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Homo sapiens

ABSTRACT: Genomic basis for clinical response to histone deacetylase inhibition in advanced urothelial carcinoma

PROVIDER: PRJNA407632 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6044760.fastq.gz	Fastqsanger.gz
	SRR6044761.fastq.gz	Fastqsanger.gz
	SRR6044762.fastq.gz	Fastqsanger.gz
	SRR6044763.fastq.gz	Fastqsanger.gz
	SRR6044764.fastq.gz	Fastqsanger.gz

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Genomic basis for clinical response to histone deacetylase inhibition in advanced urothelial carcinoma

Project description:Abstract Background: Histone deacetylase (HDAC) inhibition has shown some efficacy in urothelial carcinoma (UC); the genomic basis for clinical response is not known. Methods: In two separate phase I clinical trials testing HDAC inhibitors in advanced solid tumors, we identified one patient with advanced UC who had a complete response (CR) to belinostat and one with advanced UC who had a partial response (PR) to panobinostat. The archived tumor of the responders was genomically characterized and studied in comparison to others with UC, in the context of their response to HDAC inhibition on trial. UC cell lines treated with panobinostat were studied to elucidate the mechanisms of benefit. Results: The two patients who responded to HDAC inhibition had ARID1A and FANCD2 mutations. The patient who had a CR to HDAC inhibition had the highest tumor mutational burden of all tumors. Corroborating the basis of sensitivity, transcriptional profiling of platinum resistant ARID1A mutated HT1197 cells treated with panobinostat revealed downregulation of cyto-proliferative and DNA repair gene sets and upregulation of inflammatory gene sets. Conclusions: Clinical efficacy of HDAC inhibition in UC may be dependent on overlapping SWI/SNF pathway mutations and DNA repair defects. Tumor mutational burden may predict the depth and duration of benefit.

2018-10-31 | GSE103928 | GEO

Epigenetic regulation of mammalian Hedgehog signaling to the stroma determines the molecular subtype of human bladder cancer

Project description:In bladder, loss of mammalian Sonic Hedgehog (Shh) accompanies progression to invasive urothelial carcinoma, but the molecular mechanisms underlying this cancer-initiating event are poorly defined. Here, we show that loss of Shh results from hypermethylation of the CpG shore of the Shh gene, and that inhibition of DNA methylation increases Shh expression to halt the initiation of murine urothelial carcinoma at the early stage of progression. In full-fledged tumors, pharmacologic augmentation of Hedgehog (Hh) pathway activity impedes tumor growth, and this cancer-restraining effect of Hh signaling is mediated by the stromal response to Shh signals, which stimulates subtype conversion of basal to luminal-like urothelial carcinoma. Our findings thus provide a basis to develop subtype-specific strategies for the management of human bladder cancer.

2019-04-09 | GSE129441 | GEO

A Phase I/II Study of Ivaltinostat Combined with Gemcitabine and Erlotinib in Patients with Untreated Locally Advanced or Metastatic Pancreatic Adenocarcinoma

Project description:Histone deacetylase inhibitors (HDACi) are currently used as anticancer drugs; however, no clinical trials proved efficacy in pancreatic adenocarcinoma (PDAC). Ivaltinostat, a novel intravenous HDACi, presented cell growth inhibition and improved chemo-sensitivity in PDAC. This phase I/II study demonstrated ivaltinostat with gemcitabine and erlotinib can be administered safely to improve survivals in patients with untreated advanced PDAC. In addition, we proposed potential blood markers to predict response to ivaltinostat treatment based on correlative studies.

2021-11-29 | GSE189724 | GEO

Study of CPI-0209 in patients with advanced tumors.

Project description:Advanced bladder cancer remains a difficult cancer to treat, and for the majority of patients, current standard treatments ultimately prove ineffective. These tumors frequently harbor mutations in the BAF complex subunit ARID1A, which has been reported to confer sensitivity to EZH2 inhibition in several tumor types. Here we describe the generation of CPI-0209, a best-in-class, orally available EZH2 inhibitor. We show that mutant bladder cancer lines harboring ARID1A loss of function (LOF) mutations are preferentially sensitive to inhibition of EZH2. Treatment with CPI-0209 not only elicits a significant monotherapeutic response in ARID1A mutant models, it also outperforms cisplatin and improves response in chemo-resistant models. These findings shine light on new therapeutic opportunities for patients with advanced urothelial carcinoma.

2024-06-26 | GSE176490 | GEO

Epigenomic profile of bladder cancer cell line HT1376 treated with CPI-0209

2024-06-26 | GSE176486 | GEO

Xenograft of bladder cancer cell line HT1376 were treated with or without EZH2 inhibitors before subject to RNA-seq

2024-06-26 | GSE176485 | GEO

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

2024-06-26 | GSE176477 | GEO

Transcriptomic change of bladder cancer cell lines treated with CPI-0209 [2]

2024-06-26 | GSE176362 | GEO

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

2024-06-26 | GSE176358 | GEO

Integrated genomic and gene expression profiling identifies two major gene/genomic circuits operating in urothelial carcinoma

Project description:This SuperSeries is composed of the following subset Series: GSE32535: Integrated genomic and gene expression profiling identifies two major gene/genomic circuits operating in urothelial carcinoma (genomic) GSE32548: Integrated genomic and gene expression profiling identifies two major gene/genomic circuits operating in urothelial carcinoma (gene expression) Refer to individual Series

2012-06-17 | E-GEOD-32549 | biostudies-arrayexpress

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