- abstract = {Aptamers are short nucleic acid oligos. They may serve as both drugs and drug-carriers. Their use as diagnostic tools is also evident. They can be generated using various experimental, theoretical, and computational techniques. The systematic evolution of ligands by exponential enrichment which uses iterative screening of nucleic acid libraries is a popular experimental technique. Theory inspired methodology entropy-based seed-and-grow strategy that designs aptamer templates to bind specifically to targets is another one. Aptamers are predicted to be highly useful in producing general drugs and theranostic drugs occasionally for certain diseases like cancer, Alzheimer's disease, and so on. They bind to various targets like lipids, nucleic acids, proteins, small organic compounds, and even entire organisms. Aptamers may also serve as drug-carriers or nanoparticles helping drugs to get released in specific target regions. Due to better target specific physical binding properties aptamers cause less off-target toxicity effects. Therefore, search for aptamer based drugs, drug-carriers, and even diagnostic tools is expanding fast. The biophysical properties in relation to the target specific binding phenomena of aptamers, energetics behind the aptamer transport of drugs, and the consequent biological implications will be discussed. This review will open up avenues leading to novel drug discovery and drug delivery.},

- pmcid = {PMC4177733}

-}

-

-@article{assoulinePhaseStudyPanobinostat2016,

- title = {Phase 2 Study of Panobinostat with or without Rituximab in Relapsed Diffuse Large {{B-cell}} Lymphoma.},

- author = {Assouline, Sarit E and Nielsen, Torsten Holm and Yu, Stephen and Alcaide, Miguel and Chong, Lauren and Macdonald, David and Tosikyan, Axel and Kukreti, Vishal and Kezouh, Abbas and Petrogiannis-Haliotis, Tina and Albuquerque, Marco and Fornika, Daniel and Alamouti, Sepideh and Froment, Remi and Greenwood, Celia M T and Oros, Kathleen Klein and Camglioglu, Errol and Sharma, Ayushi and Christodoulopoulos, Rosa and Rousseau, Caroline and Johnson, Nathalie and Crump, Michael and Morin, Ryan D and Mann, Koren K},

- date = {2016-07},

- journaltitle = {Blood},

- volume = {128},

- number = {2},

- pages = {185--194}

-}

-

-@article{asterDetectionBCL2Rearrangements2002,

- title = {Detection of {{BCL2 Rearrangements}} in {{Follicular Lymphoma}}},

- author = {Aster, Jon C. and Longtine, Janina A.},

- date = {2002-03},

- journaltitle = {The American Journal of Pathology},

- shortjournal = {Am J Pathol},

- volume = {160},

- number = {3},

- eprint = {11891173},

- eprinttype = {pmid},

- pages = {759--763},

- issn = {0002-9440},

- pmcid = {PMC1867166}

-}

-

-@article{auweraFastQDataHighConfidence2013,

- title = {From {{FastQ Data}} to {{High-Confidence Variant Calls}}: {{The Genome Analysis Toolkit Best Practices Pipeline}}},

- shorttitle = {From {{FastQ Data}} to {{High-Confidence Variant Calls}}},

- author = {family=Auwera, given=Geraldine A. Van, prefix=der, useprefix=false and Carneiro, Mauricio O. and Hartl, Christopher and Poplin, Ryan and family=Angel, given=Guillermo, prefix=del, useprefix=false and Levy‐Moonshine, Ami and Jordan, Tadeusz and Shakir, Khalid and Roazen, David and Thibault, Joel and Banks, Eric and Garimella, Kiran V. and Altshuler, David and Gabriel, Stacey and DePristo, Mark A.},

- date = {2013},

- journaltitle = {Current Protocols in Bioinformatics},

- volume = {43},

- number = {1},

- pages = {11.10.1-11.10.33},

- issn = {1934-340X},

- doi = {10.1002/0471250953.bi1110s43},

- abstract = {This unit describes how to use BWA and the Genome Analysis Toolkit (GATK) to map genome sequencing data to a reference and produce high-quality variant calls that can be used in downstream analyses. The complete workflow includes the core NGS data-processing steps that are necessary to make the raw data suitable for analysis by the GATK, as well as the key methods involved in variant discovery using the GATK. Curr. Protoc. Bioinform. 43:11.10.1-11.10.33. © 2013 by John Wiley \& Sons, Inc.},

- langid = {english},

- keywords = {exome,genotyping,NGS,variant detection,WGS}

-}

-

-@article{ayyadGeneExpressionCancer2019,

- title = {Gene Expression Cancer Classification Using Modified {{K-Nearest Neighbors}} Technique},

- author = {Ayyad, Sarah M. and Saleh, Ahmed I. and Labib, Labib M.},

- date = {2019-02-01},

- journaltitle = {Biosystems},

- shortjournal = {Biosystems},

- volume = {176},

- pages = {41--51},

- issn = {0303-2647},

- doi = {10.1016/j.biosystems.2018.12.009},

- abstract = {Gene expression microarray classification is a crucial research field as it has been employed in cancer prediction and diagnosis systems. Gene expression data are composed of dozens of samples characterized by thousands of genes. Hence, an accurate and effective classification of such samples is a challenge. Machine learning techniques have been broadly utilized to build substantial and precise classification models. This paper proposes a new classification technique for gene expression data, which is called Modified k-nearest neighbor (MKNN). MKNN is applied in two scenarios namely; smallest modified KNN (SMKNN) and largest modified KNN (LMKNN). Both implementations are undertaken to enhance the performance of KNN. The key idea is to employ robust neighbors from training data by using a new weighting strategy. Several experiments have been performed on six different gene expression datasets. Experiments have shown that MKNN in its both scenarios outperforms traditional as well as recent ones. MKNN has been compared against (i) KNN, (ii) weighted KNN, (iii) support vector machine (SVM), (iv) fuzzy support vector machine, (v) brain emotional learning (BEL) in terms of classification accuracy, precision, and recall. On the other hand, results show that MKNN introduces smaller testing time than both KNN and weighted KNN.},

- langid = {english},

- keywords = {Cancer classification,Data mining,Gene expression,K-Nearest Neighbor,Microarray data classification}

-}

-

-@article{balSuperenhancerHypermutationAlters2022,

- title = {Super-Enhancer Hypermutation Alters Oncogene Expression in {{B}} Cell Lymphoma},

- author = {Bal, Elodie and Kumar, Rahul and Hadigol, Mohammad and Holmes, Antony B. and Hilton, Laura K. and Loh, Jui Wan and Dreval, Kostiantyn and Wong, Jasper C. H. and Vlasevska, Sofija and Corinaldesi, Clarissa and Soni, Rajesh Kumar and Basso, Katia and Morin, Ryan D. and Khiabanian, Hossein and Pasqualucci, Laura and Dalla-Favera, Riccardo},

- date = {2022-07},

- journaltitle = {Nature},

- shortjournal = {Nature},

- volume = {607},

- number = {7920},

- eprint = {35794478},

- eprinttype = {pmid},

- pages = {808--815},

- issn = {1476-4687},

- doi = {10.1038/s41586-022-04906-8},

- abstract = {Diffuse large B~cell lymphoma (DLBCL) is the most common B cell non-Hodgkin lymphoma and remains incurable in around 40\% of patients. Efforts to sequence the coding genome identified several genes and pathways that are altered in this disease, including potential therapeutic targets1-5. However, the non-coding genome of DLBCL remains largely unexplored. Here we show that active super-enhancers are highly and specifically hypermutated in 92\% of samples from individuals with DLBCL, display signatures of activation-induced cytidine deaminase activity, and are linked to genes that encode B cell developmental regulators and oncogenes. As evidence of oncogenic relevance, we show that the hypermutated super-enhancers linked to the BCL6, BCL2 and CXCR4 proto-oncogenes prevent the binding and transcriptional downregulation of the corresponding target gene by transcriptional repressors, including BLIMP1 (targeting BCL6) and the steroid receptor NR3C1 (targeting BCL2 and CXCR4). Genetic correction of selected mutations restored repressor DNA binding, downregulated target gene expression and led to the counter-selection of cells containing corrected alleles, indicating an oncogenic dependency on the super-enhancer mutations. This pervasive super-enhancer mutational mechanism reveals a major set of genetic lesions deregulating gene expression, which expands the involvement of known oncogenes in DLBCL pathogenesis and identifies new deregulated gene targets of therapeutic relevance.},

- langid = {english},

- pmcid = {PMC9583699},

- keywords = {Down-Regulation,Enhancer Elements Genetic,Gene Expression Regulation Neoplastic,Humans,Lymphoma Large B-Cell Diffuse,Mutation,Oncogenes,Positive Regulatory Domain I-Binding Factor 1,Proto-Oncogene Proteins c-bcl-2,Proto-Oncogene Proteins c-bcl-6,Receptors CXCR4,Receptors Glucocorticoid,Repressor Proteins}

-}

-@article{barnardPhaseClinicalTrial2014,

- title = {Phase {{I}} Clinical Trial and Pharmacodynamic Evaluation of Combination Hydroxychloroquine and Doxorubicin Treatment in Pet Dogs Treated for Spontaneously Occurring Lymphoma},

- author = {Barnard, Rebecca A and Wittenburg, Luke A and Amaravadi, Ravi K and Gustafson, Daniel L and Thorburn, Andrew and Thamm, Douglas H},

- date = {2014-08-01},

- journaltitle = {Autophagy},

- shortjournal = {Autophagy},

- volume = {10},

- number = {8},

- eprint = {24991836},

- eprinttype = {pmid},

- pages = {1415--1425},

- issn = {1554-8627},

- doi = {10.4161/auto.29165},

- abstract = {Autophagy is a lysosomal degradation process that may act as a mechanism of survival in a variety of cancers. While pharmacologic inhibition of autophagy with hydroxychloroquine (HCQ) is currently being explored in human clinical trials, it has never been evaluated in canine cancers. Non-Hodgkin lymphoma (NHL) is one of the most prevalent tumor types in dogs and has similar pathogenesis and response to treatment as human NHL. Clinical trials in canine patients are conducted in the same way as in human patients, thus, to determine a maximum dose of HCQ that can be combined with a standard chemotherapy, a Phase I, single arm, dose escalation trial was conducted in dogs with spontaneous NHL presenting as patients to an academic, tertiary-care veterinary teaching hospital. HCQ was administered daily by mouth throughout the trial, beginning 72 h prior to doxorubicin (DOX), which was given intravenously on a 21-d cycle. Peripheral blood mononuclear cells and biopsies were collected before and 3 d after HCQ treatment and assessed for autophagy inhibition and HCQ concentration. A total of 30 patients were enrolled in the trial. HCQ alone was well tolerated with only mild lethargy and gastrointestinal-related adverse events. The overall response rate (ORR) for dogs with lymphoma was 93.3\%, with median progression-free interval (PFI) of 5 mo. Pharmacokinetic analysis revealed a 100-fold increase in HCQ in tumors compared with plasma. There was a trend that supported therapy-induced increase in LC3-II (the cleaved and lipidated form of microtubule-associated protein 1 light chain 3/LC3, which serves as a maker for autophagosomes) and SQSTM1/p62 (sequestosome 1) after treatment. The superior ORR and comparable PFI to single-agent DOX provide strong support for further evaluation via randomized, placebo-controlled trials in canine and human NHL.},

- pmcid = {PMC4203518}

-}

-

-@article{barrans1418Associated2003,

- title = {The t(14;18) Is Associated with Germinal Center-Derived Diffuse Large {{B-cell}} Lymphoma and Is a Strong Predictor of Outcome.},

- author = {Barrans, Sharon L and Evans, Paul A S and O'Connor, Sheila J M and Kendall, S Jane and Owen, Roger G and Haynes, Andrew P and Morgan, Gareth J and Jack, Andrew S},

- date = {2003-06},

- journaltitle = {Clin Cancer Res},

- volume = {9},

- number = {6},

- pages = {2133--2139}

-}

-

-@article{barthOfatumumabExhibitsEnhanced2015,

- title = {Ofatumumab {{Exhibits Enhanced In Vitro}} and {{In Vivo Activity Compared}} to {{Rituximab}} in {{Preclinical Models}} of {{Mantle Cell Lymphoma}}},

- author = {Barth, M J and Mavis, C and Czuczman, M S and Hernandez-Ilizaliturri, F J},

- date = {2015-09},

- journaltitle = {Clin Cancer Res},

- volume = {21},

- number = {19},

- pages = {4391--4397}

-}

-

-@article{beaDiffuseLargeBcell2005,

- title = {Diffuse Large {{B-cell}} Lymphoma Subgroups Have Distinct Genetic Profiles That Influence Tumor Biology and Improve Gene-Expression-Based Survival Prediction.},

- author = {Bea, Silvia and Zettl, Andreas and Wright, George and Salaverria, Itziar and Jehn, Philipp and Moreno, Victor and Burek, Christof and Ott, German and Puig, Xavier and Yang, Liming and López-Guillermo, Armando and Chan, Wing C and Greiner, Timothy C and Weisenburger, Dennis D and Armitage, James O and Gascoyne, Randy D and Connors, Joseph M and Grogan, Thomas M and Braziel, Rita and Fisher, Richard I and Smeland, Erlend B and Kvaloy, Stein and Holte, Harald and Delabie, Jan and Simon, Richard and Powell, John and Wilson, Wyndham H and Jaffe, Elaine S and Montserrat, Emili and Müller-Hermelink, Hans-Konrad and Staudt, Louis M and Campo, Elias and Rosenwald, Andreas and Project, Lymphoma Leukemia Molecular Profiling},

- date = {2005-11},

- journaltitle = {Blood},

- volume = {106},

- number = {9},

- pages = {3183--3190}

-}

-

-@article{benesovaHansAlgorithmFailed,

- title = {The {{Hans}} Algorithm Failed to Predict Outcome in Patients with Diffuse Large {{B-cell}} Lymphoma Treated with Rituximab.},

- author = {Benesova, K and Forsterova, K and Votavova, H and Campr, V and Stritesky, J and Velenska, Z and Prochazka, B and Pytlik, R and Trneny, M},

- journaltitle = {Neoplasma},

- volume = {60},

- number = {1},

- pages = {68--73}

-}

-

-@article{bettegowdaDetectionCirculatingTumor2014,

- title = {Detection of {{Circulating Tumor DNA}} in {{Early-}} and {{Late-Stage Human Malignancies}}},

- author = {Bettegowda, C and Sausen, M and Leary, R J and Kinde, I and Wang, Y and Agrawal, N and Bartlett, B R and Wang, H and Luber, B and Alani, R M and Antonarakis, E S and Azad, N S and Bardelli, A and Brem, H and Cameron, J L and Lee, C C and Fecher, L A and Gallia, G L and Gibbs, P and Le, D and Giuntoli, R L and Goggins, M and Hogarty, M D and Holdhoff, M and Hong, S M and Jiao, Y and Juhl, H H and Kim, J J and Siravegna, G and Laheru, D A and Lauricella, C and Lim, M and Lipson, E J and Marie, S K N and Netto, G J and Oliner, K S and Olivi, A and Olsson, L and Riggins, G J and Sartore-Bianchi, A and Schmidt, K and Shih, l M and Oba-Shinjo, S M and Siena, S and Theodorescu, D and Tie, J and Harkins, T T and Veronese, S and Wang, T L and Weingart, J D and Wolfgang, C L and Wood, L D and Xing, D and Hruban, R H and Wu, J and Allen, P J and Schmidt, C M and Choti, M A and Velculescu, V E and Kinzler, K W and Vogelstein, B and Papadopoulos, N and Diaz, L A},

- date = {2014-02},

- journaltitle = {Science translational medicine},

- volume = {6},

- number = {224},

- pages = {224ra24--224ra24}

-}

-

-@article{biffiElevatedLevelsGQuadruplex2014,

- title = {Elevated {{Levels}} of {{G-Quadruplex Formation}} in {{Human Stomach}} and {{Liver Cancer Tissues}}},

- author = {Biffi, Giulia and Tannahill, David and Miller, Jodi and Howat, William J. and Balasubramanian, Shankar},

- date = {2014-07-17},

- journaltitle = {PLOS ONE},

- shortjournal = {PLOS ONE},

- volume = {9},

- number = {7},

- pages = {e102711},

- publisher = {Public Library of Science},

- issn = {1932-6203},

- doi = {10.1371/journal.pone.0102711},

- abstract = {Four-stranded G-quadruplex DNA secondary structures have recently been visualized in the nuclei of human cultured cells. Here, we show that BG4, a G-quadruplex-specific antibody, can be used to stain DNA G-quadruplex structures in patient-derived tissues using immunohistochemistry. We observe a significantly elevated number of G-quadruplex-positive nuclei in human cancers of the liver and stomach as compared to background non-neoplastic tissue. Our results suggest that G-quadruplex formation can be detected and measured in patient-derived material and that elevated G-quadruplex formation may be a characteristic of some cancers.},

- langid = {english},

- keywords = {Breast cancer,Cell staining,DNA structure,Gastric cancer,Hepatocellular carcinoma,Immunohistochemistry techniques,Nuclear staining,Stomach}

-}

-@article{blumSnapShotTCGAAnalyzedTumors2018,

- title = {{{SnapShot}}: {{TCGA-Analyzed Tumors}}},

- shorttitle = {{{SnapShot}}},

- author = {Blum, Amy and Wang, Peggy and Zenklusen, Jean C.},

- date = {2018-04-05},

- journaltitle = {Cell},

- shortjournal = {Cell},

- volume = {173},

- number = {2},

- eprint = {29625059},

- eprinttype = {pmid},

- pages = {530},

- publisher = {Elsevier},

- issn = {0092-8674, 1097-4172},

- doi = {10.1016/j.cell.2018.03.059},

- langid = {english}

-}

-

-@article{boevaControlFREECToolAssessing2012,

- title = {Control-{{FREEC}}: A Tool for Assessing Copy Number and Allelic Content Using next-Generation Sequencing Data},

- shorttitle = {Control-{{FREEC}}},

- author = {Boeva, Valentina and Popova, Tatiana and Bleakley, Kevin and Chiche, Pierre and Cappo, Julie and Schleiermacher, Gudrun and Janoueix-Lerosey, Isabelle and Delattre, Olivier and Barillot, Emmanuel},

- date = {2012-02-01},

- journaltitle = {Bioinformatics},

- shortjournal = {Bioinformatics},

- volume = {28},

- number = {3},

- pages = {423--425},

- issn = {1367-4803},

- doi = {10.1093/bioinformatics/btr670},

- abstract = {Abstract. Summary: More and more cancer studies use next-generation sequencing (NGS) data to detect various types of genomic variation. However, even when rese},

- langid = {english}

-}

-@article{bolotinMiXCRSoftwareComprehensive2015,

- title = {{{MiXCR}}: Software for Comprehensive Adaptive Immunity Profiling},

- shorttitle = {{{MiXCR}}},

- author = {Bolotin, Dmitriy A. and Poslavsky, Stanislav and Mitrophanov, Igor and Shugay, Mikhail and Mamedov, Ilgar Z. and Putintseva, Ekaterina V. and Chudakov, Dmitriy M.},

- date = {2015-05},

- journaltitle = {Nature Methods},

- shortjournal = {Nat Methods},

- volume = {12},

- number = {5},

- eprint = {25924071},

- eprinttype = {pmid},

- pages = {380--381},

- issn = {1548-7105},

- doi = {10.1038/nmeth.3364},

- langid = {english},

- keywords = {Adaptive Immunity,Animals,DNA,Gene Expression Regulation,Humans,Mice,RNA,Software}

-}

-

-@article{boseBortezomibTreatmentNonHodgkin2014,

- title = {Bortezomib for the Treatment of Non-{{Hodgkin}}'s Lymphoma.},

- author = {Bose, Prithviraj and Batalo, Michael S and Holkova, Beata and Grant, Steven},

- date = {2014-11},

- journaltitle = {Expert opinion on pharmacotherapy},

- volume = {15},

- number = {16},

- pages = {2443--2459}

-}

-@article{boutrosGlobalOptimizationSomatic2014,

- title = {Global Optimization of Somatic Variant Identification in Cancer Genomes with a Global Community Challenge},

- author = {Boutros, Paul C. and Ewing, Adam D. and Ellrott, Kyle and Norman, Thea C. and Dang, Kristen K. and Hu, Yin and Kellen, Michael R. and Suver, Christine and Bare, J. Christopher and Stein, Lincoln D. and Spellman, Paul T. and Stolovitzky, Gustavo and Friend, Stephen H. and Margolin, Adam A. and Stuart, Joshua M.},

- date = {2014-04},

- journaltitle = {Nature Genetics},

- shortjournal = {Nat Genet},

- volume = {46},

- number = {4},

- eprint = {24675517},

- eprinttype = {pmid},

- pages = {318--319},

- issn = {1546-1718},

- doi = {10.1038/ng.2932},

- langid = {english},

- pmcid = {PMC4035501},

- keywords = {Computational Biology,Crowdsourcing,Databases Genetic,DNA Mutational Analysis,Genetic Variation,Genome Human,High-Throughput Screening Assays,Humans,Neoplasms,Software}

-}

-

-@article{boutrosGlobalOptimizationSomatic2014a,

- title = {Global Optimization of Somatic Variant Identification in Cancer Genomes with a Global Community Challenge},

- author = {Boutros, Paul C. and Ewing, Adam D. and Ellrott, Kyle and Norman, Thea C. and Dang, Kristen K. and Hu, Yin and Kellen, Michael R. and Suver, Christine and Bare, J. Christopher and Stein, Lincoln D. and Spellman, Paul T. and Stolovitzky, Gustavo and Friend, Stephen H. and Margolin, Adam A. and Stuart, Joshua M.},

- date = {2014-04},

- journaltitle = {Nature Genetics},

- shortjournal = {Nat Genet},

- volume = {46},

- number = {4},

- eprint = {24675517},

- eprinttype = {pmid},

- pages = {318--319},

- issn = {1546-1718},

- doi = {10.1038/ng.2932},

- langid = {english},

- pmcid = {PMC4035501},

- keywords = {Computational Biology,Crowdsourcing,Databases Genetic,DNA Mutational Analysis,Genetic Variation,Genome Human,High-Throughput Screening Assays,Humans,Neoplasms,Software}

-}

-@article{brazmaMinimumInformationMicroarray2001,

- title = {Minimum Information about a Microarray Experiment ({{MIAME}})-toward Standards for Microarray Data},

- author = {Brazma, A. and Hingamp, P. and Quackenbush, J. and Sherlock, G. and Spellman, P. and Stoeckert, C. and Aach, J. and Ansorge, W. and Ball, C. A. and Causton, H. C. and Gaasterland, T. and Glenisson, P. and Holstege, F. C. and Kim, I. F. and Markowitz, V. and Matese, J. C. and Parkinson, H. and Robinson, A. and Sarkans, U. and Schulze-Kremer, S. and Stewart, J. and Taylor, R. and Vilo, J. and Vingron, M.},

- date = {2001-12},

- journaltitle = {Nature Genetics},

- shortjournal = {Nat Genet},

- volume = {29},

- number = {4},

- eprint = {11726920},

- eprinttype = {pmid},

- pages = {365--371},

- issn = {1061-4036},

- doi = {10.1038/ng1201-365},

- abstract = {Microarray analysis has become a widely used tool for the generation of gene expression data on a genomic scale. Although many significant results have been derived from microarray studies, one limitation has been the lack of standards for presenting and exchanging such data. Here we present a proposal, the Minimum Information About a Microarray Experiment (MIAME), that describes the minimum information required to ensure that microarray data can be easily interpreted and that results derived from its analysis can be independently verified. The ultimate goal of this work is to establish a standard for recording and reporting microarray-based gene expression data, which will in turn facilitate the establishment of databases and public repositories and enable the development of data analysis tools. With respect to MIAME, we concentrate on defining the content and structure of the necessary information rather than the technical format for capturing it.},

- langid = {english},

- keywords = {Computational Biology,Gene Expression Profiling,Oligonucleotide Array Sequence Analysis}

-}

-

-@article{brazmaMINSEQEMinimumInformation2012,

- title = {{{MINSEQE}}: {{Minimum Information}} about a High-Throughput {{Nucleotide SeQuencing Experiment}} - a Proposal for Standards in Functional Genomic Data Reporting},

- shorttitle = {{{MINSEQE}}},

- author = {Brazma, Alvis and Ball, Catherine and Bumgarner, Roger and Furlanello, Cesare and Miller, Michael and Quackenbush, John and Reich, Michael and Rustici, Gabriella and Stoeckert, Chris and Trutane, Stephen Chervitz and Taylor, Ronald C},

- date = {2012-06-01},

- publisher = {Zenodo},

- doi = {10.5281/zenodo.5706412},

- abstract = {MINSEQE~describes the~Minimum Information about a high-throughput nucleotide SEQuencing Experiment~that is needed to enable the unambiguous interpretation and facilitate reproduction of the results of the~experiment. By analogy to the~MIAME~guidelines for microarray experiments, adherence to the MINSEQE guidelines will improve~integration of multiple experiments across different modalities, thereby maximising the value of high-throughput research.~ The five elements of experimental description considered essential when making data available supporting published high-throughput sequencing experiments are as follows: The description of the biological system, samples, and the experimental variables being studied: “compound” and “dose” in dose-response experiments or “antibody” in ChIP-Seq experiments,~the organism, tissue, and the ~treatment(s) applied. The sequence read data for each assay: read sequences and base-level quality scores for each assay;~FASTQ~format is recommended, with a description of the scale used for quality scores. The ‘final’ processed (or summary) data for the set of assays in the study: the data on which the conclusions in the related publication are based, and~descriptions of the data format. General information about the experiment and sample-data relationships: a summary of the experiment and its goals, contact information, any associated publication, and a~table specifying sample-data relationships. Essential experimental and data processing protocols: how the nucleic acid samples were isolated, purified and processed prior to sequencing,~a summary of the instrumentation used, library preparation strategy, labelling and amplification methodologies, alignment algorithms and data filtering plus data processing \& analysis protocols. The present document contains version 1.0 of the MINSEQE guidelines, which~originated from discussions at an FGED-organized workshop held in Berkeley in March 2008.},

- langid = {english},

- keywords = {nucleotide sequencing genome transcriptome genomics transcriptomics reproducibility standards publication}

-}

-

-@article{breenEvolutionarilyConservedCytogenetic2008,

- title = {Evolutionarily Conserved Cytogenetic Changes in Hematological Malignancies of Dogs and Humans – Man and His Best Friend Share More than Companionship},

- author = {Breen, Matthew and Modiano, Jaime F.},

- date = {2008-03-01},

- journaltitle = {Chromosome Research},

- shortjournal = {Chromosome Res},

- volume = {16},

- number = {1},

- pages = {145--154},

- issn = {1573-6849},

- doi = {10.1007/s10577-007-1212-4},

- abstract = {The pathophysiological similarities shared by many forms of human and canine disease, combined with the sophisticated genomic resources now available for the dog, have placed ‘man’s best friend’ in a position of high visibility as a model system for a variety of biomedical concerns, including cancer. The importance of nonrandom cytogenetic abnormalities in human leukemia and lymphoma was recognized over 40~years ago, but the mechanisms of genome reorganization remain incompletely understood. The development of molecular cytogenetics, using fluorescence in situ hybridization (FISH) technology, has played a significant role in our understanding of cancer biology by providing a means for ‘interrogating’ tumor cells for a variety of gross genetic changes in the form of either numerical or structural chromosome aberrations. Here, we have identified cytogenetic abnormalities in naturally occurring canine hematopoietic tumors that are evolutionarily conserved compared with those that are considered characteristic of the corresponding human condition. These data suggest that humans and dogs share an ancestrally retained pathogenetic basis for cancer and that cytogenetic evaluation of canine tumors may provide greater insight into the biology of tumorigenesis.},

- langid = {english}

-}

-

-@article{bresciaMEF2BInstructsGerminal2018,

- title = {{{MEF2B Instructs Germinal Center Development}} and {{Acts}} as an {{Oncogene}} in {{B Cell Lymphomagenesis}}},

- author = {Brescia, Paola and Schneider, Christof and Holmes, Antony B. and Shen, Qiong and Hussein, Shafinaz and Pasqualucci, Laura and Basso, Katia and Dalla-Favera, Riccardo},

- date = {2018-09-10},

- journaltitle = {Cancer Cell},

- shortjournal = {Cancer Cell},

- volume = {34},

- number = {3},

- eprint = {30205047},

- eprinttype = {pmid},

- pages = {453-465.e9},

- issn = {1535-6108, 1878-3686},

- doi = {10.1016/j.ccell.2018.08.006},

- langid = {english},

- keywords = {B cell,germinal center,lymphoma,MEF2B,mouse model}

-}

-

-@article{breunisCopyNumberVariation2009,

- title = {Copy Number Variation at the {{FCGR}} Locus Includes {{FCGR3A}}, {{FCGR2C}} and {{FCGR3B}} but Not {{FCGR2A}} and {{FCGR2B}}.},

- author = {Breunis, Willemijn B and family=Mirre, given=Edwin, prefix=van, useprefix=true and Geissler, Judy and Laddach, Nadja and Wolbink, Gertjan and family=Schoot, given=Ellen, prefix=van der, useprefix=true and family=Haas, given=Masja, prefix=de, useprefix=true and family=Boer, given=Martin, prefix=de, useprefix=true and Roos, Dirk and Kuijpers, Taco W},

- date = {2009-05},

- journaltitle = {Human mutation},

- volume = {30},

- number = {5},

- pages = {E640--50}

-}

-

-@article{brooksPanCancerAnalysisTranscriptome2014,

- title = {A {{Pan-Cancer Analysis}} of {{Transcriptome Changes Associated}} with {{Somatic Mutations}} in {{U2AF1 Reveals Commonly Altered Splicing Events}}},

- author = {Brooks, Angela N. and Choi, Peter S. and family=Waal, given=Luc, prefix=de, useprefix=false and Sharifnia, Tanaz and Imielinski, Marcin and Saksena, Gordon and Pedamallu, Chandra Sekhar and Sivachenko, Andrey and Rosenberg, Mara and Chmielecki, Juliann and Lawrence, Michael S. and DeLuca, David S. and Getz, Gad and Meyerson, Matthew},

- date = {2014-01-31},

- journaltitle = {PLOS ONE},

- shortjournal = {PLOS ONE},

- volume = {9},

- number = {1},

- pages = {e87361},

- publisher = {Public Library of Science},

- issn = {1932-6203},

- doi = {10.1371/journal.pone.0087361},

- abstract = {Although recurrent somatic mutations in the splicing factor U2AF1 (also known as U2AF35) have been identified in multiple cancer types, the effects of these mutations on the cancer transcriptome have yet to be fully elucidated. Here, we identified splicing alterations associated with U2AF1 mutations across distinct cancers using DNA and RNA sequencing data from The Cancer Genome Atlas (TCGA). Using RNA-Seq data from 182 lung adenocarcinomas and 167 acute myeloid leukemias (AML), in which U2AF1 is somatically mutated in 3–4\% of cases, we identified 131 and 369 splicing alterations, respectively, that were significantly associated with U2AF1 mutation. Of these, 30 splicing alterations were statistically significant in both lung adenocarcinoma and AML, including three genes in the Cancer Gene Census, CTNNB1, CHCHD7, and PICALM. Cell line experiments expressing U2AF1 S34F in HeLa cells and in 293T cells provide further support that these altered splicing events are caused by U2AF1 mutation. Consistent with the function of U2AF1 in 3′ splice site recognition, we found that S34F/Y mutations cause preferences for CAG over UAG 3′ splice site sequences. This report demonstrates consistent effects of U2AF1 mutation on splicing in distinct cancer cell types.},

- langid = {english},

- keywords = {Acute myeloid leukemia,Adenocarcinoma,Adenocarcinoma of the lung,Alternative splicing,HeLa cells,Lung and intrathoracic tumors,Mutation,Somatic mutation}

-}

-

-@article{bruunGlobalIdentificationHnRNP2016,

- title = {Global Identification of {{hnRNP A1}} Binding Sites for {{SSO-based}} Splicing Modulation},

- author = {Bruun, Gitte H. and Doktor, Thomas K. and Borch-Jensen, Jonas and Masuda, Akio and Krainer, Adrian R. and Ohno, Kinji and Andresen, Brage S.},

- date = {2016-07-05},

- journaltitle = {BMC Biology},

- shortjournal = {BMC Biology},

- volume = {14},

- number = {1},

- pages = {54},

- issn = {1741-7007},

- doi = {10.1186/s12915-016-0279-9},

- abstract = {Many pathogenic genetic variants have been shown to disrupt mRNA splicing. Besides splice mutations in the well-conserved splice sites, mutations in splicing regulatory elements (SREs) may deregulate splicing and cause disease. A promising therapeutic approach is to compensate for this deregulation by blocking other SREs with splice-switching oligonucleotides (SSOs). However, the location and sequence of most SREs are not well known.},

- keywords = {Alternative splicing,Cross-linking immunoprecipitation (CLIP),hnRNP A1,iCLIP,Pseudoexons,RNA-seq,Splicing silencer,Splicing splice-switching oligonucleotides (SSOs),Surface plasmon resonance imaging (SPRi)}

-}

-

-@article{buntingNewEffectorFunctions2013,

- title = {New Effector Functions and Regulatory Mechanisms of {{BCL6}} in Normal and Malignant Lymphocytes},

- author = {Bunting, Karen L. and Melnick, Ari M.},

- date = {2013-06},

- journaltitle = {Current opinion in immunology},

- shortjournal = {Curr Opin Immunol},

- volume = {25},

- number = {3},

- eprint = {23725655},

- eprinttype = {pmid},

- pages = {339--346},

- issn = {0952-7915},

- doi = {10.1016/j.coi.2013.05.003},

- abstract = {The BCL6 oncogenic repressor is a master regulator of humoral immunity and B-cell lymphoma survival. Whereas much research has focused on its regulation and function in germinal center B-cells, its role in other mature lymphoid cell compartments is less clear. A novel role for BCL6 in follicular T helper cell development was recently uncovered. The latest discoveries reveal that BCL6 is also an important regulator of other specialized helper T-cell subsets within germinal centers, pre-germinal center events, and peripheral T-cells effector functions. Here, we review newly discovered roles for BCL6 in lymphocyte subsets residing within and outside of germinal centers, and discuss their implications with respect to the molecular mechanisms of BCL6 regulation and potential links to B and T-cell lymphomas.},

- pmcid = {PMC4075446}

-}

-@article{burrowsCellDevelopmentDifferentiation1997,

- title = {B Cell Development and Differentiation},

- author = {Burrows, Peter D and Cooper, Max D},

- date = {1997-04-01},

- journaltitle = {Current Opinion in Immunology},

- shortjournal = {Current Opinion in Immunology},

- volume = {9},

- number = {2},

- pages = {239--244},

- issn = {0952-7915},

- doi = {10.1016/S0952-7915(97)80142-2},

- abstract = {The initial phases of B cell development depend on interactions between the cell surface molecules and secreted products of stromal cells with their receptor-ligand partners on lymphoid progenitors. Recent research in this area has greatly advanced our understanding of B cell development and differentiation. Antigen receptors on pre-B and B cells play key roles in the progression of this differentiation process, as revealed by targeted and inherited gene mutations that disrupt B cell development and by the transgenic repair of these mutations in mice.},

- langid = {english}

-}

-

-@article{burtonNCIComparativeOncology2018,

- title = {{{NCI Comparative Oncology Program Testing}} of {{Non-Camptothecin Indenoisoquinoline Topoisomerase I Inhibitors}} in {{Naturally Occurring Canine Lymphoma}}},

- author = {Burton, Jenna H. and Mazcko, Christina and LeBlanc, Amy and Covey, Joseph M. and Ji, Jiuping and Kinders, Robert J. and Parchment, Ralph E. and Khanna, Chand and Paoloni, Melissa and Lana, Sue and Weishaar, Kristen and London, Cheryl and Kisseberth, William and Krick, Erika and Vail, David and Childress, Michael and Bryan, Jeffrey N. and Barber, Lisa and Ehrhart, E. J. and Kent, Michael and Fan, Timothy and Kow, Kelvin and Northup, Nicole and Wilson-Robles, Heather and Tomaszewski, Joseph and Holleran, Julianne L. and Muzzio, Miguel and Eiseman, Julie and Beumer, Jan H. and Doroshow, James H. and Pommier, Yves},

- date = {2018-12-01},

- journaltitle = {Clinical Cancer Research},

- shortjournal = {Clin Cancer Res},

- volume = {24},

- number = {23},

- eprint = {30061364},

- eprinttype = {pmid},

- pages = {5830--5840},

- publisher = {American Association for Cancer Research},

- issn = {1078-0432, 1557-3265},

- doi = {10.1158/1078-0432.CCR-18-1498},

- abstract = {Purpose: Only one chemical class of topoisomerase I (TOP1) inhibitors is FDA approved, the camptothecins with irinotecan and topotecan widely used. Because of their limitations (chemical instability, drug efflux-mediated resistance, and diarrhea), novel TOP1 inhibitors are warranted. Indenoisoquinoline non-camptothecin topoisomerase I (TOP1) inhibitors overcome chemical instability and drug resistance that limit camptothecin use. Three indenoisoquinolines, LMP400 (indotecan), LMP776 (indimitecan), and LMP744, were examined in a phase I study for lymphoma-bearing dogs to evaluate differential efficacy, pharmacodynamics, toxicology, and pharmacokinetics. Experimental Design: Eighty-four client-owned dogs with lymphomas were enrolled in dose-escalation cohorts for each indenoisoquinoline, with an expansion phase for LMP744. Efficacy, tolerability, pharmacokinetics, and target engagement were determined. Results: The MTDs were 17.5 mg/m2 for LMP 776 and 100 mg/m2 for LMP744; bone marrow toxicity was dose-limiting; up to 65 mg/m2 LMP400 was well-tolerated and MTD was not reached. None of the drugs induced notable diarrhea. Sustained tumor accumulation was observed for LMP744; γH2AX induction was demonstrated in tumors 2 and 6 hours after treatment; a decrease in TOP1 protein was observed in most lymphoma samples across all compounds and dose levels, which is consistent with the fact that tumor response was also observed at low doses LMP744. Objective responses were documented for all indenoisoquinolines; efficacy (13/19 dogs) was greatest for LMP744. Conclusions: These results demonstrate proof-of-mechanism for indenoisoquinoline TOP1 inhibitors supporting their further clinical development. They also highlight the value of the NCI Comparative Oncology Program (https://ccr.cancer.gov/Comparative-Oncology-Program) for evaluating novel therapies in immunocompetent pets with cancers.},

- langid = {english}

-}

-

-@article{bushellGeneticInactivationTRAF32015,

- title = {Genetic Inactivation of {{TRAF3}} in Canine and Human {{B-cell}} Lymphoma},

- author = {Bushell, Kevin R. and Kim, Yukyoung and Chan, Fong Chun and Ben-Neriah, Susana and Jenks, Andrew and Alcaide, Miguel and Fornika, Daniel and Grande, Bruno M. and Arthur, Sarah and Gascoyne, Randy D. and Steidl, Christian and Morin, Ryan D.},

- date = {2015-02-05},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {125},

- number = {6},

- eprint = {25468570},

- eprinttype = {pmid},

- pages = {999--1005},

- issn = {1528-0020},

- doi = {10.1182/blood-2014-10-602714},

- abstract = {Non-Hodgkin lymphomas (NHLs) are the most common cancer to affect pet dogs. In contrast to the many genes whose mutation contributes to lymphomagenesis in humans, relatively little is known about the acquired genetic alterations that lead to canine B-cell lymphomas (cBCLs). We performed a survey of 84 canine NHL tumors to identify genes affected by somatic point mutations. We found mutations affecting TRAF3, which encodes a negative regulator of nuclear factor (NF)-κB, to be a common feature of cBCLs, with mutations observed in 44\% of tumors including a combination of somatic and rare germ-line variants. Overall, 30\% of the tumors contained ≥1 somatic TRAF3 mutation. The majority of mutations are predicted to cause loss of TRAF3 protein including those impacting reading frame and splicing. To determine whether TRAF3 loss might be relevant to human NHL, we also analyzed 148 human diffuse large B-cell lymphoma (DLBCL) tumors and identified loss of TRAF3 as a common event, affecting ∼9\% of DLBCLs, and reduced expression of TRAF3 among deleted cases. This study implicates mutations affecting NF-κB activity as a novel genetic commonality between human and canine NHLs and supports the potential utility of cBCLs with mutated TRAF3 as a model of the more aggressive activated B-cell subgroup of DLBCL.},

- langid = {english},

- keywords = {Animals,B-Lymphocytes,Dogs,Gene Deletion,Gene Expression Regulation Neoplastic,Humans,Lymphoma B-Cell,Lymphoma Large B-Cell Diffuse,Mutation,NF-kappa B,TNF Receptor-Associated Factor 3}

-}

-

-@article{bustinMIQEGuidelinesMinimum2009,

- title = {The {{MIQE Guidelines}}: {{Minimum Information}} for {{Publication}} of {{Quantitative Real-Time PCR Experiments}}},

- shorttitle = {The {{MIQE Guidelines}}},

- author = {Bustin, Stephen A and Benes, Vladimir and Garson, Jeremy A and Hellemans, Jan and Huggett, Jim and Kubista, Mikael and Mueller, Reinhold and Nolan, Tania and Pfaffl, Michael W and Shipley, Gregory L and Vandesompele, Jo and Wittwer, Carl T},

- date = {2009-04-01},

- journaltitle = {Clinical Chemistry},

- shortjournal = {Clinical Chemistry},

- volume = {55},

- number = {4},

- pages = {611--622},

- issn = {0009-9147},

- doi = {10.1373/clinchem.2008.112797},

- abstract = {Background: Currently, a lack of consensus exists on how best to perform and interpret quantitative real-time PCR (qPCR) experiments. The problem is exacerbated by a lack of sufficient experimental detail in many publications, which impedes a reader’s ability to evaluate critically the quality of the results presented or to repeat the experiments.Content: The Minimum Information for Publication of Quantitative Real-Time PCR Experiments (MIQE) guidelines target the reliability of results to help ensure the integrity of the scientific literature, promote consistency between laboratories, and increase experimental transparency. MIQE is a set of guidelines that describe the minimum information necessary for evaluating qPCR experiments. Included is a checklist to accompany the initial submission of a manuscript to the publisher. By providing all relevant experimental conditions and assay characteristics, reviewers can assess the validity of the protocols used. Full disclosure of all reagents, sequences, and analysis methods is necessary to enable other investigators to reproduce results. MIQE details should be published either in abbreviated form or as an online supplement.Summary: Following these guidelines will encourage better experimental practice, allowing more reliable and unequivocal interpretation of qPCR results.}

-}

-

-@article{butcharReciprocalRegulationActivating2010,

- title = {Reciprocal {{Regulation}} of {{Activating}} and {{Inhibitory Fcγ Receptors}} by {{TLR7}}/8 {{Activation}}: {{Implications}} for {{Tumor Immunotherapy}}},

- author = {Butchar, J P and Mehta, P and Justiniano, S E and Guenterberg, K D and Kondadasula, S V and Mo, X and Chemudupati, M and Kanneganti, T D and Amer, A and Muthusamy, N and Jarjoura, D and Marsh, C B and Carson, W E and Byrd, J C and Tridandapani, S},

- date = {2010-03},

- journaltitle = {Clin Cancer Res},

- volume = {16},

- number = {7},

- pages = {1--12}

-}

-

-@article{callananIgGFcReceptor2000,

- title = {The {{IgG Fc}} Receptor, {{FcγRIIB}}, Is a Target for Deregulation by Chromosomal Translocation in Malignant Lymphoma},

- author = {Callanan, Mary B. and Baccon, Patricia Le and Mossuz, Pascal and Duley, Samuel and Bastard, Christian and Hamoudi, Rifat and Dyer, Martin J. and Klobeck, Gustav and Rimokh, Ruth and Sotto, Jean Jacques and Leroux, Dominique},

- date = {2000},

- journaltitle = {Proceedings of the National Academy of Sciences},

- volume = {97},

- number = {1},

- eprint = {10618414},

- eprinttype = {pmid},

- pages = {309--314},

- issn = {0027-8424},

- doi = {10.1073/pnas.97.1.309},

- url = {http://dx.doi.org/10.1073/pnas.97.1.309},

- abstract = {Rearrangement of chromosomal bands 1q21–23 is one of the most frequent chromosomal aberrations observed in hematological malignancy. The genes affected by these rearrangements remain poorly characterized. Typically, 1q21–23 rearrangements arise during tumor evolution and accompany disease-specific chromosomal rearrangements such as t(14;18) (BCL2) and t(8;14) (MYC), where they are thus thought to play an important role in tumor progression. The pathogenetic basis of this 1q21–23-associated disease progression is currently unknown. In this setting, we surveyed our series of follicular lymphoma for evidence of recurring 1q21–23 breaks and identified three cases in which a t(14;18)(q32;q21) was accompanied by a novel balanced t(1;22)(q22;q11). Molecular cloning of the t(1;22) in a cell line (B593) derived from one of these cases and detailed fluorescent in situ hybridization mapping in the two remaining cases identified the FCGR2B gene, which encodes the immunoreceptor tyrosine-based inhibition motif-bearing IgG Fc receptor, FcγRIIB, as the target gene of the t(1;22)(q22;q11). We demonstrate deregulation of FCGR2B leading to hyperexpression of FcγRIIb2 as the principal consequence of the t(1;22). This is evidence that IgG Fc receptors can be targets for deregulation through chromosomal translocation in lymphoma. It suggests that dysregulation of FCGR2B may play a role in tumor progression in follicular lymphoma.}

-}

-

-@article{camilleri-broetFcgammaRIIBDifferentiallyExpressed2004,

- title = {{{FcgammaRIIB}} Is Differentially Expressed during {{B}} Cell Maturation and in {{B-cell}} Lymphomas.},

- author = {Camilleri-Broët, Sophie and Cassard, Lydie and Broët, Philippe and Delmer, Alain and Le Touneau, Agnès and Diebold, Jacques and Fridman, Wolf Herman and Molina, Thierry Jo and Sautès-Fridman, Catherine},

- date = {2004-01},

- journaltitle = {Br J Haematol},

- volume = {124},

- number = {1},

- pages = {55--62}

-}

-

-@article{campoInternationalConsensusClassification2022,

- title = {The {{International Consensus Classification}} of {{Mature Lymphoid Neoplasms}}: A Report from the {{Clinical Advisory Committee}}},

- shorttitle = {The {{International Consensus Classification}} of {{Mature Lymphoid Neoplasms}}},

- author = {Campo, Elias and Jaffe, Elaine S. and Cook, James R. and Quintanilla-Martinez, Leticia and Swerdlow, Steven H. and Anderson, Kenneth C. and Brousset, Pierre and Cerroni, Lorenzo and family=Leval, given=Laurence, prefix=de, useprefix=true and Dirnhofer, Stefan and Dogan, Ahmet and Feldman, Andrew L. and Fend, Falko and Friedberg, Jonathan W. and Gaulard, Philippe and Ghia, Paolo and Horwitz, Steven M. and King, Rebecca L. and Salles, Gilles and San-Miguel, Jesus and Seymour, John F. and Treon, Steven P. and Vose, Julie M. and Zucca, Emanuele and Advani, Ranjana and Ansell, Stephen and Au, Wing-Yan and Barrionuevo, Carlos and Bergsagel, Leif and Chan, Wing C. and Cohen, Jeffrey I. and family=Amore, given=Francesco, prefix=d', useprefix=true and Davies, Andrew and Falini, Brunangelo and Ghobrial, Irene M. and Goodlad, John R. and Gribben, John G. and Hsi, Eric D. and Kahl, Brad S. and Kim, Won-Seog and Kumar, Shaji and LaCasce, Ann S. and Laurent, Camille and Lenz, Georg and Leonard, John P. and Link, Michael P. and Lopez-Guillermo, Armando and Mateos, Maria Victoria and Macintyre, Elizabeth and Melnick, Ari M. and Morschhauser, Franck and Nakamura, Shigeo and Narbaitz, Marina and Pavlovsky, Astrid and Pileri, Stefano A. and Piris, Miguel and Pro, Barbara and Rajkumar, Vincent and Rosen, Steven T. and Sander, Birgitta and Sehn, Laurie and Shipp, Margaret A. and Smith, Sonali M. and Staudt, Louis M. and Thieblemont, Catherine and Tousseyn, Thomas and Wilson, Wyndham H. and Yoshino, Tadashi and Zinzani, Pier-Luigi and Dreyling, Martin and Scott, David W. and Winter, Jane N. and Zelenetz, Andrew D.},

- date = {2022-09-15},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {140},

- number = {11},

- eprint = {35653592},

- eprinttype = {pmid},

- pages = {1229--1253},

- issn = {1528-0020},

- doi = {10.1182/blood.2022015851},

- abstract = {Since the publication of the Revised European-American Classification of Lymphoid Neoplasms in 1994, subsequent updates of the classification of lymphoid neoplasms have been generated through iterative international efforts to achieve broad consensus among hematopathologists, geneticists, molecular scientists, and clinicians. Significant progress has recently been made in the characterization of malignancies of the immune system, with many new insights provided by genomic studies. They have led to this proposal. We have followed the same process that was successfully used for the third and fourth editions of the World Health Organization Classification of Hematologic Neoplasms. The definition, recommended studies, and criteria for the diagnosis of many entities have been extensively refined. Some categories considered provisional have now been upgraded to definite entities. Terminology for some diseases has been revised to adapt nomenclature to the current knowledge of their biology, but these modifications have been restricted to well-justified situations. Major findings from recent genomic studies have impacted the conceptual framework and diagnostic criteria for many disease entities. These changes will have an impact on optimal clinical management. The conclusions of this work are summarized in this report as the proposed International Consensus Classification of mature lymphoid, histiocytic, and dendritic cell tumors.},

- langid = {english},

- pmcid = {PMC9479027},

- keywords = {Advisory Committees,Consensus,Hematologic Neoplasms,Humans,Lymphoma,World Health Organization}

-}

-

-@article{cannellPleiotropicRNABindingProtein2015,

- title = {A {{Pleiotropic RNA-Binding Protein Controls Distinct Cell Cycle Checkpoints}} to {{Drive Resistance}} of P53-Defective {{Tumors}} to {{Chemotherapy}}},

- author = {Cannell, Ian G and Merrick, Karl A and Morandell, Sandra and Zhu, Chang-Qi and Braun, Christian J and Grant, Robert A and Cameron, Eleanor R and Tsao, Ming-Sound and Hemann, Michael T and Yaffe, Michael B},

- date = {2015-11-09},

- journaltitle = {Cancer cell},

- shortjournal = {Cancer Cell},

- volume = {28},

- number = {5},

- eprint = {26602816},

- eprinttype = {pmid},

- pages = {623--637},

- issn = {1535-6108},

- doi = {10.1016/j.ccell.2015.09.009},

- abstract = {In normal cells p53 is activated by DNA damage checkpoint kinases to simultaneously control the G1/S and G2/M cell cycle checkpoints through transcriptional induction of p21cip1 and Gadd45α. In p53 mutant tumors, cell cycle checkpoints are rewired, leading to dependency on the p38/MK2 pathway to survive DNA-damaging chemotherapy. Here we show that the RNA binding protein hnRNPA0 is the “successor” to p53 for checkpoint control. Like p53, hnRNPA0 is activated by a checkpoint kinase (MK2) and simultaneously controls both cell cycle checkpoints through distinct target mRNAs, but unlike p53 this is through the post-transcriptional stabilization of p27Kip1 and Gadd45α mRNAs. This pathway drives cisplatin resistance in lung cancer demonstrating the importance of post-transcriptional RNA control to chemotherapy response.,},

- pmcid = {PMC4830093}

-}

-

-@article{cannonEarlyStorageSedentism2006,

- title = {Early {{Storage}} and {{Sedentism}} on the {{Pacific Northwest Coast}}: {{Ancient DNA Analysis}} of {{Salmon Remains}} from {{Namu}}, {{British Columbia}}},

- shorttitle = {Early {{Storage}} and {{Sedentism}} on the {{Pacific Northwest Coast}}},

- author = {Cannon, Aubrey and Yang, Dongya Y.},

- date = {2006-01},

- journaltitle = {American Antiquity},

- volume = {71},

- number = {1},

- pages = {123--140},

- issn = {0002-7316, 2325-5064},

- doi = {10.2307/40035324},

- url = {https://www.cambridge.org/core/journals/american-antiquity/article/early-storage-and-sedentism-on-the-pacific-northwest-coast-ancient-dna-analysis-of-salmon-remains-from-namu-british-columbia/55BF5175B9F47DCB521786EF5F8EF3BC},

- urldate = {2018-10-27},

- abstract = {Ancient DNA identification of salmon remains from the site of Namu on the central coast of British Columbia shows use of a variety of species and an emphasis on pink salmon over the course of the past 7,000 years. These results support arguments that Namu was a permanent village settlement dependent on a salmon storage economy throughout this time. This pattern of subsistence and settlement predates by several millennia the first substantial evidence for population expansion or social differentiation in the region. Periodic salmon shortages in the period after 2000 cal B.C., which are associated with local and regional disruptions in settlement and increased reliance on more marginal resources, appear to be the result of failures in the pink salmon fishery. , Résumé La identificación del ADN antiguo en remanentes de salmón obtenidos en el sitio Namu en la costa central de la Columbia Británica, constituye evidencia de la utilización de una variedad de especies, con preferencia por el salmón rosado, a través de los últimos 7000 años. Dichos resultados vendrían a apoyar la hipótesis de que Namu sería un asentamiento permanente, que dependería económicamente del almacenamiento de salmón. Este patrón de subsistencia y de asentamiento vendría a ser más temprano, por varios milenios, que la importante primera evidencia de una expansión poblacional o de una diferenciación social en esta región. La escasez periódica del salmón en el período posterior al 2000 cal B.C., asociada con trastornos en los asentamientos locales y regionales y con un incremento de la dependencia sobre recursos más marginales, vendrían a ser producto del fracaso en la pesca del salmón rosado.},

- langid = {english}

-}

-

-@article{caoControlAlternativeSplicing2012,

- title = {Control of Alternative Splicing by Forskolin through {{hnRNP K}} during Neuronal Differentiation},

- author = {Cao, Wenguang and Razanau, Aleh and Feng, Dairong and Lobo, Vincent G. and Xie, Jiuyong},

- date = {2012-09},

- journaltitle = {Nucleic Acids Research},

- shortjournal = {Nucleic Acids Res},

- volume = {40},

- number = {16},

- eprint = {22684629},

- eprinttype = {pmid},

- pages = {8059--8071},

- issn = {0305-1048},

- doi = {10.1093/nar/gks504},

- url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3439897/},

- urldate = {2022-09-22},

- abstract = {The molecular basis of cell signal-regulated alternative splicing at the 3′ splice site remains largely unknown. We isolated a protein kinase A-responsive ribonucleic acid (RNA) element from a 3′ splice site of the synaptosomal-associated protein 25 (Snap25) gene for forskolin-inhibited splicing during neuronal differentiation of rat pheochromocytoma PC12 cells. The element binds specifically to heterogeneous nuclear ribonucleo protein (hnRNP) K in a phosphatase-sensitive way, which directly competes with the U2 auxiliary factor U2AF65, an essential component of early spliceosomes. Transcripts with similarly localized hnRNP K target motifs upstream of alternative exons are enriched in genes often associated with neurological diseases. We show that such motifs upstream of the Runx1 exon 6 also bind hnRNP K, and importantly, hnRNP K is required for forskolin-induced repression of the exon. Interestingly, this exon encodes the peptide domain that determines the switch of the transcriptional repressor/activator activity of Runx1, a change known to be critical in specifying neuron lineages. Consistent with an important role of the target genes in neurons, knocking down hnRNP K severely disrupts forskolin-induced neurite growth. Thus, through hnRNP K, the neuronal differentiation stimulus forskolin targets a critical 3′ splice site component of the splicing machinery to control alternative splicing of crucial genes. This also provides a regulated direct competitor of U2AF65 for cell signal control of 3′ splice site usage.},

- pmcid = {PMC3439897}

-}

-

-@article{caputiDeterminationRNABinding2001,

- title = {Determination of the {{RNA Binding Specificity}} of the {{Heterogeneous Nuclear Ribonucleoprotein}} ({{hnRNP}}) {{H}}/{{H}}′/{{F}}/{{2H9 Family}} *},

- author = {Caputi, Massimo and Zahler, Alan M.},

- date = {2001-11-23},

- journaltitle = {Journal of Biological Chemistry},

- shortjournal = {Journal of Biological Chemistry},

- volume = {276},

- number = {47},

- eprint = {11571276},

- eprinttype = {pmid},

- pages = {43850--43859},

- publisher = {Elsevier},

- issn = {0021-9258, 1083-351X},

- doi = {10.1074/jbc.M102861200},

- url = {https://www.jbc.org/article/S0021-9258(19)82817-X/abstract},

- urldate = {2022-09-26},

- abstract = {{$<$}p{$>$}Members of the heterogeneous nuclear ribonucleoprotein (hnRNP) H protein family, H, H′, F, and 2H9, are involved in pre-mRNA processing. We analyzed the assembly of these proteins from splicing extracts onto four RNA regulatory elements as follows: a high affinity hnRNP A1-binding site (WA1), a sequence involved in Rev-dependent export (p17gag INS), an exonic splicing silencer from the β-tropomyosin gene, and an intronic splicing regulator (downstream control sequence (DCS) from the c-\emph{src} gene. The entire family binds the WA1, instability (INS), and β-tropomyosin substrates, and the core-binding site for each is a run of three G residues followed by an A. Transfer of small regions containing this sequence to a substrate lacking hnRNP H binding activity is sufficient to promote binding of all family members. The c-\emph{src} DCS has been shown to assemble hnRNP H, not hnRNP F, from HeLa cell extracts, and we show that hnRNP 2H9 does not bind this element. The DCS contains five G residues followed by a C. Mutation of the C to an A changes the specificity of the DCS from a substrate that binds only hnRNP H/H′ to a binding site for all hnRNP H family members. We conclude that the sequence GGGA is recognized by all hnRNP H family proteins.{$<$}/p{$>$}},

- langid = {english}

-}

-

-@article{carabetComputerAidedDiscoverySmall2019,

- title = {Computer-{{Aided Discovery}} of {{Small Molecules Targeting}} the {{RNA Splicing Activity}} of {{hnRNP A1}} in {{Castration-Resistant Prostate Cancer}}},

- author = {Carabet, Lavinia A. and Leblanc, Eric and Lallous, Nada and Morin, Helene and Ghaidi, Fariba and Lee, Joseph and Rennie, Paul S. and Cherkasov, Artem},

- date = {2019-02-20},

- journaltitle = {Molecules (Basel, Switzerland)},

- shortjournal = {Molecules},

- volume = {24},

- number = {4},

- eprint = {30791548},

- eprinttype = {pmid},

- pages = {E763},

- issn = {1420-3049},

- doi = {10.3390/molecules24040763},

- abstract = {The heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) is a versatile RNA-binding protein playing a critical role in alternative pre-mRNA splicing regulation in cancer. Emerging data have implicated hnRNP A1 as a central player in a splicing regulatory circuit involving its direct transcriptional control by c-Myc oncoprotein and the production of the constitutively active ligand-independent alternative splice variant of androgen receptor, AR-V7, which promotes castration-resistant prostate cancer (CRPC). As there is an urgent need for effective CRPC drugs, targeting hnRNP A1 could, therefore, serve a dual purpose of preventing AR-V7 generation as well as reducing c-Myc transcriptional output. Herein, we report compound VPC-80051 as the first small molecule inhibitor of hnRNP A1 splicing activity discovered to date by using a computer-aided drug discovery approach. The inhibitor was developed to target the RNA-binding domain (RBD) of hnRNP A1. Further experimental evaluation demonstrated that VPC-80051 interacts directly with hnRNP A1 RBD and reduces AR-V7 messenger levels in 22Rv1 CRPC cell line. This study lays the groundwork for future structure-based development of more potent and selective small molecule inhibitors of hnRNP A1⁻RNA interactions aimed at altering the production of cancer-specific alternative splice isoforms.},

- langid = {english},

- pmcid = {PMC6413181},

- keywords = {alternative splicing,Binding Sites,castration-resistant prostate cancer,Cell Line Tumor,Computational Biology,Computer Simulation,computer-aided drug discovery,Drug Discovery,Gene Expression Regulation Neoplastic,Heterogeneous Nuclear Ribonucleoprotein A1,hnRNP A1,Humans,Male,Models Molecular,Molecular Conformation,Prostatic Neoplasms Castration-Resistant,protein–RNA interactions,RNA Splicing,small molecule inhibitors,Structure-Activity Relationship}

-}

-@article{carnetrecessonBCLXLDirectlyModulates2017,

- title = {{{BCL-XL}} Directly Modulates {{RAS}} Signalling to Favour Cancer Cell Stemness},

- author = {family=Carné Trécesson, given=Sophie, prefix=de, useprefix=false and Souazé, Frédérique and Basseville, Agnès and Bernard, Anne-Charlotte and Pécot, Jessie and Lopez, Jonathan and Bessou, Margaux and Sarosiek, Kristopher A. and Letai, Anthony and Barillé-Nion, Sophie and Valo, Isabelle and Coqueret, Olivier and Guette, Catherine and Campone, Mario and Gautier, Fabien and Juin, Philippe Paul},

- date = {2017-10-24},

- journaltitle = {Nature Communications},

- shortjournal = {Nat Commun},

- volume = {8},

- eprint = {29066722},

- eprinttype = {pmid},

- pages = {1123},

- issn = {2041-1723},

- doi = {10.1038/s41467-017-01079-1},

- url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5654832/},

- urldate = {2022-10-04},

- abstract = {In tumours, accumulation of chemoresistant cells that express high levels of anti-apoptotic proteins such as BCL-XL is thought to result from the counter selection of sensitive, low expresser clones during progression and/or initial treatment. We herein show that BCL-XL expression is selectively advantageous to cancer cell populations even in the absence of pro-apoptotic pressure. In transformed human mammary epithelial cells BCL-XL favours full activation of signalling downstream of constitutively active RAS with which it interacts in a BH4-dependent manner. Comparative proteomic analysis and functional assays indicate that this is critical for RAS-induced expression of stemness regulators and maintenance of a cancer initiating cell (CIC) phenotype. Resistant cancer cells thus arise from a positive selection driven by BCL-XL modulation of RAS-induced self-renewal, and during which apoptotic resistance is not necessarily the directly selected trait., BCL-XL provides a survival advantage to cancer cells even in the absence of apoptotic pressures. In this study, the authors show that BCL-XL interacts with RAS in a BH4-dependent manner and regulates RAS-mediated activation of pathways involved in the stemness feature of breast cancer cells.},

- pmcid = {PMC5654832}

-}

-

-@article{carpenterHeterogeneousNuclearRibonucleoprotein2006,

- title = {Heterogeneous Nuclear Ribonucleoprotein {{K}} Is over Expressed, Aberrantly Localised and Is Associated with Poor Prognosis in Colorectal Cancer},

- author = {Carpenter, B. and McKay, M. and Dundas, S. R. and Lawrie, L. C. and Telfer, C. and Murray, G. I.},

- date = {2006-10},

- journaltitle = {British Journal of Cancer},

- shortjournal = {Br J Cancer},

- volume = {95},

- number = {7},

- pages = {921--927},

- publisher = {Nature Publishing Group},

- issn = {1532-1827},

- doi = {10.1038/sj.bjc.6603349},

- url = {https://www.nature.com/articles/6603349},

- urldate = {2023-01-09},

- abstract = {Heterogeneous ribonucleoprotein K (hnRNP K) is a member of the hnRNP family which has several different cellular roles including transcription, mRNA shuttling, RNA editing and translation. Several reports implicate hnRNP K having a role in tumorigenesis, for instance hnRNP K increases transcription of the oncogene c-myc and hnRNP K expression is regulated by the p53/MDM 2 pathway. In this study comparing normal colon to colorectal cancer by proteomics, hnRNP K was identified as being overexpressed in this type of cancer. Immunohistochemistry with a monoclonal antibody to hnRNP K (which we developed) on colorectal cancer tissue microarray, confirmed that hnRNP K was overexpressed in colorectal cancer (P{$<$}0.001) and also showed that hnRNP K had an aberrant subcellular localisation in cancer cells. In normal colon hnRNP K was exclusively nuclear whereas in colorectal cancer the protein localised both in the cytoplasm and the nucleus. There were significant increases in both nuclear (P=0.007) and cytoplasmic (P=0.001) expression of hnRNP K in Dukes C tumours compared with early stage tumours. In Dukes C patient's good survival was associated with increased hnRNP K nuclear expression (P=0.0093). To elaborate on the recent observation that hnRNP K is regulated by p53, the expression profiles of these two proteins were also analysed. There was no correlation between hnRNP K and p53 expression, however, patients who presented tumours that were positive for hnRNP K and p53 had a poorer survival outcome (P=0.045).},

- issue = {7},

- langid = {english},

- keywords = {Biomedicine,Cancer Research,Drug Resistance,Epidemiology,general,Molecular Medicine,Oncology}

-}

-

-@article{castelo-brancoPolypyrimidineTractBinding2004,

- title = {Polypyrimidine {{Tract Binding Protein Modulates Efficiency}} of {{Polyadenylation}}},

- author = {Castelo-Branco, Pedro and Furger, Andre and Wollerton, Matthew and Smith, Christopher and Moreira, Alexandra and Proudfoot, Nick},

- date = {2004-05-15},

- journaltitle = {Molecular and Cellular Biology},

- volume = {24},

- number = {10},

- pages = {4174--4183},

- publisher = {American Society for Microbiology},

- doi = {10.1128/MCB.24.10.4174-4183.2004},

- url = {https://journals.asm.org/doi/full/10.1128/MCB.24.10.4174-4183.2004},

- urldate = {2022-09-27}

-}

-

-@article{cattorettiDeregulatedBCL6Expression,

- title = {Deregulated {{BCL6}} Expression Recapitulates the Pathogenesis of Human Diffuse Large {{B}} Cell Lymphomas in Mice},

- author = {Cattoretti, Giorgio and Pasqualucci, Laura and Ballon, Gianna and Tam, Wayne and Nandula, Subhadra V and Shen, Qiong and Mo, Tongwei and Murty, Vundavalli V and Dalla-Favera, Riccardo},

- journaltitle = {Cancer Cell},

- volume = {7},

- number = {5},

- pages = {445--455}

-}

-

-@article{cattorettiTargetedDisruptionS1P22009,

- title = {Targeted {{Disruption}} of the {{S1P2 Sphingosine}} 1-{{Phosphate Receptor Gene Leads}} to {{Diffuse Large B-Cell Lymphoma Formation}}},

- author = {Cattoretti, G and Cattoretti, G and Mandelbaum, J and Mandelbaum, J and Lee, N and Lee, N and Chaves, A H and Chaves, A H and Mahler, A M and Mahler, A M and Chadburn, A and Dalla-Favera, R and Pasqualucci, L and MacLennan, A J and MacLennan, A J},

- date = {2009-11},

- journaltitle = {Cancer Res},

- volume = {69},

- number = {22},

- pages = {8686--8692}

-}

-

-@online{CellDevelopmentPathways,

- title = {B Cell Development Pathways - {{ProQuest}}},

- url = {https://www.proquest.com/openview/dd4dd441a1e721485aa871b6e812c2d9/1?casa_token=oL4JXwb4PmAAAAAA:a05XBzPaGKSPDIrAWvwnlVXDB-bn8l3cKX0AQ5lllmjo9zPxpqzckoiCzUkPoAs0C7TDTeBPQuw&cbl=47332&pq-origsite=gscholar&parentSessionId=vkSsFp6eiGXrMO9pT3aWhVFysFqfdTwKAN1ymj7w48c%3D},

- urldate = {2022-10-06},

- abstract = {Explore millions of resources from scholarly journals, books, newspapers, videos and more, on the ProQuest Platform.},

- langid = {english}

-}

-

-@article{cerchiettiPurineScaffoldHsp902009,

- title = {A Purine Scaffold {{Hsp90}} Inhibitor Destabilizes {{BCL-6}} and Has Specific Antitumor Activity in {{BCL-6}}–Dependent {{B}} Cell Lymphomas},

- author = {Cerchietti, Leandro C. and Lopes, Eloisi C. and Yang, Shao Ning and Hatzi, Katerina and Bunting, Karen L. and Tsikitas, Lucas A. and Mallik, Alka and Robles, Ana I. and Walling, Jennifer and Varticovski, Lyuba and Shaknovich, Rita and Bhalla, Kapil N. and Chiosis, Gabriela and Melnick, Ari},

- date = {2009-12},

- journaltitle = {Nature Medicine},

- shortjournal = {Nat Med},

- volume = {15},

- number = {12},

- pages = {1369--1376},

- publisher = {Nature Publishing Group},

- issn = {1546-170X},

- doi = {10.1038/nm.2059},

- url = {https://www.nature.com/articles/nm.2059},

- urldate = {2022-10-04},

- abstract = {By taking advantage of the direct interaction between heat shock protein 90 (Hsp90) and the transcriptional repressor Bcl-6, a purine-derived inhibitor of Hsp90 selectively kills diffuse large B cell lymphomas that depend on the expression of Bcl-6 for their survival.},

- issue = {12},

- langid = {english},

- keywords = {Biomedicine,Cancer Research,general,Infectious Diseases,Metabolic Diseases,Molecular Medicine,Neurosciences}

-}

-

-@article{chadburnImmunophenotypicAnalysisAIDSrelated,

- title = {Immunophenotypic Analysis of {{AIDS-related}} Diffuse Large {{B-cell}} Lymphoma and Clinical Implications in Patients from {{AIDS Malignancies Consortium}} Clinical Trials 010 and 034.},

- author = {Chadburn, Amy and Chiu, April and Lee, Jeannette Y and Chen, Xia and Hyjek, Elizabeth and Banham, Alison H and Noy, Ariela and Kaplan, Lawrence D and Sparano, Joseph A and Bhatia, Kishor and Cesarman, Ethel},

- journaltitle = {J Clin Oncol},

- volume = {27},

- number = {30},

- pages = {5039--5048}

-}

-

-@article{changRNAbindingProteinHnRNPLL2015,

- title = {{{RNA-binding}} Protein {{hnRNPLL}} Regulates {{mRNA}} Splicing and Stability during {{B-cell}} to Plasma-Cell Differentiation},

- author = {Chang, Xing and Li, Bin and Rao, Anjana},

- date = {2015-04-14},

- journaltitle = {Proceedings of the National Academy of Sciences},

- volume = {112},

- number = {15},

- pages = {E1888-E1897},

- publisher = {Proceedings of the National Academy of Sciences},

- doi = {10.1073/pnas.1422490112},

- url = {https://www.pnas.org/doi/10.1073/pnas.1422490112},

- urldate = {2022-10-06}

-}

-

-@article{changTargetingPanessentialGenes2021,

- title = {Targeting Pan-Essential Genes in Cancer: {{Challenges}} and Opportunities},

- shorttitle = {Targeting Pan-Essential Genes in Cancer},

- author = {Chang, Liang and Ruiz, Paloma and Ito, Takahiro and Sellers, William R.},

- date = {2021-04-12},

- journaltitle = {Cancer Cell},

- shortjournal = {Cancer Cell},

- volume = {39},

- number = {4},

- pages = {466--479},

- issn = {1535-6108},

- doi = {10.1016/j.ccell.2020.12.008},

- url = {https://www.sciencedirect.com/science/article/pii/S1535610820306565},

- urldate = {2023-01-09},

- abstract = {Despite remarkable successes in the clinic, cancer targeted therapy development remains challenging and the failure rate is disappointingly high. This problem is partly due to the misapplication of the targeted therapy paradigm to therapeutics targeting pan-essential genes, which can result in therapeutics whereby efficacy is attenuated by dose-limiting toxicity. Here we summarize the key features of successful chemotherapy and targeted therapy agents, and use case studies to outline recurrent challenges to drug development efforts targeting pan-essential genes. Finally, we suggest strategies to avoid previous pitfalls for ongoing and future development of pan-essential therapeutics.},

- langid = {english},

- keywords = {drug development,pan-essential genes,target identification,target validation,targeted therapies}

-}

-

-@article{chanPathogenesisDiffuseLarge2010,

- title = {Pathogenesis of Diffuse Large {{B}} Cell Lymphoma},

- author = {Chan, Wing John C},

- date = {2010-06},

- journaltitle = {International journal of hematology},

- volume = {92},

- number = {2},

- pages = {219--230}

-}

-

-@article{chaudhuryHeterogeneousNuclearRibonucleoproteins2010,

- title = {Heterogeneous Nuclear Ribonucleoproteins ({{hnRNPs}}) in Cellular Processes: {{Focus}} on {{hnRNP E1}}'s Multifunctional Regulatory Roles},

- shorttitle = {Heterogeneous Nuclear Ribonucleoproteins ({{hnRNPs}}) in Cellular Processes},

- author = {Chaudhury, Arindam and Chander, Praveen and Howe, Philip H.},

- date = {2010-08},

- journaltitle = {RNA},

- shortjournal = {RNA},

- volume = {16},

- number = {8},

- eprint = {20584894},

- eprinttype = {pmid},

- pages = {1449--1462},

- issn = {1355-8382},

- doi = {10.1261/rna.2254110},

- url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2905745/},

- urldate = {2022-09-28},

- abstract = {Heterogeneous nuclear ribonucleoproteins (hnRNPs) comprise a family of RNA-binding proteins. The complexity and diversity associated with the hnRNPs render them multifunctional, involved not only in processing heterogeneous nuclear RNAs (hnRNAs) into mature mRNAs, but also acting as trans-factors in regulating gene expression. Heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1), a subgroup of hnRNPs, is a KH-triple repeat containing RNA-binding protein. It is encoded by an intronless gene arising from hnRNP E2 through a retrotransposition event. hnRNP E1 is ubiquitously expressed and functions in regulating major steps of gene expression, including pre-mRNA processing, mRNA stability, and translation. Given its wide-ranging functions in the nucleus and cytoplasm and interaction with multiple proteins, we propose a post-transcriptional regulon model that explains hnRNP E1's widespread functional diversity.},

- pmcid = {PMC2905745}

-}

-

-@article{chaudhuryTGFbetamediatedPhosphorylationHnRNP2010,

- title = {{{TGF-beta-mediated}} Phosphorylation of {{hnRNP E1}} Induces {{EMT}} via Transcript-Selective Translational Induction of {{Dab2}} and {{ILEI}}},

- author = {Chaudhury, Arindam and Hussey, George S. and Ray, Partho S. and Jin, Ge and Fox, Paul L. and Howe, Philip H.},

- date = {2010-03},

- journaltitle = {Nature Cell Biology},

- shortjournal = {Nat Cell Biol},

- volume = {12},

- number = {3},

- eprint = {20154680},

- eprinttype = {pmid},

- pages = {286--293},

- issn = {1476-4679},

- doi = {10.1038/ncb2029},

- abstract = {Transforming growth factor-beta (TGF-beta) induces epithelial-mesenchymal transdifferentiation (EMT) accompanied by cellular differentiation and migration. Despite extensive transcriptomic profiling, the identification of TGF-beta-inducible, EMT-specific genes has met with limited success. Here we identify a post-transcriptional pathway by which TGF-beta modulates the expression of EMT-specific proteins and of EMT itself. We show that heterogeneous nuclear ribonucleoprotein E1 (hnRNP E1) binds a structural, 33-nucleotide TGF-beta-activated translation (BAT) element in the 3' untranslated region of disabled-2 (Dab2) and interleukin-like EMT inducer (ILEI) transcripts, and represses their translation. TGF-beta activation leads to phosphorylation at Ser 43 of hnRNP E1 by protein kinase Bbeta/Akt2, inducing its release from the BAT element and translational activation of Dab2 and ILEI messenger RNAs. Modulation of hnRNP E1 expression or its post-translational modification alters the TGF-beta-mediated reversal of translational silencing of the target transcripts and EMT. These results suggest the existence of a TGF-beta-inducible post-transcriptional regulon that controls EMT during the development and metastatic progression of tumours.},

- langid = {english},

- pmcid = {PMC2830561},

- keywords = {3' Untranslated Regions,Adaptor Proteins Signal Transducing,Adaptor Proteins Vesicular Transport,Animals,Apoptosis Regulatory Proteins,Cadherins,Carrier Proteins,Cell Line Transformed,Cell Transdifferentiation,Cytokines,DNA-Binding Proteins,Epithelial Cells,Female,Gene Expression,Gene Expression Regulation Neoplastic,Insulin,Mammary Glands Animal,Mesoderm,Mice,Neoplasm Proteins,Phosphorylation,Polyribosomes,Protein Binding,Protein Biosynthesis,Protein Isoforms,Protein Kinase Inhibitors,Proto-Oncogene Proteins c-akt,RNA Messenger,RNA Small Interfering,RNA-Binding Proteins,Signal Transduction,Transforming Growth Factor beta,Vimentin}

-}

-@article{chenBenchmarkingLongReadAssemblers2020,

- title = {Benchmarking {{Long-Read Assemblers}} for {{Genomic Analyses}} of {{Bacterial Pathogens Using Oxford Nanopore Sequencing}}},

- author = {Chen, Zhao and Erickson, David L. and Meng, Jianghong},

- date = {2020-01},

- journaltitle = {International Journal of Molecular Sciences},

- volume = {21},

- number = {23},

- pages = {9161},

- publisher = {Multidisciplinary Digital Publishing Institute},

- issn = {1422-0067},

- doi = {10.3390/ijms21239161},

- url = {https://www.mdpi.com/1422-0067/21/23/9161},

- urldate = {2022-02-07},

- abstract = {Oxford Nanopore sequencing can be used to achieve complete bacterial genomes. However, the error rates of Oxford Nanopore long reads are greater compared to Illumina short reads. Long-read assemblers using a variety of assembly algorithms have been developed to overcome this deficiency, which have not been benchmarked for genomic analyses of bacterial pathogens using Oxford Nanopore long reads. In this study, long-read assemblers, namely Canu, Flye, Miniasm/Racon, Raven, Redbean, and Shasta, were thus benchmarked using Oxford Nanopore long reads of bacterial pathogens. Ten species were tested for mediocre- and low-quality simulated reads, and 10 species were tested for real reads. Raven was the most robust assembler, obtaining complete and accurate genomes. All Miniasm/Racon and Raven assemblies of mediocre-quality reads provided accurate antimicrobial resistance (AMR) profiles, while the Raven assembly of Klebsiella variicola with low-quality reads was the only assembly with an accurate AMR profile among all assemblers and species. All assemblers functioned well for predicting virulence genes using mediocre-quality and real reads, whereas only the Raven assemblies of low-quality reads had accurate numbers of virulence genes. Regarding multilocus sequence typing (MLST), Miniasm/Racon was the most effective assembler for mediocre-quality reads, while only the Raven assemblies of Escherichia coli O157:H7 and K. variicola with low-quality reads showed positive MLST results. Miniasm/Racon and Raven were the best performers for MLST using real reads. The Miniasm/Racon and Raven assemblies showed accurate phylogenetic inference. For the pan-genome analyses, Raven was the strongest assembler for simulated reads, whereas Miniasm/Racon and Raven performed the best for real reads. Overall, the most robust and accurate assembler was Raven, closely followed by Miniasm/Racon.},

- issue = {23},

- langid = {english},

- keywords = {bacterial pathogen,benchmarking,genome assembly,genomic analysis,long-read assembler,long-read sequencing,Oxford Nanopore sequencing,whole-genome sequencing}

-}

-

-@article{chenBindingHnRNPExonic1999,

- title = {Binding of {{hnRNP H}} to an Exonic Splicing Silencer Is Involved in the Regulation of Alternative Splicing of the Rat β-Tropomyosin Gene},

- author = {Chen, Charlie Degui and Kobayashi, Ryuji and Helfman, David M.},

- date = {1999-01-03},

- journaltitle = {Genes \& Development},

- shortjournal = {Genes Dev.},

- volume = {13},

- number = {5},

- eprint = {10072387},

- eprinttype = {pmid},

- pages = {593--606},

- publisher = {Cold Spring Harbor Lab},

- issn = {0890-9369, 1549-5477},

- url = {http://genesdev.cshlp.org/content/13/5/593},

- urldate = {2022-09-27},

- abstract = {In the rat β-tropomyosin (β-TM) gene, exons 6 and 7 are spliced alternatively in a mutually exclusive manner. Exon 6 is included in mRNA encoding nonmuscle TM-1, whereas exon 7 is used in mRNA encoding skeletal muscle β-TM. Previously, we demonstrated that a six nucleotide mutation at the 5′ end of exon 7, designated as ex-1, activated exon 7 splicing in nonmuscle cells. In this study, we show that the activating effect of this mutation is not the result of creating an exonic splicing enhancer (ESE) or disrupting a putative secondary structure. The sequence in exon 7 acts as a bona fide exonic splicing silencer (ESS), which is bound specifically by atrans-acting factor. Isolation and peptide sequencing reveal that this factor is hnRNP H, a member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family. Binding of hnRNP H correlates with the ESS activity. Furthermore, addition of antibodies that specifically recognizes hnRNP H to the splicing reactions or partial depletion of hnRNP H from nuclear extract activates exon 7 splicing in vitro and this effect can be reversed by addition of purified recombinant hnRNP H. These results indicate that hnRNP H participates in exclusion of exon 7 in nonmuscle cells. The involvement of hnRNP H in the activity of an ESS may represent a prototype for the regulation of tissue- and developmental-specific alternative splicing.},

- langid = {english},

- keywords = {cis-acting element,heterogeneous nuclear ribonucleoproteins,RNA processing,RNA–protein interaction,trans-acting factor}

-}

-

-@article{chenDeregulationFCGR2BExpression2001,

- title = {Deregulation of {{FCGR2B}} Expression by 1q21 Rearrangements in Follicular Lymphomas},

- author = {Chen, Weiyi and Palanisamy, Nallasivam and Schmidt, Helmut and Teruya-Feldstein, Julie and Jhanwar, Suresh C and Zelenetz, Andrew D and Houldsworth, Jane and Chaganti, R},

- date = {2001-01},

- journaltitle = {Oncogene},

- volume = {20},

- number = {52},

- eprint = {11753646},

- eprinttype = {pmid},

- pages = {1204989},

- issn = {1476-5594},

- doi = {10.1038/sj.onc.1204989},

- url = {http://dx.doi.org/10.1038/sj.onc.1204989},

- abstract = {We report here the molecular cloning and characterization of a t(1;14)(q21;q32) in a follicular lymphoma (FL) with an unusual BCL2 aberration. Fluorescence in situ hybridization (FISH) and Southern blot analysis of tumor cells identified the translocation breakpoint within the 5′ switch region of IGHG (Sγ). We cloned the chimeric breakpoint region approximately 1.5 kbp downstream from the HindIII site of 5′Sγ2 on chromosome 14q32 and identified a 360-bp novel segment with homology to the CpG island clone 11h8. Two BAC clones containing this sequence were isolated and mapped to 1q21 by FISH. BAC 342/P13 contained sequences homologous to Fcγ receptors 2A, 3A, 2B, 3B, and a heat shock protein gene HSP70B. The translocation brought the Sγ2 region of a productive IGH allele 20∼30 kbp upstream of FCGR2B. As a result of the translocation, the b2 isoform of FCGR2B was overexpressed in the tumor. Screening of a panel of 76 B-cell lymphomas with 1q21-23 cytogenetic aberrations by Southern blot analysis using breakpoint probes identified an additional FL with a t(14;18)(q32;q21) and a breakpoint in the FCGR2B region. These results suggest that FCGR2B may be deregulated by 1q21 aberration in BCL2 rearranged FLs and possibly play a role in their progression.}

-}

-

-@article{chenIndolentMantleCell2009,

- title = {Indolent {{Mantle Cell Lymphoma}}: {{A Distinct Subgroup Characterized}} by {{Leukemic Phase Disease}} without {{Lymphadenopathy}}.},

- shorttitle = {Indolent {{Mantle Cell Lymphoma}}},

- author = {Chen, Dong and Viswanatha, David S. and Zent, Clive S. and Shanafelt, Tait D. and Call, Timothy G. and Kay, Neil E. and Van Dyke, Daniel L. and Ketterling, Rhett P. and Witzig, Thomas E. and Morice, William G. and Hanson, Curtis A.},

- date = {2009-11-20},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {114},

- number = {22},

- pages = {3937--3937},

- issn = {0006-4971},

- doi = {10.1182/blood.V114.22.3937.3937},

- url = {https://ashpublications.org/blood/article/114/22/3937/76125/Indolent-Mantle-Cell-Lymphoma-A-Distinct-Subgroup},

- urldate = {2019-12-21},

- langid = {english}

-}

-

-@article{chenMantaRapidDetection2016,

- title = {Manta: Rapid Detection of Structural Variants and Indels for Germline and Cancer Sequencing Applications},

- shorttitle = {Manta},

- author = {Chen, Xiaoyu and Schulz-Trieglaff, Ole and Shaw, Richard and Barnes, Bret and Schlesinger, Felix and Källberg, Morten and Cox, Anthony J. and Kruglyak, Semyon and Saunders, Christopher T.},

- date = {2016-04-15},

- journaltitle = {Bioinformatics (Oxford, England)},

- shortjournal = {Bioinformatics},

- volume = {32},

- number = {8},

- eprint = {26647377},

- eprinttype = {pmid},

- pages = {1220--1222},

- issn = {1367-4811},

- doi = {10.1093/bioinformatics/btv710},

- abstract = {: We describe Manta, a method to discover structural variants and indels from next generation sequencing data. Manta is optimized for rapid germline and somatic analysis, calling structural variants, medium-sized indels and large insertions on standard compute hardware in less than a tenth of the time that comparable methods require to identify only subsets of these variant types: for example NA12878 at 50× genomic coverage is analyzed in less than 20\,min. Manta can discover and score variants based on supporting paired and split-read evidence, with scoring models optimized for germline analysis of diploid individuals and somatic analysis of tumor-normal sample pairs. Call quality is similar to or better than comparable methods, as determined by pedigree consistency of germline calls and comparison of somatic calls to COSMIC database variants. Manta consistently assembles a higher fraction of its calls to base-pair resolution, allowing for improved downstream annotation and analysis of clinical significance. We provide Manta as a community resource to facilitate practical and routine structural variant analysis in clinical and research sequencing scenarios. AVAILABILITY AND IMPLEMENTATION: Manta is released under the open-source GPLv3 license. Source code, documentation and Linux binaries are available from https://github.com/Illumina/manta. CONTACT: csaunders@illumina.com SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.},

- langid = {english},

- keywords = {DNA Neoplasm,Genome,Genomics,High-Throughput Nucleotide Sequencing,Humans,INDEL Mutation,Neoplasms,Software}

-}

-@article{chenThymidinePhosphorylaseMRNA2009,

- title = {Thymidine Phosphorylase {{mRNA}} Stability and Protein Levels Are Increased through {{ERK-mediated}} Cytoplasmic Accumulation of {{hnRNP K}} in Nasopharyngeal Carcinoma Cells},

- author = {Chen, L.-C. and Liu, H.-P. and Li, H.-P. and Hsueh, C. and Yu, J.-S. and Liang, C.-L. and Chang, Y.-S.},

- date = {2009-04},

- journaltitle = {Oncogene},

- volume = {28},

- number = {17},

- pages = {1904--1915},

- publisher = {Nature Publishing Group},

- issn = {1476-5594},

- doi = {10.1038/onc.2009.55},

- url = {https://www.nature.com/articles/onc200955},

- urldate = {2022-09-28},

- abstract = {The cytoplasmic level of heterogeneous nuclear ribonucleoprotein K (hnRNP K) is significantly correlated with the elevated expression of thymidine phosphorylase (TP), and high levels of both proteins are predictive of a poor prognosis in nasopharyngeal carcinoma (NPC). We herein show that TP is highly induced by serum deprivation in NPC cells, and that this is due to an increase in the half-life of the TP mRNA, as shown by nuclear run-on and actinomycin D assays. We further show that the CU-rich element of the TP mRNA directly interacts with hnRNP K, as demonstrated by immunoprecipitation RT–PCR assays, and the nucleus-to-cytoplasm translocation of hnRNP K. Blockade of hnRNP K expression reduces TP expression, suggesting that hnRNP K acts in the upregulation of TP. Mechanistically, both MEK inhibitor and the hnRNP K ERK-phosphoacceptor-site mutant decrease cytoplasmic accumulation of hnRNP K, suggesting that ERK-dependent phosphorylation is critical for TP induction. Furthermore, we found that hnRNP K-mediated TP induction allows NPC cells to resist hypoxia-induced apoptosis. Our results collectively establish the regulation and role of ERK-mediated cytoplasmic accumulation of hnRNP K as an upstream modulator of TP, suggesting that hnRNP K may be an attractive candidate as a future therapeutic target for cancer.},

- issue = {17},

- langid = {english},

- keywords = {Apoptosis,Cell Biology,general,Human Genetics,Internal Medicine,Medicine/Public Health,Oncology}

-}

-

-@article{chesonOblimersenTreatmentPatients2007,

- title = {Oblimersen for the Treatment of Patients with Chronic Lymphocytic Leukemia},

- author = {Cheson, Bruce D},

- date = {2007-10},

- journaltitle = {Therapeutics and Clinical Risk Management},

- shortjournal = {Ther Clin Risk Manag},

- volume = {3},

- number = {5},

- eprint = {18473009},

- eprinttype = {pmid},

- pages = {855--870},

- issn = {1176-6336},

- url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2376092/},

- urldate = {2020-09-22},

- abstract = {Among adults in Western countries, chronic lymphocytic leukemia (CLL) is the most prevalent form of leukemia. CLL primarily affects the elderly and may be associated with multiple comorbidities. A cure has not been identified, and new treatment options are needed. Expression of Bcl-2 protein is associated with the pathogenesis of CLL and chemotherapy resistance. Oblimersen, a Bcl-2 antisense phosphorothioate oligonucleotide, is being evaluated in patients with CLL and other cancers; trials through Phase III have been completed. In the setting of relapsed/refractory CLL, single-agent oblimersen demonstrates modest activity, whereas the addition of oblimersen to fludarabine/cyclophosphamide significantly improves the rate of complete and nodular partial responses; moreover, these responses are durable and associated with clinical benefit. Oblimersen is more efficacious in relapsed rather than refractory patients. The side effect profile of oblimersen, alone or in combination with standard chemotherapy, is favorable compared with currently available chemotherapies. In the first cycle, an infusion reaction with or without tumor lysis syndrome is uncommon, and transient thrombocytopenia is observed. Catheter-related complications are associated with the need for continuous intravenous infusion of oblimersen over several days; other routes of administration are under clinical investigation. Oblimersen is a promising therapeutic approach for patients with relapsed CLL and should be further evaluated in the front-line setting.},

- pmcid = {PMC2376092}

-}

-@article{chouHnRNPComponentSplicing1999,

- title = {{{hnRNP H}} Is a Component of a Splicing Enhancer Complex That Activates a C-Src Alternative Exon in Neuronal Cells},

- author = {Chou, M. Y. and Rooke, N. and Turck, C. W. and Black, D. L.},

- date = {1999-01},

- journaltitle = {Molecular and Cellular Biology},

- shortjournal = {Mol Cell Biol},

- volume = {19},

- number = {1},

- eprint = {9858532},

- eprinttype = {pmid},

- pages = {69--77},

- issn = {0270-7306},

- doi = {10.1128/MCB.19.1.69},

- abstract = {The regulation of the c-src N1 exon is mediated by an intronic splicing enhancer downstream of the N1 5' splice site. Previous experiments showed that a set of proteins assembles onto the most conserved core of this enhancer sequence specifically in neuronal WERI-1 cell extracts. The most prominent components of this enhancer complex are the proteins hnRNP F, KSRP, and an unidentified protein of 58 kDa (p58). This p58 protein was purified from the WERI-1 cell nuclear extract by ammonium sulfate precipitation, Mono Q chromatography, and immunoprecipitation with anti-Sm antibody Y12. Peptide sequence analysis of purified p58 protein identified it as hnRNP H. Immunoprecipitation of hnRNP H cross-linked to the N1 enhancer RNA, as well as gel mobility shift analysis of the enhancer complex in the presence of hnRNP H-specific antibodies, confirmed that hnRNP H is a protein component of the splicing enhancer complex. Immunoprecipitation of splicing intermediates from in vitro splicing reactions with anti-hnRNP H antibody indicated that hnRNP H remains bound to the src pre-mRNA after the assembly of spliceosome. Partial immunodepletion of hnRNP H from the nuclear extract partially inactivated the splicing of the N1 exon in vitro. This inhibition of splicing can be restored by the addition of recombinant hnRNP H, indicating that hnRNP H is an important factor for N1 splicing. Finally, in vitro binding assays demonstrate that hnRNP H can interact with the related protein hnRNP F, suggesting that hnRNPs H and F may exist as a heterodimer in a single enhancer complex. These two proteins presumably cooperate with each other and with other enhancer complex proteins to direct splicing to the N1 exon upstream.},

- langid = {english},

- pmcid = {PMC83866},

- keywords = {Alternative Splicing,Dimerization,Enhancer Elements Genetic,Exons,Gene Expression Regulation,HeLa Cells,Heterogeneous-Nuclear Ribonucleoprotein Group F-H,Heterogeneous-Nuclear Ribonucleoproteins,Humans,Neurons,Proto-Oncogene Proteins pp60(c-src),Ribonucleoproteins,RNA Precursors,Spliceosomes}

-}

-

-@article{chunGenomeWideProfilesExtracranial2016,

- title = {Genome-{{Wide Profiles}} of {{Extra-cranial Malignant Rhabdoid Tumors Reveal Heterogeneity}} and {{Dysregulated Developmental Pathways}}},

- author = {Chun, Hye-Jung E. and Lim, Emilia L. and Heravi-Moussavi, Alireza and Saberi, Saeed and Mungall, Karen L. and Bilenky, Mikhail and Carles, Annaick and Tse, Kane and Shlafman, Inna and Zhu, Kelsey and Qian, Jenny Q. and Palmquist, Diana L. and He, An and Long, William and Goya, Rodrigo and Ng, Michelle and LeBlanc, Veronique G. and Pleasance, Erin and Thiessen, Nina and Wong, Tina and Chuah, Eric and Zhao, Yong-Jun and Schein, Jacquie E. and Gerhard, Daniela S. and Taylor, Michael D. and Mungall, Andrew J. and Moore, Richard A. and Ma, Yussanne and Jones, Steven J. M. and Perlman, Elizabeth J. and Hirst, Martin and Marra, Marco A.},

- date = {2016-03-14},

- journaltitle = {Cancer Cell},

- shortjournal = {Cancer Cell},

- volume = {29},

- number = {3},

- eprint = {26977886},

- eprinttype = {pmid},

- pages = {394--406},

- publisher = {Elsevier},

- issn = {1535-6108, 1878-3686},

- doi = {10.1016/j.ccell.2016.02.009},

- url = {https://www.cell.com/cancer-cell/abstract/S1535-6108(16)30043-5},

- urldate = {2022-11-23},

- langid = {english}

-}

-

-@article{chungSetNovelConserved1986,

- title = {Set of Novel, Conserved Proteins Fold Pre-Messenger {{RNA}} into Ribonucleosomes},

- author = {Chung, Su Yun and Wooley, John},

- date = {1986},

- journaltitle = {Proteins: Structure, Function, and Bioinformatics},

- volume = {1},

- number = {3},

- pages = {195--210},

- issn = {1097-0134},

- doi = {10.1002/prot.340010302},

- url = {http://onlinelibrary.wiley.com/doi/abs/10.1002/prot.340010302},

- urldate = {2022-10-06},

- langid = {english},

- keywords = {multiple binding sites,oligomeric assembly,protein domains,RNA splicing,RNP core proteins}

-}

-

-@article{ciborowskiNovelClassII2017,

- title = {Novel Class {{II}} Alpha {{MHC}} Variability in a Small Peripheral {{Atlantic}} Salmon Population},

- author = {Ciborowski, Kate L. and Jordan, William C. and García de Leániz, Carlos and Consuegra, Sofia},

- date = {2017-06},

- journaltitle = {Animal Genetics},

- shortjournal = {Anim. Genet.},

- volume = {48},

- number = {3},

- eprint = {28116806},

- eprinttype = {pmid},

- pages = {370--372},

- issn = {1365-2052},

- doi = {10.1111/age.12535},

- langid = {english},

- keywords = {Amino Acid Sequence,Animals,Genes MHC Class II,Genetic Variation,Genetics Population,Salmo salar}

-}

-

-@article{colganMechanismRegulationMRNA1997,

- title = {Mechanism and Regulation of {{mRNA}} Polyadenylation},

- author = {Colgan, Diana F. and Manley, James L.},

- date = {1997-01-11},

- journaltitle = {Genes \& Development},

- shortjournal = {Genes Dev.},

- volume = {11},

- number = {21},

- eprint = {9353246},

- eprinttype = {pmid},

- pages = {2755--2766},

- publisher = {Cold Spring Harbor Lab},

- issn = {0890-9369, 1549-5477},

- doi = {10.1101/gad.11.21.2755},

- url = {http://genesdev.cshlp.org/content/11/21/2755},

- urldate = {2022-10-06},

- abstract = {A biweekly scientific journal publishing high-quality research in molecular biology and genetics, cancer biology, biochemistry, and related fields},

- langid = {english}

-}