Chromoplexy and hypoxic microenvironment drives prostate cancer

Chromoplexy, or chromosomal change, in which the prostate cancer tumour genome advances through mutation, translocation, and other interdependent DNA rearrangements mediated by post-translational modifications such as ubiquitination and sumoylation, might be key to a series of essential cancer processes including avoidance of apoptosis, invasion, and metastasis, and therapeutic resistance.7 Hence, measures of genomic heterogeneity, instability or change might better characterise the notion of chromoplexy as a measure of cancer cells or clusters to achieve key biological functions needed for tumour progression compared with individual genetic aberrations or disordered pathway signaling.