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Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [Methylation]

ABSTRACT: Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [Methylation]

PROVIDER: PRJNA763581 | ENA |

REPOSITORIES: ENA

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Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma

Project description:Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma

| PRJNA763577 | ENA

Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [RNA-Seq]

Project description:Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [RNA-Seq]

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Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [Methylation]

Project description:To understand the global methylation patterns in MCC cell lines

2021-09-15 | GSE184206 | GEO

Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma [RNA-Seq]

Project description:To understand the global methylation pattern in MCC

2021-09-15 | GSE176466 | GEO

Viral Status Predicts the Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma.

Project description:Merkel cell carcinoma (MCC) is an aggressive cutaneous neuroendocrine carcinoma that is classified as Merkel cell polyomavirus-positive (virus positive [VP]) or Merkel cell polyomavirus-negative (virus negative [VN]). Epigenetic changes, such as DNA methylation, can alter gene expression and influence cancer progression. However, patterns of DNA methylation and the therapeutic efficacy of hypomethylating agents have not been fully explored in MCC. We characterized genome-wide DNA methylation in 16 MCC cell lines from both molecular subclasses in comparison with other cancer types and found that the overall profile of MCC is similar to that of small-cell lung carcinoma. Comparison of VP MCC with VN MCC revealed 2,260 differentially methylated positions. The hypomethylating agent decitabine upregulated the expression of antigen-presenting machinery in MCC cell lines and stimulated membrane expression of HLA-A in VP and VN MCC xenograft tumors. Decitabine also induced prominent caspase- and large T antigen‒independent cell death in VP MCC, whereas VN MCC cell lines displayed decreased proliferation without increased cell death. In mouse xenografts, decitabine significantly decreased the size of VP tumors but not that of VN tumors. Our findings indicate that viral status predicts genomic methylation patterns in MCC and that decitabine may be therapeutically effective against MCC through antiproliferative effects, cell death, and increased immune recognition.

| S-EPMC8860850 | biostudies-literature

Viral Status Predicts Patterns of Genome Methylation and Decitabine Response in Merkel Cell Carcinoma

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-09-15 | GSE184207 | GEO

DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

Project description:DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

| PRJNA453379 | ENA

Comparative Transcriptional Profiling of human Merkel cells and Merkel Cell Carcinoma

Project description:Merkel cell carcinoma is supposed to be derived from Merkel cells after infection by Merkel cell polyomavirus (MCV) and other poorly known events. A transcriptional profiling with cDNA microarrays was performed on cells from MCV+ Merkel cell carcinomas and isolated normal Merkel cells. This microarray revealed numerous significantly upregulated genes and down-regulated genes. The extensive list of genes identified in these experiments provides a large body of potentially valuable information of Merkel cell carcinoma carcinogenesis and could represent a source of potential targets for cancer therapy. Two-conditions experiment, MCV vs Normal Merkel Cell. Biological replicates : 4 MCV (Cy5), 1 control = pool of Normal Merkel cells from 3 liftings

2014-01-01 | E-GEOD-50434 | biostudies-arrayexpress

Impact of MLL5 expression on decitabine efficacy and DNA methylation in acute myeloid leukemia

Project description:We found previously that the effect of decitabine (DAC) on hematopoietic stem cell viability differed between Mll5 wildtype and null cells. We therefore investigated the role of MLL5 expression levels on outcome of AML patients who were treated with decitabine. High MLL5 expressing AML patients have improved overall survival when treated with decitabine. In transformed murine cells, loss of Mll5 was associated with resistance to low-dose decitabine, less frequent promoter methylation, and reduced demethylation upon decitabine treatment. These data suggest a biological link between MLL5 expression and decitabine response involving regulation of DNA methylation. Leukemia cell model was generated by co-transfer of HOXA9 and MEIS1 into Mll5 wildtype or knockout mouse bone marrow cells. MeDIP was performed in Mll5+/+ HOXA9/MEIS1 and Mll5-/- HOXA9/MEIS1 leukemic cells, untreated or treated with 3-day exposure of 20 nM decitabine, triplicate for each condition. MeDIP-enriched DNA was amplified with the GenomePlex Complete Whole Genome Amplification (WGA) Kit (Sigma-Aldrich). DNA from three MeDIP and WGA of each cell type and treatment was pooled for subsequent microarray analysis. The enriched DNA and corresponding input genomic DNA was labeled, hybridized and scanned on Agilent custom mouse promoter microarrays (Agilent-025976 AP_1M_Custom_CH3, assembly build mm9). The methylation value of individual probes was defined by the signal intensity ratio of MeDIP DNA (Cy3) compared to input DNA (Cy5) . Methylated DNA immunoprecipitation coupled with Agilent mouse promoter CpG arrays (MeDIP-chip)

2014-07-01 | E-GEOD-52199 | biostudies-arrayexpress

DNA methylation status predicts survival in metastasis free clear cell renal cell carcinoma

Project description:Background: Clear cell renal cell carcinomas (ccRCCs) display divergent clinical phenotypes. Up to one third of patients with local disease at diagnosis will progress. Therefore, it is a need to identify patients at risk for recurrence. In the present study, we analyzed genome-wide promoter DNA methylation at diagnosis in relation to clinicopathological parameters, in order to identify DNA methylation profiles associated with risk for progress. Method: DNA methylation status in 155,931 CpGs located in gene promoter regions was analyzed by Illumina HumanMethylation450K arrays in diagnostic tissue samples from 115 ccRCC patients. Methylation profiles were compared with genetic aberrations and clinicopathological parameters. Results: The tumors separated into two clusters based on genome-wide promoter methylation status. The tumors in these clusters differed in tumor diameter (p < 0.001), TNM stage (p < 0.001), morphological grade (p < 0.001), and patients outcome (5 year cancer specific survival (pCSS5yr) 72 % in cluster A vs 26 % in cluster B, p < 0.001). When metastasis-status (M0/M1) and cluster A/B status at diagnosis were combined, we found poor survival in M1 patients regardless of cluster A/B status (pCSS5yr 9 % vs 6 %). In M0 patients, the cluster status clearly separated in survival (pCSS5yr 81 % vs 17 %; p < 0.001). We identified a methylation profile of 398 CpGs that was associated with progress of disease, which included differently methylated CpG sites in the SMAD6, SOCS3 and MX2 genes. An integrated genomic and epigenomic analysis revealed significant correlations between the total number of genetic aberrations and hypermethylated CpGs (R = 0.435, p > 0.001), and predicted mitotic age (R = 0.407, p < 0.001). Conclusion: DNA methylation analysis at diagnosis in ccRCC has the potential to improve outcome-prediction and therapy stratification.

2019-01-23 | GSE113501 | GEO

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