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Transcriptomic change of ARDI1A mutant bladder cancer cell line treated with CPI-0209 or induced ARID1A expression

ABSTRACT: Transcriptomic change of ARDI1A mutant bladder cancer cell line treated with CPI-0209 or induced ARID1A expression

PROVIDER: PRJNA735952 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14758200_1.fastq.gz	Fastqsanger.gz
	SRR14758200_2.fastq.gz	Fastqsanger.gz
	SRR14758201_1.fastq.gz	Fastqsanger.gz
	SRR14758201_2.fastq.gz	Fastqsanger.gz
	SRR14758202_1.fastq.gz	Fastqsanger.gz

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Epigenomic change of ARDI1A mutant bladder cancer cell line treated with CPI-0209 or induced ARID1A expression

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Project description:Recurrent mutations in ARID1A occur frequently in advanced urothelial carcinoma, endometrial cancers and ovarian clear cell carcinoma, and may create an alternative chromatin state that can be exploited therapeutically. Previously, the histone methyltransferase EZH2 was identified as a targetable vulnerability in the context of ARID1A mutations. Here we describe the discovery of tulmimetostat (CPI-0209), a novel, orally available, clinical stage EZH2 inhibitor with remarkably long residence time and elucidate aspects of its application potential in ARID1A mutant tumors. Tulmimetostat administration as a single agent achieves in vivo efficacy in multiple ARID1A mutant bladder, ovarian, and endometrial tumor models and improves cisplatin response in chemotherapy-resistant models. Consistent with its potency and the comprehensive and durable level of target coverage, tulmimetostat demonstrates greater efficacy than other PRC2-targeted inhibitors at comparable or lower exposures in a bladder cancer xenograft mouse model due to greater changes in gene expression and a profound reduction of H3K27me3 levels in the tumors. Importantly, we report the identification of a tulmimetostat controlled gene expression signature in whole blood from a cohort of 32 cancer patients, whereby the number of genes altered in expression as well as the magnitude of expression changes exquisitely correlate with tulmimetostat exposure, thus representing a novel pharmacodynamic marker for the assessment of target coverage for PRC2-targeted agents in the clinic. Collectively, our data suggest tulmimetostat may unlock the full potential of EZH2 inhibition as a cancer therapeutic mechanism with potential applications in hematologic malignancies and in solid tumors, including in an ARID1A mutant setting.

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