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Cancer genetics is the study in humans and other animals of heritable gene variants that cause or confer altered risk of tumour or hematological malignancy. Individual cancer risk varies and is influenced by familial and sporadic oncogene or tumour suppressor gene mutations as well as rare and common constitutional variants present in the population.
SHP2 interacts with ACK1 kinase to erase pY54-H3 (Tyr54-phosphorylation of histones H3) epigenetic marks and triggers Androgen receptor transcriptional program. It explains genital abnormalities and infertility in LEOPARD syndrome patients, and AR upregulation in prostate cancer.
Mitotic errors promote chromosome fragmentation and rearrangements through chromothripsis. Here, the authors identify NHEJ as the primary DSB repair pathway underlying chromothripsis and investigate the kinetics of fragment reassembly across the cell cycle.
Thirty years after the discovery and cloning of the cancer susceptibility gene BRCA1, William Foulkes reflects on this defining moment for breast and ovarian cancer genetics and how far the field has come.
Parreno et al. provide evidence for epigenetically initiated cancers in Drosophila and show that cancer develops after transient loss of Polycomb group proteins in the absence of recurrent mutations.