Blocking the survival of the nastiest by HSP90 inhibition

被引：9

作者：

Workman, Paul ^{[1
]}

Clarke, Paul A. ^{[1
]}

Al-Lazikani, Bissan ^{[1
]}

机构：

[1] Inst Canc Res, Div Canc Therapeut, Canc Res UK Canc Therapeut Unit, London SW3 6JB, England

来源：

ONCOTARGET | 2016年 / 7卷 / 04期

关键词：

HSP90; CLONAL EVOLUTION; CANCER; RESISTANCE; THERAPY; MODELS;

D O I：

10.18632/oncotarget.6971

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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.

引用

页码：3658 / 3661

页数：4

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