delete extraneous refs

-@article{kishorHnRNPLdependentProtection2019,

- title = {{{hnRNP L-dependent}} Protection of Normal {{mRNAs}} from {{NMD}} Subverts Quality Control in {{B}} Cell Lymphoma},

- author = {Kishor, Aparna and Ge, Zhiyun and Hogg, J Robert},

- date = {2019-02-01},

- journaltitle = {The EMBO Journal},

- shortjournal = {The EMBO Journal},

- volume = {38},

- number = {3},

- pages = {e99128},

- issn = {0261-4189},

- doi = {10.15252/embj.201899128},

- url = {https://www.embopress.org/doi/abs/10.15252/embj.201899128},

- urldate = {2019-12-23},

- abstract = {Abstract The human nonsense-mediated mRNA decay pathway (NMD) performs quality control and regulatory functions within complex post-transcriptional regulatory networks. In addition to degradation-promoting factors, efficient and accurate detection of NMD substrates involves proteins that safeguard normal mRNAs. Here, we identify hnRNP L as a factor that protects mRNAs with NMD-inducing features including long 3?UTRs. Using biochemical and transcriptome-wide approaches, we provide evidence that the susceptibility of a given transcript to NMD can be modulated by its 3?UTR length and ability to recruit hnRNP L. Integrating these findings with the previously defined role of polypyrimidine tract binding protein 1 in NMD evasion enables enhanced prediction of transcript susceptibility to NMD. Unexpectedly, this system is subverted in B cell lymphomas harboring translocations that produce BCL2:IGH fusion mRNAs. CRISPR/Cas9 deletion of hnRNP L binding sites near the BCL2 stop codon reduces expression of the fusion mRNAs and induces apoptosis. Together, our data indicate that protection by hnRNP L overrides the presence of multiple 3?UTR introns, allowing these aberrant mRNAs to evade NMD and promoting BCL2 overexpression and neoplasia.},

- keywords = {B cell lymphoma,BCL2,hnRNP L,nonsense-mediated mRNA decay,UPF1}

-}

-

-@article{klapperPatientAgeDiagnosis2012,

- title = {Patient Age at Diagnosis Is Associated with the Molecular Characteristics of Diffuse Large {{B-cell}} Lymphoma.},

- author = {Klapper, Wolfram and Kreuz, Markus and Kohler, Christian W and Burkhardt, Birgit and Szczepanowski, Monika and Salaverria, Itziar and Hummel, Michael and Loeffler, Markus and Pellissery, Shoji and Woessmann, Wilhelm and Schwänen, Carsten and Trümper, Lorenz and Wessendorf, Swen and Spang, Rainer and Hasenclever, Dirk and Siebert, Reiner and Krebshilfe, Molecular Mechanisms in Malignant Lymphomas Network Project of the Deutsche},

- date = {2012-02},

- journaltitle = {Blood},

- volume = {119},

- number = {8},

- pages = {1882--1887}

-}

-@article{kochanIFcombinedSmRNAFISH2016,

- title = {{{IF-combined smRNA FISH}} Reveals Interaction of {{MCPIP1}} Protein with {{IER3 mRNA}}.},

- author = {Kochan, Jakub and Wawro, Mateusz and Kasza, Aneta},

- date = {2016},

- journaltitle = {Biology Open},

- volume = {5},

- number = {7},

- pages = {889--898}

-}

-

-@article{koenigDistinctPhenotypePolarized2023,

- title = {A {{Distinct Phenotype}} of {{Polarized Memory B}} Cell Holds {{IgE Memory}}},

- author = {Koenig, Joshua F. E. and Knudsen, Niels Peter H. and Phelps, Allyssa and Bruton, Kelly and Hoof, Ilka and Lund, Gitte and Libera, Danielle Della and Lund, Anders and Christensen, Lars Harder and Glass, David R. and Walker, Tina and Fang, Allison and Waserman, Susan and Jordana, Manel and Andersen, Peter S.},

- date = {2023-01-25},

- journaltitle = {bioRxiv},

- pages = {2023.01.25.525495},

- doi = {10.1101/2023.01.25.525495},

- url = {https://www.biorxiv.org/content/10.1101/2023.01.25.525495v1},

- urldate = {2023-12-16},

- abstract = {Allergen-specific IgE antibodies mediate allergic pathology in diseases such as allergic rhinitis and food allergy. Memory B cells (MBCs) contribute to circulating IgE by regenerating IgE-producing plasma cells upon allergen encounter. We report a population of type 2 polarized MBCs defined as CD23hi, IL-4Rαhi, CD32low at the transcriptional and surface protein levels. These “MBC2s” are enriched in IgG1 and IgG4-expressing cells, while constitutively expressing germline transcripts for IgE. Allergen-specific B cells from patients with allergic rhinitis and food allergy were enriched in MBC2s. MBC2s generated allergen specific-IgE during sublingual immunotherapy, thereby identifying these cells as the primary reservoir of IgE. The identification of MBC2s provides insights into the maintenance of IgE memory, which is detrimental in allergic diseases, but which could be beneficial in protection against venoms and helminths. One-Sentence Summary Identification of a novel memory B cell subset which holds allergen specific IgE memory.},

- langid = {english}

-}

-

-@article{kogureWholegenomeLandscapeAdult2022,

- title = {Whole-Genome Landscape of Adult {{T-cell}} Leukemia/Lymphoma},

- author = {Kogure, Yasunori and Kameda, Takuro and Koya, Junji and Yoshimitsu, Makoto and Nosaka, Kisato and Yasunaga, Jun-Ichirou and Imaizumi, Yoshitaka and Watanabe, Mizuki and Saito, Yuki and Ito, Yuta and McClure, Marni B. and Tabata, Mariko and Shingaki, Sumito and Yoshifuji, Kota and Chiba, Kenichi and Okada, Ai and Kakiuchi, Nobuyuki and Nannya, Yasuhito and Kamiunten, Ayako and Tahira, Yuki and Akizuki, Keiichi and Sekine, Masaaki and Shide, Kotaro and Hidaka, Tomonori and Kubuki, Yoko and Kitanaka, Akira and Hidaka, Michihiro and Nakano, Nobuaki and Utsunomiya, Atae and Sica, R. Alejandro and Acuna-Villaorduna, Ana and Janakiram, Murali and Shah, Urvi and Ramos, Juan Carlos and Shibata, Tatsuhiro and Takeuchi, Kengo and Takaori-Kondo, Akifumi and Miyazaki, Yasushi and Matsuoka, Masao and Ishitsuka, Kenji and Shiraishi, Yuichi and Miyano, Satoru and Ogawa, Seishi and Ye, B. Hilda and Shimoda, Kazuya and Kataoka, Keisuke},

- date = {2022-02-17},

- journaltitle = {Blood},

- shortjournal = {Blood},

- volume = {139},

- number = {7},

- eprint = {34695199},

- eprinttype = {pmid},

- pages = {967--982},

- issn = {1528-0020},

- doi = {10.1182/blood.2021013568},

- abstract = {Adult T-cell leukemia/lymphoma (ATL) is an aggressive neoplasm immunophenotypically resembling regulatory T cells, associated with human T-cell leukemia virus type-1. Here, we performed whole-genome sequencing (WGS) of 150 ATL cases to reveal the overarching landscape of genetic alterations in ATL. We discovered frequent (33\%) loss-of-function alterations preferentially targeting the CIC long isoform, which were overlooked by previous exome-centric studies of various cancer types. Long but not short isoform-specific inactivation of Cic selectively increased CD4+CD25+Foxp3+ T cells in~vivo. We also found recurrent (13\%) 3'-truncations of REL, which induce transcriptional upregulation and generate gain-of-function proteins. More importantly, REL truncations are also common in diffuse large B-cell lymphoma, especially in germinal center B-cell-like subtype (12\%). In the non-coding genome, we identified recurrent mutations in regulatory elements, particularly splice sites, of several driver genes. In addition, we characterized the different mutational processes operative in clustered hypermutation sites within and outside immunoglobulin/T-cell receptor genes and identified the mutational enrichment at the binding sites of host and viral transcription factors, suggesting their activities in ATL. By combining the analyses for coding and noncoding mutations, structural variations, and copy number alterations, we discovered 56 recurrently altered driver genes, including 11 novel ones. Finally, ATL cases were classified into 2 molecular groups with distinct clinical and genetic characteristics based on the driver alteration profile. Our findings not only help to improve diagnostic and therapeutic strategies in ATL, but also provide insights into T-cell biology and have implications for genome-wide cancer driver discovery.},

- langid = {english},

- pmcid = {PMC8854674},

- keywords = {Animals,Ataxin-1,Biomarkers Tumor,DNA Copy Number Variations,Female,Gene Expression Regulation Neoplastic,Genome Human,Humans,Leukemia-Lymphoma Adult T-Cell,Mice,Mice Inbred C57BL,Mutation,Prognosis,Proto-Oncogene Proteins c-rel,Repressor Proteins,Survival Rate,Whole Exome Sequencing}

-}

-

-@article{kopetzGenomicClassifierColoPrint2015,

- title = {Genomic Classifier {{ColoPrint}} Predicts Recurrence in Stage {{II}} Colorectal Cancer Patients More Accurately than Clinical Factors},

- author = {Kopetz, Scott and Tabernero, Josep and Rosenberg, Robert and Jiang, Zhi-Qin and Moreno, Víctor and Bachleitner-Hofmann, Thomas and Lanza, Giovanni and Stork-Sloots, Lisette and Maru, Dipen and Simon, Iris and Capellà, Gabriel and Salazar, Ramon},

- date = {2015-02},

- journaltitle = {The Oncologist},

- shortjournal = {Oncologist},

- volume = {20},

- number = {2},

- eprint = {25561511},

- eprinttype = {pmid},

- pages = {127--133},

- issn = {1549-490X},

- doi = {10.1634/theoncologist.2014-0325},

- abstract = {BACKGROUND: Approximately 20\% of patients with stage II colorectal cancer will experience a relapse. Current clinical-pathologic stratification factors do not allow clear identification of these high-risk patients. ColoPrint (Agendia, Amsterdam, The Netherlands, http://www.agendia.com) is a gene expression classifier that distinguishes patients with low or high risk of disease relapse. METHODS: ColoPrint was developed using whole-genome expression data and validated in several independent validation cohorts. Stage II patients from these studies were pooled (n = 416), and ColoPrint was compared with clinical risk factors described in the National Comprehensive Cancer Network (NCCN) 2013 Guidelines for Colon Cancer. Median follow-up was 81 months. Most patients (70\%) did not receive adjuvant chemotherapy. Risk of relapse (ROR) was defined as survival until first event of recurrence or death from cancer. RESULTS: In the pooled stage II data set, ColoPrint identified 63\% of patients as low risk with a 5-year ROR of 10\%, whereas high-risk patients (37\%) had a 5-year ROR of 21\%, with a hazard ratio (HR) of 2.16 (p = .004). This remained significant in a multivariate model that included number of lymph nodes retrieved and microsatellite instability. In the T3 microsatellite-stable subgroup (n = 301), ColoPrint classified 59\% of patients as low risk with a 5-year ROR of 9.9\%. High-risk patients (31\%) had a 22.4\% ROR (HR: 2.41; p = .005). In contrast, the NCCN clinical high-risk factors were unable to distinguish high- and low-risk patients (15\% vs. 13\% ROR; p = .55). CONCLUSION: ColoPrint significantly improved prognostic accuracy independent of microsatellite status or clinical variables, facilitating the identification of patients at higher risk who might be considered for additional treatment.},

- langid = {english},

- pmcid = {PMC4319631},

- keywords = {Adult,Aged,Aged 80 and over,Colorectal Neoplasms,Female,Gene Expression Profiling,Gene Expression Regulation Neoplastic,Gene expression signature,Genomics,Humans,Male,Middle Aged,Neoplasm Recurrence Local,Neoplasm Staging,Netherlands,Prognosis,Risk Assessment,Risk classification,Risk prediction,Stage II colon cancer}

-}

-@article{kubuschokLearningFailuresDrug2017,

- title = {Learning from the Failures of Drug Discovery in {{B-cell}} Non-{{Hodgkin}} Lymphomas and Perspectives for the Future: Chronic Lymphocytic Leukemia and Diffuse Large {{B-cell}} Lymphoma as Two Ends of a Spectrum in Drug Development},

- author = {Kubuschok, Boris and Trepel, Martin},

- date = {2017},

- journaltitle = {Expert Opinion on Drug Discovery},

- volume = {12},

- number = {7},

- eprint = {28494631},

- eprinttype = {pmid},

- pages = {733--745},

- issn = {1746-0441},

- doi = {10.1080/17460441.2017.1329293},

- url = {http://dx.doi.org/10.1080/17460441.2017.1329293},

- abstract = {Introduction: Despite substantial recent advances, there is still an unmet need for better therapies in B-cell non Hodgkin lymphomas (B-NHL), especially in relapsed or refractory disease. Many novel targeted drugs have been developed based on a better molecular understanding of B-NHL. Areas covered: This article focuses on chronic lymphocytic leukemia (CLL) as a representative for indolent lymphomas and paradigmatic for the tremendous progress in treating B-NHL on the one hand and diffuse large B-cell lymphoma (DLBCL) as a representative for aggressive lymphomas and paradigmatic for many unsolved problems in lymphoma treatment or the other hand. We highlight salient points in current therapies targeting genetic, epigenetic, immunological and microenvironmental alterations. Possible reasons for drug failure in clinical trials like tumor heterogeneity, clonal evolution and drug resistance mechanisms are discussed. Based thereon, some perspectives for further drug discovery are given. Expert opinion: In view of the pathogenetic complexity of lymphomas, therapies targeting exclusively a single alteration may fail because resistance mechanisms are present either initially or evolve during treatment. Therefore, future therapies in B-NHL may have to target the greatest possible number of genetic, immunological or epigenetic alterations still allowing tolerability and to monitor these alterations during therapy.}

-}

-

-@article{kukalevActinHnRNPCooperate2005,

- title = {Actin and {{hnRNP U}} Cooperate for Productive Transcription by {{RNA}} Polymerase {{II}}},

- author = {Kukalev, Alexander and Nord, Ylva and Palmberg, Carina and Bergman, Tomas and Percipalle, Piergiorgio},

- date = {2005-03},

- journaltitle = {Nature Structural \& Molecular Biology},

- shortjournal = {Nat Struct Mol Biol},

- volume = {12},

- number = {3},

- pages = {238--244},

- publisher = {Nature Publishing Group},

- issn = {1545-9985},

- doi = {10.1038/nsmb904},

- url = {https://www.nature.com/articles/nsmb904},

- urldate = {2022-09-27},

- abstract = {To determine the role of actin–ribonucleoprotein complexes in transcription, we set out to identify novel actin-binding proteins associated with RNA polymerase II (Pol II). Using affinity chromatography on fractionated HeLa cells, we found that hnRNP U binds actin through a short amino acid sequence in its C-terminal domain. Post-transcriptional gene silencing of hnRNP U and nuclear microinjections of a short peptide encompassing the hnRNP U actin-binding sequence inhibited BrUTP incorporation in vivo. In living cells, we found that both actin and hnRNP U are associated with the phosphorylated C-terminal domain of Pol II, and antibodies to actin and hnRNP U blocked Pol II–mediated transcription. Taken together, our results indicate that a general actin-based mechanism is implicated in the transcription of most Pol II genes. Actin in complex with hnRNP U may carry out its regulatory role during the initial phases of transcription activation.},

- issue = {3},

- langid = {english},

- keywords = {Biochemistry,Biological Microscopy,general,Life Sciences,Membrane Biology,Protein Structure}

-}

-

-@article{kulkarniPosttranscriptionalRegulationHLAA2017,

- title = {Posttranscriptional {{Regulation}} of {{HLA-A Protein Expression}} by {{Alternative Polyadenylation Signals Involving}} the {{RNA-Binding Protein Syncrip}}},

- author = {Kulkarni, Smita and Ramsuran, Veron and Rucevic, Marijana and Singh, Sukhvinder and Lied, Alexandra and Kulkarni, Viraj and O'hUigin, Colm and Le Gall, Sylvie and Carrington, Mary},

- date = {2017-12-01},

- journaltitle = {Journal of Immunology (Baltimore, Md.: 1950)},

- shortjournal = {J Immunol},

- volume = {199},

- number = {11},

- eprint = {29055006},

- eprinttype = {pmid},

- pages = {3892--3899},

- issn = {1550-6606},

- doi = {10.4049/jimmunol.1700697},

- abstract = {Genomic variation in the untranslated region (UTR) has been shown to influence HLA class I expression level and associate with disease outcomes. Sequencing of the 3'UTR of common HLA-A alleles indicated the presence of two polyadenylation signals (PAS). The proximal PAS is conserved, whereas the distal PAS is disrupted within certain alleles by sequence variants. Using 3'RACE, we confirmed expression of two distinct forms of the HLA-A 3'UTR based on use of either the proximal or the distal PAS, which differ in length by 100 bp. Specific HLA-A alleles varied in the usage of the proximal versus distal PAS, with some alleles using only the proximal PAS, and others using both the proximal and distal PAS to differing degrees. We show that the short and the long 3'UTR produced similar mRNA expression levels. However, the long 3'UTR conferred lower luciferase activity as compared with the short form, indicating translation inhibition of the long 3'UTR. RNA affinity pull-down followed by mass spectrometry analysis as well as RNA coimmunoprecipitation indicated differential binding of Syncrip to the long versus short 3'UTR. Depletion of Syncrip by small interfering RNA increased surface expression of an HLA-A allotype that uses primarily the long 3'UTR, whereas an allotype expressing only the short form was unaffected. Furthermore, specific blocking of the proximal 3'UTR reduced surface expression without decreasing mRNA expression. These data demonstrate HLA-A allele-specific variation in PAS usage, which modulates their cell surface expression posttranscriptionally.},

- langid = {english},

- pmcid = {PMC5812486},

- keywords = {3' Untranslated Regions,Gene Expression Regulation,Genotype,Heterogeneous-Nuclear Ribonucleoproteins,HLA-A Antigens,Humans,Jurkat Cells,Polyadenylation,Polymorphism Genetic,Protein Binding,Protein Isoforms,RNA Processing Post-Transcriptional,RNA Small Interfering,RNA Splice Sites,RNA-Binding Motifs}

-}

-@article{kumarMultipleMyeloma2017,

- title = {Multiple Myeloma},

- author = {Kumar, Shaji K. and Rajkumar, Vincent and Kyle, Robert A. and family=Duin, given=Mark, prefix=van, useprefix=true and Sonneveld, Pieter and Mateos, María-Victoria and Gay, Francesca and Anderson, Kenneth C.},

- date = {2017-07-20},

- journaltitle = {Nature Reviews Disease Primers},

- shortjournal = {Nat Rev Dis Primers},

- volume = {3},

- number = {1},

- pages = {1--20},

- publisher = {Nature Publishing Group},

- issn = {2056-676X},

- doi = {10.1038/nrdp.2017.46},

- url = {https://www.nature.com/articles/nrdp201746},

- urldate = {2022-10-05},

- abstract = {Multiple myeloma is a malignancy of terminally differentiated plasma cells, and patients typically present with bone marrow infiltration of clonal plasma cells and monoclonal protein in the serum and/or urine. The diagnosis of multiple myeloma is made when clear end-organ damage attributable to the plasma cell proliferative disorder or when findings that suggest a high likelihood of their development are present. Distinguishing symptomatic multiple myeloma that requires treatment from the precursor stages of monoclonal gammopathy of undetermined significance and smouldering multiple myeloma is important, as observation is the standard for those conditions. Much progress has been made over the past decade in the understanding of disease biology and individualized treatment approaches. Several new classes of drugs, such as proteasome inhibitors and immunomodulatory drugs, have joined the traditional armamentarium (corticosteroids, alkylating agents and anthracyclines) and, along with high-dose therapy and autologous haemopoietic stem cell transplantation, have led to deeper and durable clinical responses. Indeed, an increasing proportion of patients are achieving lasting remissions, raising the possibility of cure for this disease. Success will probably depend on using combinations of effective agents and treating patients in the early stages of disease, such as patients with smouldering multiple myeloma.},

- issue = {1},

- langid = {english},

- keywords = {Cancer genetics,Cancer microenvironment,Cancer therapy,Myeloma}

-}

-

-@article{kurtzNoninvasiveMonitoringDiffuse2015,

- title = {Noninvasive Monitoring of Diffuse Large {{B-cell}} Lymphoma by Immunoglobulin High-Throughput Sequencing.},

- author = {Kurtz, David M and Green, Michael R and Bratman, Scott V and Scherer, Florian and Liu, Chih Long and Kunder, Christian A and Takahashi, Kazuhiro and Glover, Cynthia and Keane, Colm and Kihira, Shingo and Visser, Brendan and Callahan, Jason and Kong, Katherine A and Faham, Malek and Corbelli, Karen S and Miklos, David and Advani, Ranjana H and Levy, Ronald and Hicks, Rodney J and Hertzberg, Mark and Ohgami, Robert S and Gandhi, Maher K and Diehn, Maximilian and Alizadeh, Ash A},

- date = {2015-06},

- journaltitle = {Blood},

- volume = {125},

- number = {24},

- pages = {3679--3687}

-}

-@article{kwanGenomeStellerSea2019,

- title = {The {{Genome}} of the {{Steller Sea Lion}} ({{Eumetopias}} Jubatus)},

- author = {Kwan, Harwood H. and Culibrk, Luka and Taylor, Gregory A. and Leelakumari, Sreeja and Tan, Ryan and Jackman, Shaun D. and Tse, Kane and MacLeod, Tina and Cheng, Dean and Chuah, Eric and Kirk, Heather and Pandoh, Pawan and Carlsen, Rebecca and Zhao, Yongjun and Mungall, Andrew J. and Moore, Richard and Birol, Inanc and Marra, Marco A. and Rosen, David A.S. and Haulena, Martin and Jones, Steven J. M.},

- date = {2019-06-26},

- journaltitle = {Genes},

- shortjournal = {Genes (Basel)},

- volume = {10},

- number = {7},

- eprint = {31248052},

- eprinttype = {pmid},

- pages = {486},

- issn = {2073-4425},

- doi = {10.3390/genes10070486},

- url = {https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6678222/},

- urldate = {2022-02-01},

- abstract = {The Steller sea lion is the largest member of the Otariidae family and is found in the coastal waters of the northern Pacific Rim. Here, we present the Steller sea lion genome, determined through DNA sequencing approaches that utilized microfluidic partitioning library construction, as well as nanopore technologies. These methods constructed a highly contiguous assembly with a scaffold N50 length of over 14 megabases, a contig N50 length of over 242 kilobases and a total length of 2.404 gigabases. As a measure of completeness, 95.1\% of 4104 highly conserved mammalian genes were found to be complete within the assembly. Further annotation identified 19,668 protein coding genes. The assembled genome sequence and underlying sequence data can be found at the National Center for Biotechnology Information (NCBI) under the BioProject accession number PRJNA475770.},

- pmcid = {PMC6678222}

-}

-@article{kwonOPOSSUM3AdvancedAnalysis2012,

- title = {{{oPOSSUM-3}}: Advanced Analysis of Regulatory Motif over-Representation across Genes or {{ChIP-Seq}} Datasets.},

- author = {Kwon, Andrew T and Arenillas, David J and Worsley Hunt, Rebecca and Wasserman, Wyeth W},

- date = {2012-09},

- journaltitle = {G3 (Bethesda, Md.)},

- volume = {2},

- number = {9},

- pages = {987--1002}

-}

-@article{lahtveeAbsoluteQuantificationProtein2017,

- title = {Absolute {{Quantification}} of {{Protein}} and {{mRNA Abundances Demonstrate Variability}} in {{Gene-Specific Translation Efficiency}} in {{Yeast}}},

- author = {Lahtvee, Petri-Jaan and Sánchez, Benjamín J. and Smialowska, Agata and Kasvandik, Sergo and Elsemman, Ibrahim E. and Gatto, Francesco and Nielsen, Jens},

- date = {2017-05-24},

- journaltitle = {Cell Systems},

- shortjournal = {Cell Syst},

- volume = {4},

- number = {5},

- eprint = {28365149},

- eprinttype = {pmid},

- pages = {495-504.e5},

- issn = {2405-4712},

- doi = {10.1016/j.cels.2017.03.003},

- abstract = {Protein synthesis is the most energy-consuming process in a proliferating cell, and understanding what controls protein abundances represents a key question in biology and biotechnology. We quantified absolute abundances of 5,354 mRNAs and 2,198 proteins in Saccharomyces cerevisiae under ten environmental conditions and protein turnover for 1,384 proteins under a reference condition. The overall correlation between mRNA and protein abundances across all conditions was low (0.46), but for differentially expressed proteins (n~= 202), the median mRNA-protein correlation was 0.88. We used these data to model translation efficiencies and found that they vary more than 400-fold between genes. Non-linear regression analysis detected that mRNA abundance and translation elongation were the dominant factors controlling protein synthesis, explaining 61\% and 15\% of its variance. Metabolic flux balance analysis further showed that only mitochondrial fluxes were positively associated with changes at the transcript level. The present dataset represents a crucial expansion to the current resources for future studies on yeast physiology.},

- langid = {english},

- keywords = {absolute proteome,absolute transcriptome,genome-scale metabolic modeling,integrative data analysis,protein degradation rates,protein turnover,translation efficiency,translational control}

-}

-@article{laksClonalDecompositionDNA2019,

- title = {Clonal {{Decomposition}} and {{DNA Replication States Defined}} by {{Scaled Single-Cell Genome Sequencing}}},

- author = {Laks, Emma and McPherson, Andrew and Zahn, Hans and Lai, Daniel and Steif, Adi and Brimhall, Jazmine and Biele, Justina and Wang, Beixi and Masud, Tehmina and Ting, Jerome and Grewal, Diljot and Nielsen, Cydney and Leung, Samantha and Bojilova, Viktoria and Smith, Maia and Golovko, Oleg and Poon, Steven and Eirew, Peter and Kabeer, Farhia and Ruiz de Algara, Teresa and Lee, So Ra and Taghiyar, M. Jafar and Huebner, Curtis and Ngo, Jessica and Chan, Tim and Vatrt-Watts, Spencer and Walters, Pascale and Abrar, Nafis and Chan, Sophia and Wiens, Matt and Martin, Lauren and Scott, R. Wilder and Underhill, T. Michael and Chavez, Elizabeth and Steidl, Christian and Da Costa, Daniel and Ma, Yussanne and Coope, Robin J. N. and Corbett, Richard and Pleasance, Stephen and Moore, Richard and Mungall, Andrew J. and Mar, Colin and Cafferty, Fergus and Gelmon, Karen and Chia, Stephen and {CRUK IMAXT Grand Challenge Team} and Marra, Marco A. and Hansen, Carl and Shah, Sohrab P. and Aparicio, Samuel},

- date = {2019-11-14},

- journaltitle = {Cell},

- shortjournal = {Cell},

- volume = {179},

- number = {5},

- eprint = {31730858},

- eprinttype = {pmid},

- pages = {1207-1221.e22},

- issn = {1097-4172},

- doi = {10.1016/j.cell.2019.10.026},

- abstract = {Accurate measurement of clonal genotypes, mutational processes, and replication states from individual tumor-cell genomes will facilitate improved understanding of tumor evolution. We have developed DLP+, a scalable single-cell whole-genome sequencing platform implemented using commodity instruments, image-based object recognition, and open source computational methods. Using DLP+, we have generated a resource of 51,926 single-cell genomes and matched cell images from diverse cell types including cell lines, xenografts, and diagnostic samples with limited material. From this resource we have defined variation in mitotic mis-segregation rates across tissue types and genotypes. Analysis of matched genomic and image measurements revealed correlations between cellular morphology and genome ploidy states. Aggregation of cells sharing copy number profiles allowed for calculation of single-nucleotide resolution clonal genotypes and inference of clonal phylogenies and avoided the limitations of bulk deconvolution. Finally, joint analysis over the above features defined clone-specific chromosomal aneuploidy in polyclonal populations.},

- langid = {english},

- pmcid = {PMC6912164},

- keywords = {aneuploidy,Aneuploidy,Animals,cancer genomics,cell cycle,Cell Cycle,Cell Line Tumor,Cell Shape,Cell Survival,Chromosomes Human,Clone Cells,copy number,Diploidy,DNA Replication,DNA sequencing,DNA Transposable Elements,Female,Genome Human,genomic instability,Genotype,High-Throughput Nucleotide Sequencing,Humans,Male,Mice,Mutation,Phylogeny,Polymorphism Single Nucleotide,single cell,Single-Cell Analysis,tumor evolution,tumor heterogeneity}

-}

-

-@article{lamSmallMoleculeInhibitors,

- title = {Small Molecule Inhibitors of {{IkappaB}} Kinase Are Selectively Toxic for Subgroups of Diffuse Large {{B-cell}} Lymphoma Defined by Gene Expression Profiling.},

- author = {Lam, Lloyd T and Davis, R Eric and Pierce, Jackie and Hepperle, Michael and Xu, Yajun and Hottelet, Maria and Nong, Yuhua and Wen, Danyi and Adams, Julian and Dang, Lenny and Staudt, Louis M},

- journaltitle = {Clin Cancer Res},

- volume = {11},

- number = {1},

- pages = {28--40}

-}

-@article{lawrieDetectionElevatedLevels2008,

- title = {Detection of Elevated Levels of Tumour-Associated {{microRNAs}} in Serum of Patients with Diffuse Large {{B-cell}} Lymphoma},

- author = {Lawrie, Charles and Gal, Shira and Dunlop, Heather and Pushkaran, Beena and Liggins, Amanda and Pulford, Karen and Banham, Alison and Pezzella, Francesco and Boultwood, Jacqueline and Wainscoat, James and Hatton, Christian and Harris, Adrian},

- date = {2008},

- journaltitle = {Br J Haematol},

- volume = {141},

- number = {5},

- pages = {672--675}

-}

-@article{leeGenomedefinedAfricanAncestry2020,

- title = {Genome-Defined {{African}} Ancestry Is Associated with Distinct Mutations and Worse Survival in Patients with Diffuse Large {{B-cell}} Lymphoma},

- author = {Lee, Michelle J. and Koff, Jean L. and Switchenko, Jeffrey M. and Jhaney, C. Ileen and Harkins, R. Andrew and Patel, Sharvil P. and Dave, Sandeep S. and Flowers, Christopher R.},

- date = {2020-08-01},

- journaltitle = {Cancer},

- shortjournal = {Cancer},

- volume = {126},

- number = {15},

- eprint = {32469082},

- eprinttype = {pmid},

- pages = {3493--3503},

- issn = {1097-0142},

- doi = {10.1002/cncr.32866},

- abstract = {BACKGROUND: Significant racial differences have been observed in the incidence and clinical outcomes of diffuse large B-cell lymphoma (DLBCL) in the United States, but to the authors' knowledge it remains unclear whether genomic differences contribute to these disparities. METHODS: To understand the influences of genetic ancestry on tumor genomic alterations, the authors estimated the genetic ancestry of 1001 previously described patients with DLBCL using unsupervised model-based Admixture global ancestry analysis applied to exome sequencing data and examined the mutational profile of 150 DLBCL driver genes in tumors obtained from this cohort. RESULTS: Global ancestry prediction identified 619 patients with {$>$}90\% European ancestry, 81 patients with {$>$}90\% African ancestry, and 50 patients with {$>$}90\% Asian ancestry. Compared with patients with DLBCL with European ancestry, patients with African ancestry were aged {$>$}10~years younger at the time of diagnosis and were more likely to present with B symptoms, elevated serum lactate dehydrogenase, extranodal disease, and advanced stage disease. Patients with African ancestry demonstrated worse overall survival compared with patients with European ancestry (median, 4.9~years vs 8.8~years; P~=~.04). Recurrent mutations of MLL2 (KMT2D), HIST1H1E, MYD88, BCL2, and PIM1 were found across all ancestry groups, suggesting shared mechanisms underlying tumor biology. The authors also identified 6 DLBCL driver genes that were more commonly mutated in patients with African ancestry compared with patients with European ancestry: ATM (21.0\% vs 7.75\%; P~{$<~$}.001), MGA (19.7\% vs 5.33\%; P~{$<~$}.001), SETD2 (17.3\% vs 5.17\%; P~{$<~$}.001), TET2 (12.3\% vs 5.82\%; P~=~.029), MLL3 (KMT2C) (11.1\% vs 4.36\%; P~=~.013), and DNMT3A (11.1\% vs 4.52\%; P~=~.016). CONCLUSIONS: Distinct prevalence and patterns of mutation highlight an important difference in the mutational landscapes of DLBCL arising in different ancestry groups. To the authors' knowledge, the results of the current study provide the first-ever characterization of genetic alterations among patients with African descent who are diagnosed with DLBCL.},

- langid = {english},

- pmcid = {PMC7494053},

- keywords = {Adult,African continental ancestry group,Aged,Asians,Blacks,Cohort Studies,diffuse large B-cell lymphoma,Disease-Free Survival,DNA-Binding Proteins,Exome,Female,Genome Human,Histones,Humans,Lymphoma Large B-Cell Diffuse,Male,Middle Aged,mutation,Mutation,Myeloid Differentiation Factor 88,Neoplasm Proteins,Prognosis,Proto-Oncogene Proteins c-bcl-2,racial factors,Whites,Whole Exome Sequencing,Young Adult}

-}

-@article{lefrancIMGTInternationalImMunoGeneTics2015,

- title = {{{IMGT}}®, the International {{ImMunoGeneTics}} Information System® 25 Years On},

- author = {Lefranc, Marie-Paule and Giudicelli, Véronique and Duroux, Patrice and Jabado-Michaloud, Joumana and Folch, Géraldine and Aouinti, Safa and Carillon, Emilie and Duvergey, Hugo and Houles, Amélie and Paysan-Lafosse, Typhaine and Hadi-Saljoqi, Saida and Sasorith, Souphatta and Lefranc, Gérard and Kossida, Sofia},

- date = {2015-01},

- journaltitle = {Nucleic Acids Research},

- shortjournal = {Nucleic Acids Res},

- volume = {43},

- eprint = {25378316},

- eprinttype = {pmid},

- pages = {D413-422},

- issn = {1362-4962},

- doi = {10.1093/nar/gku1056},

- abstract = {IMGT(®), the international ImMunoGeneTics information system(®)(http://www.imgt.org) is the global reference in immunogenetics and immunoinformatics. By its creation in 1989 by Marie-Paule Lefranc (Université de Montpellier and CNRS), IMGT(®) marked the advent of immunoinformatics, which emerged at the interface between immunogenetics and bioinformatics. IMGT(®) is specialized in the immunoglobulins (IG) or antibodies, T cell receptors (TR), major histocompatibility (MH) and proteins of the IgSF and MhSF superfamilies. IMGT(®) is built on the IMGT-ONTOLOGY axioms and concepts, which bridged the gap between genes, sequences and 3D structures. The concepts include the IMGT(®) standardized keywords (identification), IMGT(®) standardized labels (description), IMGT(®) standardized nomenclature (classification), IMGT unique numbering and IMGT Colliers de Perles (numerotation). IMGT(®) comprises 7 databases, 17 online tools and 15,000 pages of web resources, and provides a high-quality and integrated system for analysis of the genomic and expressed IG and TR repertoire of the adaptive immune responses, including NGS high-throughput data. Tools and databases are used in basic, veterinary and medical research, in clinical applications (mutation analysis in leukemia and lymphoma) and in antibody engineering and humanization. The IMGT/mAb-DB interface was developed for therapeutic antibodies and fusion proteins for immunological applications (FPIA). IMGT(®) is freely available at http://www.imgt.org.},

- issue = {Database issue},

- langid = {english},

- pmcid = {PMC4383898},

- keywords = {Alleles,Animals,Biological Ontologies,Computational Biology,Databases Genetic,Genes Immunoglobulin,Genes T-Cell Receptor,Histocompatibility Antigens,Humans,Immunogenetics,Immunoglobulins,Internet,Major Histocompatibility Complex,Receptors Antigen T-Cell,Software}

-}

-@article{lenzAberrantImmunoglobulinClass2007,

- title = {Aberrant Immunoglobulin Class Switch Recombination and Switch Translocations in Activated {{B}} Cell-like Diffuse Large {{B}} Cell Lymphoma},

- author = {Lenz, G and Nagel, I and Siebert, R and Roschke, A and Sanger, W and Wright, G and Dave, S and Tan, B and Zhao, H and Rosenwald, A and Muller-Hermelink, H and Gascoyne, R and Campo, E and Jaffe, E and Smeland, E and Fisher, R and Kuehl, W and Chan, W and Staudt, L},

- date = {2007},

- journaltitle = {J Exp Med},

- volume = {204},

- number = {3},

- pages = {633--643}

-}

-@article{leonardTargetedTreatmentNew2008,

- title = {Targeted Treatment and New Agents in Diffuse Large {{B-cell}} Lymphoma},

- author = {Leonard, John P and Martin, Peter and Barrientos, Jacqueline and Elstrom, Rebecca},

- date = {2008-07},

- journaltitle = {Seminars in hematology},

- volume = {45},

- pages = {S11--6},

- issue = {3 Suppl 2}

-}

-

-@article{liAligningSequenceReads2013,

- title = {Aligning Sequence Reads, Clone Sequences and Assembly Contigs with {{BWA-MEM}}},

- author = {Li, Heng},

- date = {2013-03-16},

- journaltitle = {arXiv},

- volume = {arXiv:1303.3997},

- eprint = {1303.3997},

- eprinttype = {arxiv},

- url = {http://arxiv.org/abs/1303.3997},

- urldate = {2019-07-08},

- abstract = {Summary: BWA-MEM is a new alignment algorithm for aligning sequence reads or long query sequences against a large reference genome such as human. It automatically chooses between local and end-to-end alignments, supports paired-end reads and performs chimeric alignment. The algorithm is robust to sequencing errors and applicable to a wide range of sequence lengths from 70bp to a few megabases. For mapping 100bp sequences, BWA-MEM shows better performance than several state-of-art read aligners to date. Availability and implementation: BWA-MEM is implemented as a component of BWA, which is available at http://github.com/lh3/bwa. Contact: hengli@broadinstitute.org},

- keywords = {Quantitative Biology - Genomics}

-}

-@article{liaoFeatureCountsEfficientGeneral2014,

- title = {{{featureCounts}}: An Efficient General Purpose Program for Assigning Sequence Reads to Genomic Features},

- shorttitle = {{{featureCounts}}},

- author = {Liao, Yang and Smyth, Gordon K. and Shi, Wei},

- date = {2014-04-01},

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

- shortjournal = {Bioinformatics},

- volume = {30},

- number = {7},

- eprint = {24227677},

- eprinttype = {pmid},

- pages = {923--930},

- issn = {1367-4811},

- doi = {10.1093/bioinformatics/btt656},

- abstract = {MOTIVATION: Next-generation sequencing technologies generate millions of short sequence reads, which are usually aligned to a reference genome. In many applications, the key information required for downstream analysis is the number of reads mapping to each genomic feature, for example to each exon or each gene. The process of counting reads is called read summarization. Read summarization is required for a great variety of genomic analyses but has so far received relatively little attention in the literature. RESULTS: We present featureCounts, a read summarization program suitable for counting reads generated from either RNA or genomic DNA sequencing experiments. featureCounts implements highly efficient chromosome hashing and feature blocking techniques. It is considerably faster than existing methods (by an order of magnitude for gene-level summarization) and requires far less computer memory. It works with either single or paired-end reads and provides a wide range of options appropriate for different sequencing applications. AVAILABILITY AND IMPLEMENTATION: featureCounts is available under GNU General Public License as part of the Subread (http://subread.sourceforge.net) or Rsubread (http://www.bioconductor.org) software packages.},

- langid = {english},

- keywords = {Algorithms,Genome,Genomics,High-Throughput Nucleotide Sequencing,Histones,Sequence Analysis RNA,Software}

-}