Format

Send to

Choose Destination
Curr Drug Metab. 2020 Jan 2. doi: 10.2174/1389200221666200103111539. [Epub ahead of print]

Genetic and epigenetic modulation of drug resistance in cancer: Challenges and opportunities.

Author information

1
Department of Life Science, School of Sciences, Gujarat University, India.

Abstract

Cancer is a complex disease that has the ability to develop resistance to traditional therapies. The current chemotherapeutic treatment has become increasingly sophisticated, yet it is not 100% effective against disseminated tumours. Anticancer drugs resistance is an intricate process that ascends from modifications in the drug targets suggesting the need for better targeted therapies in the therapeutic arsenal. Advances in the modern techniques such as DNA microarray, proteomics along with development of newer targeted drug therapies might provide better strategies to overcome drug resistance. This drug resistance in tumours can be attributed to an individual's genetic differences, especially in tumoral somatic cells but acquired drug resistance is due to different mechanisms such as cell death inhibition (apoptosis suppression) altered expression of drug transporters, alteration in drug metabolism epigenetic and drug targets, enhancing DNA repair and gene amplification. This review also focusses on the epigenetic modifications and microRNAs which induce drug resistance and contributes to the formation of tumour progenitor cells that are not destroyed by conventional cancer therapies. Lastly, this review highlights the different means to prevent the formation of drug resistant tumours and provides future directions for the better treatment of these resistant tumours.

KEYWORDS:

Drug response; Drug target alteration; Epigenetics; Epithelial – mesenchymal transitions; Resistance mechanisms; microRNAs

Supplemental Content

Full text links

Icon for Bentham Science Publishers Ltd.
Loading ...
Support Center