Journal
GENES CHROMOSOMES & CANCER
Volume 61, Issue 7, Pages 432-436Publisher
WILEY
DOI: 10.1002/gcc.23034
Keywords
epigenetic; genomic; micro-RNAs; T-cell prolymphocytic leukemia; T-cells
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Funding
- German Research Foundation (DFG) [SFB 1074, B9N/B9]
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Deregulation of micro(mi)-RNAs is a common mechanism in tumorigenesis. In T-cell prolymphocytic leukemia (T-PLL), 111 miRNAs were found to be differentially expressed compared to normal T-cell subsets, with 33 of them belonging to cancer-related miRNA gene clusters. Upregulation of the miR-200c/-141 cluster in T-PLL was associated with DNA hypomethylation and active promoter marks, suggesting that copy number aberrations and epigenetic changes could contribute to miRNA deregulation in T-PLL.
Deregulation of micro(mi)-RNAs is a common mechanism in tumorigenesis. We investigated the expression of 2083 miRNAs in T-cell prolymphocytic leukemia (T-PLL). Compared to physiologic CD4+ and CD8+ T-cell subsets, 111 miRNAs were differentially expressed in T-PLL. Of these, 33 belonged to miRNA gene clusters linked to cancer. Genomic variants affecting miRNAs were infrequent with the notable exception of copy number aberrations. Remarkably, we found strong upregulation of the miR-200c/-141 cluster in T-PLL to be associated with DNA hypomethylation and active promoter marks. Our findings suggest that copy number aberrations and epigenetic changes could contribute to miRNA deregulation in T-PLL.
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