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免疫病理疾病及治疗学论文学
SJR: 0.309 SNIP: 0.041 CiteScore™: 0.18

ISSN 打印: 2151-8017
ISSN 在线: 2151-8025

Archives: Volume 1, 2010 to Volume 7, 2016

免疫病理疾病及治疗学论文学

DOI: 10.1615/ForumImmunDisTher.v1.i1-2.120
pages 149-151

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

Natale D'Alessandro
Pharmacology Unit, University of Palermo Department of Health Sciences and Mother and Child Care "Giuseppe D'Alessandro" Palermo, Italy
Maria C. Mazzarino
Department of Biomedical Sciences, University of Catania, Catania
James A. McCubrey
Department of Microbiology and Immunology, Brody School of Medicine at East Carolina University, Greenville, North Carolina, USA

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.


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