Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations

Benjamin G. Bitler; Katherine M. Aird; Rugang Zhang

doi:10.1080/23723556.2015.1032476

Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations

Benjamin G. Bitler
, Katherine M. Aird
, Rugang Zhang

Research output: Contribution to journal › Article › peer-review

22 Scopus citations

Abstract

The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50% of ovarian clear cell carcinomas (OCCCs). We reported that inhibition of enhancer of zeste homology 2 (EZH2) is synthetically lethal in ARID1A-mutated OCCC.

Original language	English (US)
Article number	e1032476
Journal	Molecular and Cellular Oncology
Volume	3
Issue number	1
DOIs	https://doi.org/10.1080/23723556.2015.1032476
State	Published - Jan 2 2016

All Science Journal Classification (ASJC) codes

Molecular Medicine
Cancer Research

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10.1080/23723556.2015.1032476

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title = "Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations",

abstract = "The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20\% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50\% of ovarian clear cell carcinomas (OCCCs). We reported that inhibition of enhancer of zeste homology 2 (EZH2) is synthetically lethal in ARID1A-mutated OCCC.",

author = "Bitler, \{Benjamin G.\} and Aird, \{Katherine M.\} and Rugang Zhang",

note = "Funding Information: This work was supported by grants from the US National Institutes of Health/National Cancer Institute (R01CA160331 and R01CA163377 to R. Z. and Cancer Center Support grant CA010815 to the Wistar Institute), a US Department of Defense Ovarian Cancer Academy award (OC093420 to R.Z.), and an Ovarian Cancer Research Fund Program project (to R.Z.). R.Z. is an Ovarian Cancer Research Fund Liz Tilbe- ris Scholar. B.G.B. is supported by an American Cancer Society postdoctoral fellowship (PF-13–058–01-TBE). K.M.A. is supported by a training grant from the US National Institutes of Health/National Cancer Institute (T32CA9171–35). Publisher Copyright: {\textcopyright} 2016, {\textcopyright} 2016 Taylor \& Francis Group, LLC.",

year = "2016",

month = jan,

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doi = "10.1080/23723556.2015.1032476",

language = "English (US)",

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T1 - Epigenetic synthetic lethality in ovarian clear cell carcinoma

T2 - EZH2 and ARID1A mutations

AU - Bitler, Benjamin G.

AU - Aird, Katherine M.

AU - Zhang, Rugang

N1 - Funding Information: This work was supported by grants from the US National Institutes of Health/National Cancer Institute (R01CA160331 and R01CA163377 to R. Z. and Cancer Center Support grant CA010815 to the Wistar Institute), a US Department of Defense Ovarian Cancer Academy award (OC093420 to R.Z.), and an Ovarian Cancer Research Fund Program project (to R.Z.). R.Z. is an Ovarian Cancer Research Fund Liz Tilbe- ris Scholar. B.G.B. is supported by an American Cancer Society postdoctoral fellowship (PF-13–058–01-TBE). K.M.A. is supported by a training grant from the US National Institutes of Health/National Cancer Institute (T32CA9171–35). Publisher Copyright: © 2016, © 2016 Taylor & Francis Group, LLC.

PY - 2016/1/2

Y1 - 2016/1/2

N2 - The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50% of ovarian clear cell carcinomas (OCCCs). We reported that inhibition of enhancer of zeste homology 2 (EZH2) is synthetically lethal in ARID1A-mutated OCCC.

AB - The components of the Switch/Sucrose non-fermentable (SWI/SNF) complex are mutated in approximately 20% of human cancers. The A/T-rich interacting domain 1A (ARID1A) subunit has one of the highest mutation rates. Most notably, ARID1A is mutated in over 50% of ovarian clear cell carcinomas (OCCCs). We reported that inhibition of enhancer of zeste homology 2 (EZH2) is synthetically lethal in ARID1A-mutated OCCC.

UR - https://www.scopus.com/pages/publications/85020005446

UR - https://www.scopus.com/pages/publications/85020005446#tab=citedBy

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DO - 10.1080/23723556.2015.1032476

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JF - Molecular and Cellular Oncology

IS - 1

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Epigenetic synthetic lethality in ovarian clear cell carcinoma: EZH2 and ARID1A mutations

Abstract

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