Prostate cancer is a multifactorial disease. It harbours a miscellany of fusion transcripts originating from chromosomal rearrangements. Additionally, susceptibility to genomic rearrangements is particularly enhanced in prostate cancer which is triggered by androgen. These fusion transcripts hijack the promoters of androgen regulated genes and exploit them for triggering anomalies. These chimeric transcripts vary in various cancer foci. A complex barcode underlies the heterogeneous response of these entities to stress. Nonetheless these transcripts create a formidable state of affairs within the cell. Exacerbation of the disease which is mediated by fusion transcripts culminates into a poor survival.
Currently there are unsatisfactory and inefficient measures to circumscribe this rapidly growing threat. The review will encompass various mechanistic insights of the androgen receptor mediated genomic instability and the mediators entailed in rendering cell error prone. Moreover efficacy of therapeutic interventions recently designed keeping in view the molecular hierarchy will be evaluated.
ATM; Prostate cancer; TMPRSS2-ERG