Resistance From The Flanks

摘要

Cancer cells are notorious for their ability to acquire resistance to chemotherapeutic agents. Drug resistance can be acquired through a variety of adaptation mechanisms, including changes that modulate drug influx, eflux, and chemical activity. In some instances, drug resistance is established through tolerance of DNA damage induced by many chemotherapeutic drugs. This ability to survive in the presence of damaged DNA is a hallmark of many cancer cells, and may be an essential driving force for tumor cell evolution. In a recent study using gastric carcinoma cell lines, Ning et al. demonstrated that resistance to several different chemotherapeutic drugs correlated with an increase in telomere repeat binding factor 2 (TRF2), and that TRF2 overexpression confered resistance to a variety of DNA damaging chemotherapeutic agents.11 These findings provide a new link between telomere regulation, DNA damage response, and human carcinogenesis.