Cancer cells acquire resistance to anticancer drugs: an update

Biomed J. Nov-Dec 2012;35(6):464-72. doi: 10.4103/2319-4170.104411.

Abstract

The efficacy of cancer chemotherapy is often affected by the emergence of resistant can-cer cells. While biochemical and pharmaco-logical mechanisms have been proposed to ex-plain chemo-resistance, the genes involved in this process have not been fully identified. We previously used genomic DNA microarrays and quantitative RT-PCR to identify the genes associated with resistance to chemotherapeutic drugs, particularly to the genotoxic agent cisplatin. Notably, knockdown of the cisplatin resistance (CPR) genes that we identified was shown to reduce chemoresistance and to suppress the growth of tumor xenographs in cisplatin-treated mice, indicating that the newly identified CPR genes may represent potential therapy candidates to limit chemo-resistance and to improve the efficacy of anticancer drugs. In addition to genetic mutations, re-searchers have found that epigenetic changes and alternative splicing of specific genes may also allow cancer cells to become resistant to chemotherapeutic drugs. In this article, the authors present an overview of the latest findings in this field, including genetic changes, epigenetic changes and alternative splicing.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antineoplastic Agents / therapeutic use*
  • Drug Resistance, Neoplasm / drug effects*
  • Drug Resistance, Neoplasm / genetics
  • Gene Expression Regulation, Neoplastic / drug effects*
  • Humans
  • Mutation / genetics
  • Neoplasms / drug therapy*
  • Neoplasms / genetics
  • Oligonucleotide Array Sequence Analysis / methods

Substances

  • Antineoplastic Agents