Library Subscription: Guest

COMMENTARY. Regulation of Drug and Immune Resistance by YY1 in Cancer

Volume 1, Issue 1-2, 2010, pp. 149-151
DOI: 10.1615/ForumImmunDisTher.v1.i1-2.120
Get accessGet access

ABSTRACT

Drug resistance, especially multidrug resistance (MDR), remains a major and difficult problem to resolve in the therapy of many cancer types. This process has previously been investigated mainly in a "pharmacologic" manner focused on the ability of tumor cells to extrude or inactivate the cytotoxic agents or to modify their targets of action. Much attention has focused on the overexpression of multidrug efflux transporters such as P-glycoprotein (MDR1, ABCB1) and many others. Nevertheless, evidence suggests that the sole reversion of the overexpression of such transporters has clinical success only in a few situations. On the other hand, today it is recognized that clinical MDR is often a multifactorial and heterogeneous process; many different molecular alterations, known to be involved in the malignant transformation and progression, may also be responsible for tumor drug resistance. Clearly, induction of tumor cell killing is fundamental for the efficacy of anticancer drugs. Mechanisms of cellular protection from their attacks include the loss of pro-apoptotic factors (e.g., functional p53 or Bax) or the overexpression of antiapoptotic factors (e.g., Bcl-2, Bcl-XL, or IAPs [inhibitor of apoptosis proteins]). Moreover, the many mechanisms of drug resistance may coincide with those responsible for resistance to immunotherapy, because the drugs and the immunologic effectors often use common pathways to evoke tumor cell damage.

Begell Digital Portal Begell Digital Library eBooks Journals References & Proceedings Research Collections Prices and Subscription Policies Begell House Contact Us Language English 中文 Русский Português German French Spain