Explaining cancer type specific mutations with transcriptomic and epigenomic features in normal tissues.

ABSTRACT: Most cancer driver genes are involved in generic cellular processes such as DNA repair, cell proliferation and cell adhesion, yet their mutations are often confined to specific cancer types. To resolve this paradox, we explained mutation frequencies of selected genes across tumor types with four features in the corresponding normal tissues from cancer-free subjects: mRNA expression and chromatin accessibility of mutated genes, mRNA expressions of their neighbors in curated pathways and the protein-protein interaction network. Encouragingly, these transcriptomic/epigenomic features in normal tissues were closely associated with mutational/functional characteristics in tumors. First, chromatin accessibility was a necessary but not sufficient condition for frequent mutations. Second, variatio

SUBMITTER: Tiong KL 

PROVIDER: S-EPMC6065413 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature