Drug resistance in cancer: molecular evolution and compensatory proliferation

Oncotarget
Ran Friedman

Abstract

Targeted therapies have revolutionized cancer treatment. Unfortunately, their success is limited due to the development of drug resistance within the tumor, which is an evolutionary process. Understanding how drug resistance evolves is a prerequisite to a better success of targeted therapies. Resistance is usually explained as a response to evolutionary pressure imposed by treatment. Thus, evolutionary understanding can and should be used in the design and treatment of cancer. In this article, drug-resistance to targeted therapies is reviewed from an evolutionary standpoint. The concept of apoptosis-induced compensatory proliferation (AICP) is developed. It is shown that AICP helps to explain some of the phenomena that are observed experimentally in cancers. Finally, potential drug targets are suggested in light of AICP.

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Citations

Feb 9, 2017·Protein Science : a Publication of the Protein Society·Stella Hernandez MaganhiRan Friedman
Jan 17, 2020·The FEBS Journal·Panagiota S GeorgouliaRan Friedman
May 20, 2020·Chemical Communications : Chem Comm·María José Dávila-RodríguezRan Friedman
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Mar 17, 2019·Pharmacology & Therapeutics·Asurayya WorredeAlessandro Fatatis
Mar 27, 2021·Frontiers in Molecular Biosciences·Zhu-Jun LawHui Poh Goh
Oct 15, 2021·Journal of Chemical Theory and Computation·Baswanth Oruganti, Ran Friedman

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Software Mentioned

UCSF Chimera
UCSF Chimera package

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