Oncotarget

Research Perspectives:

Blocking the survival of the nastiest by HSP90 inhibition

Paul Workman _, Paul A. Clarke, Bissan Al-Lazikani

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Oncotarget. 2016; 7:3658-3661. https://doi.org/10.18632/oncotarget.6971

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Abstract

Paul Workman1, Paul A. Clarke1 and Bissan Al-Lazikani1

1 Cancer Research UK Cancer Therapeutics Unit, Division of Cancer Therapeutics, The Institute of Cancer Research, London, UK

Correspondence to:

Paul Workman, email:

Keywords: HSP90

Received: November 20, 2015 Accepted: January 21, 2016 Published: January 21, 2016

Abstract

It is now recognised that genetic, epigenetic and phenotypic heterogeneity within individual human cancers is responsible for therapeutic resistance – knowledge that is having a profound impact on current thinking and experimentation. There has been concern that molecularly targeted therapy is doomed to failure, with resistant clones emerging in response to the Darwinian selective pressure of any drug treatment. However, two studies have shown that the evolution of drug resistance can be restrained by co-administration of a pharmacologic inhibitor of the HSP90 molecular chaperone.


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