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Expression profile of PBMCs following decitabine treatment

ABSTRACT: The epigenetic regulation, for example, DNA methylation, controls the development and differentiation of both tumor cells and immunocytes. Treatment with DNA demethylating agent (such as decitabine) has shown a dramatic clinical benefit in hematological malignancies and solid tumors. However, the influence of epigenetic therapy on host immune system remains unclear.

ORGANISM(S): Homo sapiens

PROVIDER: GSE72686 | GEO | 2016/06/30

SECONDARY ACCESSION(S): PRJNA294667

REPOSITORIES: GEO

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Expression profile of PBMCs following decitabine treatment

Project description:The epigenetic regulation, for example, DNA methylation, controls the development and differentiation of both tumor cells and immunocytes. Treatment with DNA demethylating agent (such as decitabine) has shown a dramatic clinical benefit in hematological malignancies and solid tumors. However, the influence of epigenetic therapy on host immune system remains unclear. To investigate the effects of low-dose decitabine therapy on T cells, We collected whole blood samples from two solid tumor patients pre and post low-dose decitabine therapy, and detected the expression profiles of PBMCs.

2016-06-30 | E-GEOD-72686 | biostudies-arrayexpress

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SUM159 BrCa Decitabine Gene Expression

Project description:Dysregulation of DNA methylation is an established feature of breast cancers. DNA demethylating therapies like decitabine are proposed for the treatment of triple-negative breast cancers (TNBCs) and indicators of response need to be identified. For this purpose, we characterized the effects of decitabine in a panel of 10 breast cancer cell lines and observed a range of sensitivity to decitabine that was not subtype-specific. Knockdown of potential key effectors demonstrated the requirement of deoxycytidine kinase (DCK) for decitabine response in breast cancer cells. In treatment-naive breast tumors, DCK was higher in TNBCs, and DCK levels were sustained or increased post chemotherapy treatment. This suggests that limited DCK levels will not be a barrier to response in TNBC patients treated with decitabine as a second line treatment or in a clinical trial. Methylome analysis revealed that genome-wide, region-specific, tumor suppressor gene-specific methylation, and decitabine-induced demethylation did not predict response to decitabine. Gene set enrichment analysis (GSEA) of transcriptome data demonstrated that decitabine induced genes within apoptosis, cell cycle, stress, and immune pathways in decitabine treated cells. Induced genes included those characterized by the viral mimicry response; however knockdown of key effectors of the pathway did not affect decitabine sensitivity suggesting that breast cancer growth suppression by decitabine is independent of viral mimicry. Finally, taxol-resistant breast cancer cells expressing high levels of multidrug resistance transporter ABCB1 remained sensitive to decitabine, suggesting that the drug could be used as second-line treatment for chemoresistant patients. We used microarrays to determine genome-wide expression changes induced by DNA de-methylating agent decitabine in breast cancer cell lines

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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.

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