The Histone Mark H3K36me3 Regulates Human DNA Mismatch Repair through Its Interaction with MutSα

TL;DR: A more detailed understanding of histone lysine methylation is necessary for elucidating complex biological processes and, ultimately, for developing and improving disease treatments.

TL;DR: The hallmark genetic alterations that are associated with distinct epigenetic features and patient characteristics in both paediatric and adult disease are summarized, and the complex interplay between the glioblastoma genome and epigenome is examined.

TL;DR: This Review summarizes common genomic and chromosomal copy number abnormalities in ccRCC, providing a mechanistic framework with which to organize these features into initiating events, drivers of progression and factors that confer lethality.

TL;DR: Results suggest ARID1A deficiency contributes to impaired MMR and mutator phenotype in cancer, and may cooperate with immune checkpoint blockade therapy, complementing MSI-based prognosis.

TL;DR: The spectrum of microsatellite alterations in noncolonic tumors was reviewed, and it was concluded that the above recommendations apply only to colorectal neoplasms.

TL;DR: Exome and genome sequences and whole-genome sequence analysis revealed frequent structural rearrangements, including in-frame exonic alterations within EGFR and SIK2 kinases, which are attractive targets for biological characterization and therapeutic targeting of lung adenocarcinoma.

TL;DR: The mutational spectrum is similar to myeloid tumours, and moreover, the global transcriptional profile of ETP ALL was similar to that of normal andMyeloid leukaemia haematopoietic stem cells, suggesting that addition of myeloids-directed therapies might improve the poor outcome of E TP ALL.

TL;DR: Analysis of sporadic colorectal tumors for the expression of hMLH1 by immunohistochemistry indicates that DNA methylation is likely to be a common mode of mismatch repair gene inactivation in sporadic tumors.