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  • 1
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    Abstract PR06: A functional screen of the epigenome identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers.
    American Association for Cancer Research (AACR) ; 2013
    In:  Molecular Cancer Therapeutics Vol. 12, No. 11_Supplement ( 2013-11-01), p. PR06-PR06
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 12, No. 11_Supplement ( 2013-11-01), p. PR06-PR06
    Abstract: Epigenetic dysregulation is an emerging hallmark of cancers, and the identification of recurrent somatic mutations in chromatin regulators implies a causal role for altered chromatin states in tumorigenesis. As the majority of epigenetic mutations are inactivating and thus do not present directly druggable targets, we reasoned that these mutations may alter the epigenomic state of cancer cells and thereby expose novel epigenetic vulnerabilities. To systematically search for epigenetic synthetic lethal interactions, we performed a deep coverage pooled shRNA screen across a large collection of cancer cell lines using a library targeting a diverse set of epigenetic regulators. Strikingly, this unbiased screen revealed that silencing of the SWI/SNF ATPase subunit BRM/SMARCA2, selectively inhibits the proliferation of BRG1-deficient cancer cells. The mammalian SWI/SNF complexes (mSWI/SNF) regulate chromatin structure through ATP-dependent nucleosome remodeling. Recent cancer genome studies have revealed a significant frequency of mutations in several components of the mSWI/SNF complexes including loss of the catalytic subunit BRG1 in non-small cell lung cancers. Our studies reveal that BRM knockdown selectively induced cell cycle arrest in BRG1-mutant cancer cells and significantly impaired the growth of BRG1-mutant lung tumor xenografts. BRM is the paralog of BRG1, suggesting a model in which mSWI/SNF mutations lead to a hypomorphic complex that promotes tumorigenesis but cannot tolerate complete inactivation. Therefore, our studies present BRM as an attractive therapeutic target in BRG1-mutant cancers. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):PR06. Citation Format: Zainab Jagani, Gregory Hoffman, Rami Rahal, Frank Buxton, Gregory McAllister, Kay Xiang, Elizabeth Frias, Janina Huber, Alicia Lindeman, Dongshu Chen, Linda Bagdasarian, Rodrigo Romero, Nadire Ramadan, Tanushree Phadke, Kristy Haas, Mariela Jaskelioff, Boris Wilson, Matthew Meyer, Margaret E. McLaughlin, Charles WM Roberts, Vic Myer, Jeff Porter, Nicholas Keen, Craig Mickanin, Frank Stegmeier. A functional screen of the epigenome identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr PR06.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-13-PR06
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 2
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    Functional epigenetics approach identifies BRM/SMARCA2 as a critical synthetic lethal target in BRG1-deficient cancers
    Proceedings of the National Academy of Sciences ; 2014
    In:  Proceedings of the National Academy of Sciences Vol. 111, No. 8 ( 2014-02-25), p. 3128-3133
    Details
    In: Proceedings of the National Academy of Sciences, Proceedings of the National Academy of Sciences, Vol. 111, No. 8 ( 2014-02-25), p. 3128-3133
    Abstract: Defects in epigenetic regulation play a fundamental role in the development of cancer, and epigenetic regulators have recently emerged as promising therapeutic candidates. We therefore set out to systematically interrogate epigenetic cancer dependencies by screening an epigenome-focused deep-coverage design shRNA (DECODER) library across 58 cancer cell lines. This screen identified BRM/SMARCA2, a DNA-dependent ATPase of the mammalian SWI/SNF (mSWI/SNF) chromatin remodeling complex, as being essential for the growth of tumor cells that harbor loss of function mutations in BRG1/SMARCA4. Depletion of BRM in BRG1-deficient cancer cells leads to a cell cycle arrest, induction of senescence, and increased levels of global H3K9me3. We further demonstrate the selective dependency of BRG1 -mutant tumors on BRM in vivo. Genetic alterations of the mSWI/SNF chromatin remodeling complexes are the most frequent among chromatin regulators in cancers, with BRG1/SMARCA4 mutations occurring in ∼10–15% of lung adenocarcinomas. Our findings position BRM as an attractive therapeutic target for BRG1 mutated cancers. Because BRG1 and BRM function as mutually exclusive catalytic subunits of the mSWI/SNF complex, we propose that such synthetic lethality may be explained by paralog insufficiency, in which loss of one family member unveils critical dependence on paralogous subunits. This concept of “cancer-selective paralog dependency” may provide a more general strategy for targeting other tumor suppressor lesions/complexes with paralogous subunits.
    Type of Medium: Online Resource
    ISSN: 0027-8424 , 1091-6490
    URL: Article
    DOI: 10.1073/pnas.1316793111
    RVK:
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    RVK:
    WA 15000
    Language: English
    Publisher: Proceedings of the National Academy of Sciences
    Publication Date: 2014
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  • 3
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    Project DRIVE: A Compendium of Cancer Dependencies and Synthetic Lethal Relationships Uncovered by Large-Scale, Deep RNAi Screening
    Elsevier BV ; 2017
    In:  Cell Vol. 170, No. 3 ( 2017-07), p. 577-592.e10
    Details
    In: Cell, Elsevier BV, Vol. 170, No. 3 ( 2017-07), p. 577-592.e10
    Type of Medium: Online Resource
    ISSN: 0092-8674
    URL: Article
    DOI: 10.1016/j.cell.2017.07.005
    RVK:
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    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2017
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    SSG: 12
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  • 4
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    Studying clonal dynamics in response to cancer therapy using high-complexity barcoding
    Springer Science and Business Media LLC ; 2015
    In:  Nature Medicine Vol. 21, No. 5 ( 2015-5), p. 440-448
    Details
    In: Nature Medicine, Springer Science and Business Media LLC, Vol. 21, No. 5 ( 2015-5), p. 440-448
    Type of Medium: Online Resource
    ISSN: 1078-8956 , 1546-170X
    URL: Article
    DOI: 10.1038/nm.3841
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2015
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  • 5
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    Abstract 444: BRM/SMARCA2 is a critical synthetic lethal target in BRG1-deficient cancers
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Research Vol. 74, No. 19_Supplement ( 2014-10-01), p. 444-444
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 74, No. 19_Supplement ( 2014-10-01), p. 444-444
    Abstract: The mammalian SWI/SNF complexes (mSWI/SNF) regulate chromatin structure through ATP-dependent nucleosome remodeling and thereby control key cellular processes. Recent cancer genome studies have revealed a significant frequency of mutations in several components of the mSWI/SNF complexes including the catalytic subunit BRG1. Emerging evidence is supportive of tumor suppressor roles for mSWI/SNF subunits, yet the inactivating nature of these mutations presents a challenge for devising targeted therapeutic strategies against cancers harboring such mutations. In this study, we interrogated epigenetic cancer dependencies by screening a deep-coverage design (DeCoDe) shRNA library targeting the epigenome across a broad range of 50+ cancer cell lines. Strikingly, this unbiased screen revealed that silencing of the SWI/SNF ATPase subunit BRM/SMARCA2, selectively inhibits the proliferation of BRG1-deficient cancer cells. BRM knockdown selectively induced cell cycle arrest in BRG1-mutant cancer cells and significantly impaired the growth of BRG1-mutant lung tumor xenografts. BRM is the paralog of BRG1, suggesting a model in which mSWI/SNF mutations lead to a hypomorphic complex that promotes tumorigenesis but cannot tolerate complete inactivation. Thus, targeting mSWI/SNF subunits that exhibit redundant activities to the residual mutated complexes may present a general strategy for SWI/SNF mutated cancers. Citation Format: Mariela Jaskelioff, Gregory Hoffman, Rami Rahal, Kay Xiang, Kristy Haas, Veronica Saenz-Vash, Huili Zhai, Nicholas Keen, Frank Stegmeier, Zainab Jagani. BRM/SMARCA2 is a critical synthetic lethal target in BRG1-deficient cancers. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 444. doi:10.1158/1538-7445.AM2014-444
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2014-444
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
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  • 6
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    Abstract LB-017: Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to marked dependence on PRMT5
    American Association for Cancer Research (AACR) ; 2016
    In:  Cancer Research Vol. 76, No. 14_Supplement ( 2016-07-15), p. LB-017-LB-017
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 76, No. 14_Supplement ( 2016-07-15), p. LB-017-LB-017
    Abstract: Metabolic genes are increasingly recognized as targets of somatic genetic alteration in human cancer often leading to profound changes in intracellular metabolite concentrations. 5-Methylthioadenosine Phosphorylase (MTAP) is a key enzyme in the methionine salvage pathway that metabolizes methylthioadenosine (MTA) to adenine and methionine. Its chromosomal position proximal to CDKN2A results in frequent collateral homozygous deletion in a wide range of human cancers. By interrogating data from a large scale deep-coverage pooled shRNA screen across 390 cancer cell line models we found that the viability of MTAP null cancer cells is strongly impaired upon shRNA-mediated depletion of the protein arginine methyltransferase PRMT5. In MTAP deleted cells there is marked accumulation of the substrate MTA and surprisingly, we find that MTA is a specific inhibitor of the catalytic activity of PRMT5. In keeping with these data, knockout of MTAP in an MTAP-proficient cell line led to increased MTA levels and rendered them sensitive to PRMT5 depletion. Moreover, reconstitution of MTAP in an MTAP-deficient cell line fully rescued PRMT5 dependence. Collectively, these findings indicate that the collateral loss of MTAP in CDNK2A deleted cancers leads to accumulation of MTA that thereby creates a hypomorphic PRMT5 state that is selectively sensitized towards further PRMT5 inhibition. Citation Format: Konstantinos Mavrakis, E Robert McDonald III, Michael R. Schlabach, Eric Billy, Gregory R. Hoffman, Antoine deWeck, David A. Ruddy, Kavitha Venkatesan, Greg McAllister, Rosalie deBeaumont, Samuel Ho, Yue Liu, Yan Yan-Neale, Guizhi Yang, Fallon Lin, Hong Yin, Hui Gao, David Randal Kipp, Songping Zhao, Joshua T. McNamara, Elizabeth R. Sprague, Young Shin Cho, Justin Gu, Ken Crawford, Vladimir Capka, Kristen Hurov, Jeffrey A. Porter, John Tallarico, Craig Mickanin, Emma Lees, Raymond Pagliarini, Nicholas Keen, Tobias Schmelzle, Francesco Hofmann, Frank Stegmeier, William R. Sellers. Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to marked dependence on PRMT5. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr LB-017.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2016-LB-017
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2016
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  • 7
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    Abstract PR01: Global chromatin profiling identifies NSD2 mutations in pediatric acute lymphoblastic leukemia
    American Association for Cancer Research (AACR) ; 2013
    In:  Cancer Research Vol. 73, No. 13_Supplement ( 2013-07-01), p. PR01-PR01
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 13_Supplement ( 2013-07-01), p. PR01-PR01
    Abstract: Epigenetic dysregulation is an emerging hallmark of cancers, and the identification of recurrent somatic mutations in chromatin modifying enzymes implies a causal role for altered chromatin states in tumorigenesis. While the genomic characterization of cancers is well advanced, our current understanding of cancer epigenomes is limited. Here, we developed a high-information-content mass spectrometry approach to profile global histone modifications in human cancer cells. When applied to 115 cell lines of the Cancer Cell Line Encyclopedia, this approach identified distinct molecular chromatin signatures (MCS) that provided novel insights into their epigenetic states. One MCS cluster, characterized by high H3K27 trimethylation, strongly correlated with EZH2 gain-of-function mutations, whereas another MCS cluster provided functional epigenetic correlates of EZH2 loss-of-function mutations. A third MCS cluster was characterized by increased H3K36 dimethylation and contained several cell lines harboring NSD2 translocations. Analysis of genomic correlates of the remaining cell lines within this third cluster identified a novel NSD2 E1099K variant in acute lymphoblastic leukemia (ALL) lines. Ectopic expression of the NSD2 E1099K variant induced a MCS profile characteristic of NSD2 hyperactivation and promoted transformation. Moreover, NSD2 knockdown selectively inhibited the proliferation of cell lines harboring NSD2 mutations. Massively parallel sequencing analysis of over 1000 pediatric cancer genomes identified the same NSD2 E1099K mutation in 14% of t(12;21)[ETV6-RUNX1] -containing ALLs. Together, these findings identify NSD2 as a potential therapeutic target for pediatric ALL and provide a general framework for the functional annotation of cancer epigenomes. Citation Format: Jacob Jaffe, Yan Wang, HoMan Chan, Jinghui Zhang, Roberts Huether, Gregory Kryukov, Jordan Taylor, Min Hu, Nathan Englund, Feng Yan, Zhaofu Wang, Lei Wei, Lei Wei, Jing Ma, John Easton, William R. Sellers, Nicholas Keen, Jun Liu, Jun Liu, Charles Mullighan, Steven Carr, James Downing, Levi Garraway, Frank Stegmeier. Global chromatin profiling identifies NSD2 mutations in pediatric acute lymphoblastic leukemia. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Jun 19-22, 2013; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2013;73(13 Suppl):Abstract nr PR01.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.CEC13-PR01
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 8
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    Abstract C151: Systematic discovery of cancer dependencies through deep coverage pshRNA screens
    American Association for Cancer Research (AACR) ; 2015
    In:  Molecular Cancer Therapeutics Vol. 14, No. 12_Supplement_2 ( 2015-12-01), p. C151-C151
    Details
    In: Molecular Cancer Therapeutics, American Association for Cancer Research (AACR), Vol. 14, No. 12_Supplement_2 ( 2015-12-01), p. C151-C151
    Abstract: Large scale cancer genome sequencing efforts, such as TCGA, revealed the landscape of genomic alterations across many tumor types, but the functional relevance of these alterations and genetic interdependencies cannot be fully assessed from these datasets. Thus, functional genomic screens, such as pooled shRNA 9pshRNA) screens, hold great promise to systematically identify cancer dependencies. However, RNAi discovery screens have been plagued by off target effects causing false positive results and possibly masking on-target effects. In order to address the previous problems with RNAi screens for cancer target discovery, we conducted a large scale pshRNA screening campaign targeting 7500 genes at a depth of 20 shRNAs per gene, across more than 300 cell lines of the cancer cell line encyclopedia (CCLE). The substantial shRNA and cell line depth in this screen significantly increased the robustness of results relative to previous published screens, and allowed the more robust identification of cancer dependencies. Moreover, integration of those growth phenotypes with known features of the cancer cell line encyclopedia (CCLE) enabled the identification of biomarkers (genetic, epigenetic, or proteomic) that correlate with sensitivity, and thus permitted discovery of synthetic lethal relationships. The increased depth provides a robust data set that can be used to find and validate new drug targets as well as infer pathway membership of novel genes by simple phenotypic similarity. The findings of this screen will be presented here. Citation Format: Michael Schlabach, Eric Billy, Konstantinos Mavrakis, Greg Hoffman, Tobias Schmelzle, Francesco Hofmann, Nicholas Keen, Frank Stegmeier, William Sellers. Systematic discovery of cancer dependencies through deep coverage pshRNA screens. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2015 Nov 5-9; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2015;14(12 Suppl 2):Abstract nr C151.
    Type of Medium: Online Resource
    ISSN: 1535-7163 , 1538-8514
    URL: Article
    DOI: 10.1158/1535-7163.TARG-15-C151
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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    SSG: 12
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  • 9
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    Abstract 2847: High complexity barcoding to study clonal dynamics in response to cancer therapy
    American Association for Cancer Research (AACR) ; 2015
    In:  Cancer Research Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2847-2847
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 75, No. 15_Supplement ( 2015-08-01), p. 2847-2847
    Abstract: Targeted therapies, such as erlotinib and imatinib, lead to dramatic clinical responses, but the emergence of resistance presents a significant challenge. Recent studies have revealed intratumoral heterogeneity as a potential source for the emergence of therapeutic resistance. However, it is still unclear if relapse/resistance is driven predominantly by pre-existing or de novo acquired alterations. To address this question, we developed a high-complexity barcode library, ClonTracer, which contains over 27 million unique DNA barcodes and thus enables the high resolution tracking of cancer cells under drug treatment. Using this library in two clinically relevant resistance models, we demonstrate that the majority of resistant clones pre-exist as rare subpopulations that become selected in response to therapeutic challenge. Furthermore, our data provide direct evidence that both genetic and non-genetic resistance mechanisms pre-exist in cancer cell populations. The ClonTracer barcoding strategy, together with mathematical modeling, enabled us to quantitatively dissect the frequency of drug-resistant subpopulations and evaluate the impact of combination treatments on the clonal complexity of these cancer models. Hence, monitoring of clonal diversity in drug-resistant cell populations by the ClonTracer barcoding strategy described here may provide a valuable tool to optimize therapeutic regimens towards the goal of curative cancer therapies. Citation Format: Hyo-eun C. Bhang, David A. Ruddy, Viveksagar Krishnamurthy Radhakrishna, Rui Zhao, Iris Kao, Daniel Rakiec, Pamela Shaw, Marissa Balak, Justina X. Caushi, Elizabeth Ackley, Nicholas Keen, Michael R. Schlabach, Michael Palmer, William R. Sellers, Franziska Michor, Vesselina G. Cooke, Joshua M. Korn, Frank Stegmeier. High complexity barcoding to study clonal dynamics in response to cancer therapy. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 2847. doi:10.1158/1538-7445.AM2015-2847
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2015-2847
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2015
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    detail.hit.zdb_id: 410466-3
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  • 10
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    Disordered methionine metabolism in MTAP/CDKN2A-deleted cancers leads to dependence on PRMT5
    American Association for the Advancement of Science (AAAS) ; 2016
    In:  Science Vol. 351, No. 6278 ( 2016-03-11), p. 1208-1213
    Details
    In: Science, American Association for the Advancement of Science (AAAS), Vol. 351, No. 6278 ( 2016-03-11), p. 1208-1213
    Abstract: 5-Methylthioadenosine phosphorylase (MTAP) is a key enzyme in the methionine salvage pathway. The MTAP gene is frequently deleted in human cancers because of its chromosomal proximity to the tumor suppressor gene CDKN2A . By interrogating data from a large-scale short hairpin RNA–mediated screen across 390 cancer cell line models, we found that the viability of MTAP-deficient cancer cells is impaired by depletion of the protein arginine methyltransferase PRMT5. MTAP-deleted cells accumulate the metabolite methylthioadenosine (MTA), which we found to inhibit PRMT5 methyltransferase activity. Deletion of MTAP in MTAP-proficient cells rendered them sensitive to PRMT5 depletion. Conversely, reconstitution of MTAP in an MTAP-deficient cell line rescued PRMT5 dependence. Thus, MTA accumulation in MTAP–deleted cancers creates a hypomorphic PRMT5 state that is selectively sensitized toward further PRMT5 inhibition. Inhibitors of PRMT5 that leverage this dysregulated metabolic state merit further investigation as a potential therapy for MTAP/CDKN2A-deleted tumors.
    Type of Medium: Online Resource
    ISSN: 0036-8075 , 1095-9203
    URL: Article
    DOI: 10.1126/science.aad5944
    RVK:
    TA 1000
    RVK:
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    Language: English
    Publisher: American Association for the Advancement of Science (AAAS)
    Publication Date: 2016
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    SSG: 11
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