Lori A. Hazlehurst

TL;DR: It is demonstrated that FN-mediated adhesion confers a survival advantage for myeloma cells acutely exposed to cytotoxic drugs by inhibiting drug-induced apoptosis, which may explain how some cells survive initial drug exposure and eventually express classical mechanisms of drug resistance such as MDR1 overexpression.

TL;DR: In this form of drug resistance, tumor cells are transiently and reversibly protected from apoptosis induced by both chemotherapy and physiologic mediators of cell death, which allows tumor cells to survive the insult of chemotherapy, leading to minimal residual disease, and thereby increases the probability for the development of acquired drug resistance.

TL;DR: It is demonstrated that β1 mediated adhesion of myeloma cells to FN regulates p27Kip1 levels and that p27kip1 Levels are causally related to CAM-DR.

TL;DR: It is proposed that specific niches within the tumor microenvironment may provide a sanctuary for subpopulations of tumors cells that affords a survival advantage following initial drug exposure and may facilitate the acquisition of acquired drug resistance.

TL;DR: A mechanism by which collaborative signaling by beta1 integrin and gp130 confers an increased survival advantage to multiple myeloma cells is suggested.