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DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

ABSTRACT: DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

OTHER RELATED OMICS DATASETS IN: GSE111305

PROVIDER: PRJNA437571 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6820600.fastq.gz	Fastqsanger.gz
	SRR6820601.fastq.gz	Fastqsanger.gz
	SRR6820602.fastq.gz	Fastqsanger.gz
	SRR6820599.fastq.gz	Fastqsanger.gz

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DNA methylation profile of adipocytes treated with DNMT inhibitor, guadecitabine (100nM, 3X daily).

2018-03-10 | GSE111617 | GEO

GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

Project description:GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

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Genomic and epigenomic predictors of response to Guadecitabine in relapsed/refractory Acute Myelogenous Leukemia

Project description:Guadecitabine is a second generation DNA methylation inhibitor with improved pharmacokinetics and clinical activity in relapsed/refractory AML (rrAML). Here we report genome-wide DNA methylation profiles in pre-treatment samples from 116 rrAML patients treated at therapeutic doses of guadecitabine in a phase I/II study. Response rate to guadecitabine was 22 % (16CR, 42 12CRi/CRp). There were no strong mutation or methylation predictors of response. Gene expression defined a subset of patients (~20%) that had (i) high DNMT3B and low CDKN2B, CTCF and CDA expression, (ii) enrichment for KRAS/NRAS mutations, (iii) frequent CpG island hypermethylation (iv) low LINE1 hypomethylation after treatment and (v) resistance to guadecitabine in both phase I (response rate 0 % vs 33 %, p=0.07) and phase II components of the study (response rate 5 % vs. 30 %, p=0.02). Multivariate analysis identified peripheral blood blasts and hemoglobin as predictors of response and cytogenetics, gene expression, RAS mutations and hemoglobin as predictors of survival. Thus, a subset of patients (∿ 20%) with rrAML are unlikely to benefit from single agent guadecitabine. In the remaining 80%, guadecitabine is a viable option with a median survival of ∿ 8 months and a three year survival rate of over 20%.

2019-08-06 | GSE112838 | GEO

GSF1243: RNA-seq data of adipocytes treated with DNMT1 inhibitor, guadecitabine (100nM), for 3 days

Project description:Ovarian cancer (OC) cells frequently metastasize to the omentum and adipocytes play a significant role in ovarian tumor progression. Therapeutic interventions targeting aberrant DNA methylation in ovarian tumors have shown promise in the clinic but the effects of epigenetic therapy on the tumor microenvironment are understudied. Here, we examined the effect of adipocytes on OC cell behavior in culture and impact of targeting DNA methylation in adipocytes on OC metastasis. The presence of adipocytes increased OC cell migration and invasion and proximal and direct co-culture of adipocytes .increased OC proliferation alone or after treatment with carboplatin. Treatment of adipocytes with hypomethylating agent guadecitabine decreased migration and invasion of OC cells towards adipocytes. Due to this result, we performed RNA-seq of adipocytes treated with DNMT1 inhibitor to analyze differential gene expression changes that occur in the adipocyte that may explain the above observation that hypomethylating agent treatment of adipocytes decrease migration and invasion.

2018-03-02 | GSE111305 | GEO

Guadecitabine and Nivolumab in Treating Refractory Metastatic Colorectal Cancer

Project description:This phase Ib/II trial studies the side effects and best dose of guadecitabine when given together with nivolumab and to see how well they work in treating participants with colorectal cancer that does not respond to treatment and has spread to other places in the body. Drugs used in chemotherapy, such as guadecitabine, work in different ways to stop the growth of tumor cells, either by killing the cells, by stopping them from dividing, or by stopping them from spreading. Monoclonal antibodies, such as nivolumab, may interfere with the ability of tumor cells to grow and spread. Giving guadecitabine and nivolumab may work better in treating participants with colorectal cancer.

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A phase 1 study of guadecitabine plus cisplatin in platinum refractory germ cell tumors [Methylation]

Project description:Germ cell tumors (GCTs) can be cured with cisplatin-based therapy, although a clinically significant number of patents are refractory and die of progressive disease. Based on preclinical studies indicating that refractory testicular GCTs are hypersensitive to hypomethylating agents (HMA), we conducted a phase I trial [NCT02429466] of the next-generation HMA guadecitabine (SGI-110) in combination with cisplatin in patients with recurrent, cisplatin-resistant GCTs. The primary endpoint was safety and toxicity including DLT and MTD. A total of 14 patients were enrolled. The majority of patients were heavily pretreated. MTD was determined to be 30 mg/m2 guadecitabine followed by cisplatin 100 mg/m2. DLTs were neutropenia and thrombocytopenia. Three patients had partial responses by RECIST criteria, two of these patients qualified as complete responses by serum tumor marker criteria with survival of 16 and 26 months. Three patients also had stable disease for an overall response rate of 23% and clinical benefit rate of 46%. Genome-wide analysis pre- and post-guadecitabine indicated dramatic and widespread global DNA demethylation in cell-free plasma samples including in the promoters of genes of cancer related pathways. In summary, the combination of guadecitabine followed by cisplatin was tolerable and demonstrated biological activity in patients with platinum refractory GCTs.

2020-12-25 | GSE152802 | GEO

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Refractory testicular germ cell tumors are highly sensitive to the second generation DNA methlation inhibitor guadecitabine

Project description:Comparison of gene expression in cisplatin resistant testicular germ cell tumor xenografts treated with vehicle (PBS) or the DNA methylation inhibitor guadecitabine

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The type of DNA damage response after Decitabine treatment depends on the level of DNMT activity

Project description:Decitabine and Azacytidine are considered as epigenetic drugs that induce DNA-methyltransferase (DNMT)-DNA crosslinks, resulting in DNA-hypomethylation and -damage. Although they are already applied against myeloid cancers, important aspects of their mode of action remain unknown, highly limiting their clinical potential. Using a combinatorial approach, we reveal that the efficacy profile of both compounds primarily depends on the level of induced DNA-damage. Under low DNMT-activity, only Decitabine has a substantial impact. Conversely, when DNMT-activity is high, toxicity and cellular response to both compounds are dramatically increased, but do not primarily depend on DNA-hypomethylation or RNA-associated processes. By investigating proteome dynamics on chromatin, we show that Decitabine induces a strictly DNMT-dependent multifaceted DNA-damage response based on chromatin-recruitment, but not expression level changes of repair-associated proteins. The choice of DNA-repair pathway herby depends on the severity of Decitabine-induced DNA-lesions. While under moderate DNMT-activity, mismatch (MMR), base-excision (BER) and Fanconi anemia-dependent DNA-repair combined with homologous recombination are activated in response to Decitabine, high DNMT-activity and therefore immense replication stress, induce activation of MMR and BER followed by non-homologous end-joining.

2024-06-19 | PXD045353 | Pride

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