Prakash Kulkarni

TL;DR: It is illustrated how phenotypic plasticity and consequent mutation-independent or non-genetic heterogeneity possibly driven by protein conformational dynamics can stochastically give rise to androgen independence in PCa, and it is suggested that dynamic phenotyping plasticity should be considered in devising therapeutic dosing strategies designed to treat and manage PCa.

TL;DR: This work discusses the phenotypic transitions in cancer from a dynamical systems perspective and invoke the concept of “cancer attractors”—hidden stable states of the underlying regulatory network that are not occupied by normal cells.

TL;DR: Multiple biophysical approaches that report conformational preferences of the intrinsically disordered protein (IDP) Prostate-Associated Gene 4 with human cancer biology and nonlinear dynamics suggest that the phosphorylation-induced conformational dynamics of PAGE4 may play a role in modulating changes between PCa cell phenotypes.

TL;DR: It is suggested that targeting IDPs implicated in EMT in PCa may be a new strategy to gain additional insights and develop novel treatments for this disease, which is the most common form of cancer in adult men.

TL;DR: A mechanism-based mathematical model is constructed that allows us to capture the interactions ofdifferent phosphoforms of PAGE4 with AP-1 and its downstream target, the androgen receptor (AR)-a key therapeutic target in prostate cancer.