Getting personal with prostate cancer: adding new pieces to an incomplete jigsaw puzzle.

Prostate cancer is a multifaceted molecular anomaly that is insurmountable to date because of the orchestrated network of negative regulators that drive carcinogenesis. A substantial fraction of information has been added that gives yet an unclear snapshot of therapeutic interventions in prostate cancer. Increasing sophisticated interpretations point towards some important aspects of prostate cancer aggressiveness like microRNAs, prostate cancer stem cells and TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) refractoriness.

ATM protein kinase: the linchpin of cellular defenses to stress.

ATM is the most significant molecule involved in monitoring the genomic integrity of the cell. Any damage done to DNA relentlessly challenges the cellular machinery involved in recognition, processing and repair of these insults. ATM kinase is activated early to detect and signal lesions in DNA, arrest the cell cycle, establish DNA repair signaling and faithfully restore the damaged chromatin.

Therapeutic Effect of Epigallocatechin-3-gallate (EGCG) and Silibinin on ATM Dynamics in Prostate Cancer Cell Line LNCaP.

Background: Epigallocatechin-3-gallate (EGCG) is a major ingredient of green tea (GT) and silibinin (SB), the active component of Silymarin presumably hold a potential to prevent pathogenomics. Prostate cancer exacerbation is triggered by fusion transcripts formed because of genomic instability induced by juxtapositioning of two genes. This chimeric transcript is implicated in androgen dependent and independent prostate cancer.