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Year Number of Results
1996 1
2001 1
2002 1
2005 2
2008 2
2009 2
2010 2
2011 5
2012 15
2013 24
2014 25
2015 35
2016 30
2017 52
2018 52
2019 42
2020 83
2021 76
2022 78
2023 62
2024 27

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540 results

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Page 1
PBRM1 Deficiency Confers Synthetic Lethality to DNA Repair Inhibitors in Cancer.
Chabanon RM, Morel D, Eychenne T, Colmet-Daage L, Bajrami I, Dorvault N, Garrido M, Meisenberg C, Lamb A, Ngo C, Hopkins SR, Roumeliotis TI, Jouny S, Hénon C, Kawai-Kawachi A, Astier C, Konde A, Del Nery E, Massard C, Pettitt SJ, Margueron R, Choudhary JS, Almouzni G, Soria JC, Deutsch E, Downs JA, Lord CJ, Postel-Vinay S. Chabanon RM, et al. Cancer Res. 2021 Jun 1;81(11):2888-2902. doi: 10.1158/0008-5472.CAN-21-0628. Cancer Res. 2021. PMID: 33888468
To identify novel therapeutic approaches to targeting PBRM1-defective cancers, we used a series of orthogonal functional genomic screens that identified PARP and ATR inhibitors as being synthetic lethal with PBRM1 deficiency. ...SIGNIFICANCE: This study demon …
To identify novel therapeutic approaches to targeting PBRM1-defective cancers, we used a series of orthogonal functional genom …
Molecular Subsets in Renal Cancer Determine Outcome to Checkpoint and Angiogenesis Blockade.
Motzer RJ, Banchereau R, Hamidi H, Powles T, McDermott D, Atkins MB, Escudier B, Liu LF, Leng N, Abbas AR, Fan J, Koeppen H, Lin J, Carroll S, Hashimoto K, Mariathasan S, Green M, Tayama D, Hegde PS, Schiff C, Huseni MA, Rini B. Motzer RJ, et al. Cancer Cell. 2020 Dec 14;38(6):803-817.e4. doi: 10.1016/j.ccell.2020.10.011. Epub 2020 Nov 5. Cancer Cell. 2020. PMID: 33157048 Free PMC article.
While sunitinib and atezolizumab + bevacizumab are effective in subsets with high angiogenesis, atezolizumab + bevacizumab improves clinical benefit in tumors with high T-effector and/or cell-cycle transcription. Somatic mutations in PBRM1 and KDM5C associate with high ang …
While sunitinib and atezolizumab + bevacizumab are effective in subsets with high angiogenesis, atezolizumab + bevacizumab improves clinical …
SWI/SNF nucleosome remodellers and cancer.
Wilson BG, Roberts CW. Wilson BG, et al. Nat Rev Cancer. 2011 Jun 9;11(7):481-92. doi: 10.1038/nrc3068. Nat Rev Cancer. 2011. PMID: 21654818 Review.
Growing evidence indicates that these complexes have a widespread role in tumour suppression, as inactivating mutations in several SWI/SNF subunits have recently been identified at a high frequency in a variety of cancers. However, the mechanisms by which mutations in thes …
Growing evidence indicates that these complexes have a widespread role in tumour suppression, as inactivating mutations in several SWI/SNF s …
BAF complex vulnerabilities in cancer demonstrated via structure-based PROTAC design.
Farnaby W, Koegl M, Roy MJ, Whitworth C, Diers E, Trainor N, Zollman D, Steurer S, Karolyi-Oezguer J, Riedmueller C, Gmaschitz T, Wachter J, Dank C, Galant M, Sharps B, Rumpel K, Traxler E, Gerstberger T, Schnitzer R, Petermann O, Greb P, Weinstabl H, Bader G, Zoephel A, Weiss-Puxbaum A, Ehrenhöfer-Wölfer K, Wöhrle S, Boehmelt G, Rinnenthal J, Arnhof H, Wiechens N, Wu MY, Owen-Hughes T, Ettmayer P, Pearson M, McConnell DB, Ciulli A. Farnaby W, et al. Nat Chem Biol. 2019 Jul;15(7):672-680. doi: 10.1038/s41589-019-0294-6. Epub 2019 Jun 10. Nat Chem Biol. 2019. PMID: 31178587 Free PMC article.
Targeting subunits of BAF/PBAF chromatin remodeling complexes has been proposed as an approach to exploit cancer vulnerabilities. Here, we develop proteolysis targeting chimera (PROTAC) degraders of the BAF ATPase subunits SMARCA2 and SMARCA4 using a bromodomain ligand and …
Targeting subunits of BAF/PBAF chromatin remodeling complexes has been proposed as an approach to exploit cancer vulnerabilities. Her …
A Pan-Cancer Analysis of the Role of PBRM1 in Human Tumors.
Liu J, Xie X, Xue M, Wang J, Chen Q, Zhao Z, Sheng X. Liu J, et al. Stem Cells Int. 2022 Oct 12;2022:7676541. doi: 10.1155/2022/7676541. eCollection 2022. Stem Cells Int. 2022. PMID: 36277039 Free PMC article. Retracted.
PBRM1 mutation was most frequent in renal cell carcinoma and showed better disease outcomes of pan-cancer. ...The analysis of pan-cancer offers us an outline of PBRM1's functions in various human cancers, which could promote a comprehensive unde …
PBRM1 mutation was most frequent in renal cell carcinoma and showed better disease outcomes of pan-cancer. ...The analysis of …
Comprehensive Analysis of Genetic Ancestry and Its Molecular Correlates in Cancer.
Carrot-Zhang J, Chambwe N, Damrauer JS, Knijnenburg TA, Robertson AG, Yau C, Zhou W, Berger AC, Huang KL, Newberg JY, Mashl RJ, Romanel A, Sayaman RW, Demichelis F, Felau I, Frampton GM, Han S, Hoadley KA, Kemal A, Laird PW, Lazar AJ, Le X, Oak N, Shen H, Wong CK, Zenklusen JC, Ziv E; Cancer Genome Atlas Analysis Network; Cherniack AD, Beroukhim R. Carrot-Zhang J, et al. Cancer Cell. 2020 May 11;37(5):639-654.e6. doi: 10.1016/j.ccell.2020.04.012. Cancer Cell. 2020. PMID: 32396860 Free PMC article.
We evaluated ancestry effects on mutation rates, DNA methylation, and mRNA and miRNA expression among 10,678 patients across 33 cancer types from The Cancer Genome Atlas. We demonstrated that cancer subtypes and ancestry-related technical artifacts are import …
We evaluated ancestry effects on mutation rates, DNA methylation, and mRNA and miRNA expression among 10,678 patients across 33 cancer …
PBRM1 Deficiency Sensitizes Renal Cancer Cells to DNMT Inhibitor 5-Fluoro-2'-Deoxycytidine.
Gu D, Dong K, Jiang A, Jiang S, Fu Z, Bao Y, Huang F, Yang C, Wang L. Gu D, et al. Front Oncol. 2022 Jun 3;12:870229. doi: 10.3389/fonc.2022.870229. eCollection 2022. Front Oncol. 2022. PMID: 35719970 Free PMC article.
PBRM1 is a tumor suppressor frequently mutated in clear cell renal cell carcinoma. However, no effective targeted therapies exist for ccRCC with PBRM1 loss. To identify novel therapeutic approaches to targeting PBRM1-deficient renal cancers, we employe …
PBRM1 is a tumor suppressor frequently mutated in clear cell renal cell carcinoma. However, no effective targeted therapies exist for …
Tumor and immune reprogramming during immunotherapy in advanced renal cell carcinoma.
Bi K, He MX, Bakouny Z, Kanodia A, Napolitano S, Wu J, Grimaldi G, Braun DA, Cuoco MS, Mayorga A, DelloStritto L, Bouchard G, Steinharter J, Tewari AK, Vokes NI, Shannon E, Sun M, Park J, Chang SL, McGregor BA, Haq R, Denize T, Signoretti S, Guerriero JL, Vigneau S, Rozenblatt-Rosen O, Rotem A, Regev A, Choueiri TK, Van Allen EM. Bi K, et al. Cancer Cell. 2021 May 10;39(5):649-661.e5. doi: 10.1016/j.ccell.2021.02.015. Epub 2021 Mar 11. Cancer Cell. 2021. PMID: 33711272 Free PMC article.
Expression signatures for cancer cell subpopulations and immune evasion are associated with PBRM1 mutation and survival in primary and ICB-treated advanced RCC. Our findings demonstrate that ICB remodels the RCC microenvironment and modifies the interplay between …
Expression signatures for cancer cell subpopulations and immune evasion are associated with PBRM1 mutation and survival in pri …
The Cancer Genome Atlas of renal cell carcinoma: findings and clinical implications.
Linehan WM, Ricketts CJ. Linehan WM, et al. Nat Rev Urol. 2019 Sep;16(9):539-552. doi: 10.1038/s41585-019-0211-5. Epub 2019 Jul 5. Nat Rev Urol. 2019. PMID: 31278395 Review.
The Cancer Genome Atlas (TCGA) characterized the somatic genetic and genomic alterations in renal cell carcinoma (RCC) encompassing the major RCC histological subtypes, including clear cell RCC (ccRCC), papillary RCC (pRCC) and chromophobe RCC (chRCC). ...Two new RCC subty …
The Cancer Genome Atlas (TCGA) characterized the somatic genetic and genomic alterations in renal cell carcinoma (RCC) encompassing t …
Integrated Genomic Characterization of Pancreatic Ductal Adenocarcinoma.
Cancer Genome Atlas Research Network. Electronic address: andrew_aguirre@dfci.harvard.edu; Cancer Genome Atlas Research Network. Cancer Genome Atlas Research Network. Electronic address: andrew_aguirre@dfci.harvard.edu, et al. Cancer Cell. 2017 Aug 14;32(2):185-203.e13. doi: 10.1016/j.ccell.2017.07.007. Cancer Cell. 2017. PMID: 28810144 Free PMC article.
Deep whole-exome sequencing revealed recurrent somatic mutations in KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFbetaR2, GNAS, RREB1, and PBRM1. KRAS wild-type tumors harbored alterations in other oncogenic drivers, including GNAS, BRAF, CTNNB1, and additional RAS pathway …
Deep whole-exome sequencing revealed recurrent somatic mutations in KRAS, TP53, CDKN2A, SMAD4, RNF43, ARID1A, TGFbetaR2, GNAS, RREB1, and …
540 results