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Drug resistance in cancer: molecular evolution and compensatory proliferation
Linnaeus University, Faculty of Health and Life Sciences, Department of Chemistry and Biomedical Sciences. (CCBG)ORCID iD: 0000-0001-8696-3104
2016 (English)In: OncoTarget, ISSN 1949-2553, E-ISSN 1949-2553, Vol. 7, no 11, 11746-11755 p.Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2016. Vol. 7, no 11, 11746-11755 p.
Keyword [en]
nearly neutral theory, neoplasm, leukemia, bladder cancer, somatic mutations
National Category
Cancer and Oncology
Research subject
Natural Science, Biomedical Sciences
URN: urn:nbn:se:lnu:diva-49818DOI: 10.18632/oncotarget.7459ISI: 000375679600002PubMedID: 26909596ScopusID: 2-s2.0-84962798373OAI: diva2:904119
Swedish Research Council, VR 2014-4406Swedish Cancer Society, CAN 2015/387
Available from: 2016-02-18 Created: 2016-02-18 Last updated: 2016-09-02Bibliographically approved

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