b1256a5a38c0e0f3658854596bc8f87f23afe137
morinlab.bib
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| 1 | +@article{campos-martinClinicalDiagnosticRelevance2017, |
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| 2 | + title = {Clinical and Diagnostic Relevance of {{NOTCH2-and KLF2-mutations}} in Splenic Marginal Zone Lymphoma}, |
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| 3 | + 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}, |
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| 4 | + date = {2017-08-01}, |
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| 5 | + journaltitle = {Haematologica}, |
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| 6 | + volume = {102}, |
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| 7 | + number = {8}, |
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| 8 | + pages = {e310-e312}, |
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| 9 | + issn = {1592-8721}, |
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| 10 | + doi = {10.3324/haematol.2016.161711}, |
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| 11 | + url = {https://haematologica.org/article/view/8174}, |
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| 12 | + urldate = {2024-07-24}, |
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| 13 | + issue = {8}, |
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| 14 | + langid = {english}, |
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| 15 | + file = {/Users/rmorin/Zotero/storage/W8D2249V/Campos-Martín et al. - 2017 - Clinical and diagnostic relevance of NOTCH2-and KL.pdf} |
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| 16 | +} |
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| 17 | + |
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| 18 | +@article{ennishiTMEM30ALossoffunctionMutations2020b, |
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| 19 | + title = {{{TMEM30A}} Loss-of-Function Mutations Drive Lymphomagenesis and Confer Therapeutically Exploitable Vulnerability in {{B-cell}} Lymphoma}, |
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| 20 | + author = {Ennishi, Daisuke and Healy, Shannon and Bashashati, Ali and Saberi, Saeed and Hother, Christoffer and Mottok, Anja and Chan, Fong Chun and Chong, Lauren and Abraham, Libin and Kridel, Robert and Boyle, Merrill and Meissner, Barbara and Aoki, Tomohiro and Takata, Katsuyoshi and Woolcock, Bruce W. and Viganò, Elena and Gold, Michael and Molday, Laurie L. and Molday, Robert S. and Telenius, Adele and Li, Michael Y. and Wretham, Nicole and Dos Santos, Nancy and Wong, Mark and Viller, Natasja N. and Uger, Robert A. and Duns, Gerben and Baticados, Abigail and Madero, Angel and Bristow, Brianna N. and Farinha, Pedro and Slack, Graham W. and Ben-Neriah, Susana and Lai, Daniel and Zhang, Allen W. and Salehi, Sohrab and Shulha, Hennady P. and Chiu, Derek S. and Mostafavi, Sara and Gerrie, Alina S. and Huang, Da Wei and Rushton, Christopher and Villa, Diego and Sehn, Laurie H. and Savage, Kerry J. and Mungall, Andrew J. and Weng, Andrew P. and Bally, Marcel B. and Morin, Ryan D. and Cohen Freue, Gabriela V. and Staudt, Louis M. and Connors, Joseph M. and Marra, Marco A. and Shah, Sohrab P. and Gascoyne, Randy D. and Scott, David W. and Steidl, Christian}, |
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| 21 | + date = {2020-04}, |
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| 22 | + journaltitle = {Nature Medicine}, |
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| 23 | + shortjournal = {Nat Med}, |
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| 24 | + volume = {26}, |
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| 25 | + number = {4}, |
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| 26 | + eprint = {32094924}, |
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| 27 | + eprinttype = {pmid}, |
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| 28 | + pages = {577--588}, |
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| 29 | + issn = {1546-170X}, |
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| 30 | + doi = {10.1038/s41591-020-0757-z}, |
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| 31 | + abstract = {Transmembrane protein 30A (TMEM30A) maintains the asymmetric distribution of phosphatidylserine, an integral component of the cell membrane and 'eat-me' signal recognized by macrophages. Integrative genomic and transcriptomic analysis of diffuse large B-cell lymphoma (DLBCL) from the British Columbia population-based registry uncovered recurrent biallelic TMEM30A loss-of-function mutations, which were associated with a favorable outcome and uniquely observed in DLBCL. Using TMEM30A-knockout systems, increased accumulation of chemotherapy drugs was observed in TMEM30A-knockout cell lines and TMEM30A-mutated primary cells, explaining the improved treatment outcome. Furthermore, we found increased tumor-associated macrophages and an enhanced effect of anti-CD47 blockade limiting tumor growth in TMEM30A-knockout models. By contrast, we show that TMEM30A loss-of-function increases B-cell signaling following antigen stimulation-a mechanism conferring selective advantage during B-cell lymphoma development. Our data highlight a multifaceted role for TMEM30A in B-cell lymphomagenesis, and characterize intrinsic and extrinsic vulnerabilities of cancer cells that can be therapeutically exploited.}, |
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| 32 | + langid = {english}, |
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| 33 | + pmcid = {PMC8480332}, |
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| 34 | + keywords = {Adolescent,Adult,Aged,Aged 80 and over,Animals,British Columbia,Cell Transformation Neoplastic,Cells Cultured,Cohort Studies,Female,Genetic Predisposition to Disease,HEK293 Cells,Humans,Jurkat Cells,Loss of Function Mutation,Lymphoma Large B-Cell Diffuse,Male,Membrane Proteins,Mice,Mice Inbred BALB C,Mice Inbred NOD,Mice SCID,Mice Transgenic,Middle Aged,Molecular Targeted Therapy,Young Adult} |
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| 35 | +} |
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| 36 | + |
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| 1 | 37 | @article{rowhTp53DeletionLineage2011, |
| 2 | 38 | title = {Tp53 Deletion in {{B}} Lineage Cells Predisposes Mice to Lymphomas with Oncogenic Translocations}, |
| 3 | 39 | 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.}, |