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DNA methylation is tightly regulated during developme.
Recently, scientists at the Max Planck Institute for Molecular Genetics and .
Co-corresponding authors, Alexander Meissner of the Max Planck Institute for Molecular Genetics and Charles Mullighan of .
In this study, researchers used whole-genome bisulfite sequencing to analyze cytosine methylation patterns in 82 children with A.
"Through comprehensive genomic analysis of large cohorts of B-cell ALL and T-cell ALL, corresponding cell lines, and healthy samples, we delineated the unique methylome of ALL and learned about epigenomic alterations during leukemogenesis," The author explain.
When they compared the methylation profiles of the ALL samples with five B-ALL cell lines, nine T-ALL cell lines, and healthy cells, they found that CpG islands in ALL were hypermethylat.
"Overall methylation loss has long been recognized as a feature of tumorigenesis," the authors explain, noting that "T-ALL samples exhibited an overall DNA methylation landscape comparable to that of T-cell precursors in healthy infants, The B-ALL samples, however, showed varying degrees of mild methylation lo.
The research team then extended these results by comparing DNA methylation profiles of ALL, CLL, acute myeloid leukemia (AML), and eight solid tumo.
They found hypermethylation of the TET2 promoter in more than a quarter of the T-ALL sampl.
Likewise, the researchers also found an association between increased DNA methylation and enhanced DNMT3B expressi.
The authors believe that this study provides important data and insights into the non-canonical epigenetic regulation of ALL, helps focus attention on specific aspects of the cancer methylome, and contributes to a better mechanistic understanding Epigenetic changes common in canc.
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Hetzel,.