Cancer drug resistance: A brief overview from a genetic viewpoint

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Abstract

Cancer drug resistance leading to therapeutic failure in the treatment of many cancers encompasses various mechanisms and may be intrinsic relying on the patient’s genetic makeup or be acquired by tumors that are initially sensitive to cancer drugs. All in all, it may be responsible for treatment failure in over 90 % of patients with metastatic cancer. Cancer drug resistance, in particular acquired resistance, may stem from the microclonality/micro-genetic heterogeneity of the tumors whereby, among others, the following mechanisms may entail resistance: altered expression of drug influx/efflux transporters in the tumor cells mediating lower drug uptake and/or greater efflux of the drug; altered role of DNA repair and impairment of apoptosis; role of epigenomics/epistasis by methylation, acetylation, and altered levels of microRNAs leading to alterations in upstream or downstream effectors; mutation of drug targets in targeted therapy and alterations in the cell cycle and checkpoints; and tumor microenvironment that are briefly reviewed.

Original languageEnglish
Title of host publicationMethods in Molecular Biology
PublisherHumana Press Inc
Pages1-18
Number of pages18
Volume1395
DOIs
Publication statusPublished - 2016

Publication series

NameMethods in Molecular Biology
Volume1395
ISSN (Print)10643745

Keywords

  • Acquired resistance and adaptive compensatory pathways
  • Acquired resistance and tumor micro-heterogeneity
  • DNA repair and resistance
  • Epigenomics and resistance
  • Intrinsic resistance and pharmacogenetics
  • Tumor microenvironment and resistance
  • Uptake and efflux transporters in resistance

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  • Cite this

    Rueff, J., & Rodrigues, AS. (2016). Cancer drug resistance: A brief overview from a genetic viewpoint. In Methods in Molecular Biology (Vol. 1395, pp. 1-18). (Methods in Molecular Biology; Vol. 1395). Humana Press Inc. https://doi.org/10.1007/978-1-4939-3347-1_1