A new rho(D) map to diffuse gastric cancer

Dorothy Benton; Jonathan Chernoff

doi:10.1158/2159-8290.CD-19-1327

A new rho(D) map to diffuse gastric cancer

Dorothy Benton, Jonathan Chernoff

Cancer Signaling and Microenvironment (CSM)

Drexel University

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Diffuse gastric cancer (DGC) is characterized by frequent missense mutations in the small GTPase RHOA, but the effects of this mutation on enzyme activity and signaling have been widely debated. In this issue, Zhang and colleagues show that the most common RHOA mutation in DGC, encoding RHOA^Y42C, represents a gain of function; that a mouse model incorporating this mutation in association with loss of the E-cadherin gene CDH1 recapitulates many aspects of DGC; and that rationally designed therapeutics based on our understanding of RHOA signaling are promising agents for treating DGC.

Original language	English
Pages (from-to)	182-184
Number of pages	3
Journal	Cancer Discovery
Volume	10
Issue number	2
DOIs	https://doi.org/10.1158/2159-8290.CD-19-1327
State	Published - Feb 2020

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10.1158/2159-8290.CD-19-1327

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title = "A new rho(D) map to diffuse gastric cancer",

abstract = "Diffuse gastric cancer (DGC) is characterized by frequent missense mutations in the small GTPase RHOA, but the effects of this mutation on enzyme activity and signaling have been widely debated. In this issue, Zhang and colleagues show that the most common RHOA mutation in DGC, encoding RHOAY42C, represents a gain of function; that a mouse model incorporating this mutation in association with loss of the E-cadherin gene CDH1 recapitulates many aspects of DGC; and that rationally designed therapeutics based on our understanding of RHOA signaling are promising agents for treating DGC.",

author = "Dorothy Benton and Jonathan Chernoff",

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AB - Diffuse gastric cancer (DGC) is characterized by frequent missense mutations in the small GTPase RHOA, but the effects of this mutation on enzyme activity and signaling have been widely debated. In this issue, Zhang and colleagues show that the most common RHOA mutation in DGC, encoding RHOAY42C, represents a gain of function; that a mouse model incorporating this mutation in association with loss of the E-cadherin gene CDH1 recapitulates many aspects of DGC; and that rationally designed therapeutics based on our understanding of RHOA signaling are promising agents for treating DGC.

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A new rho(D) map to diffuse gastric cancer

Abstract

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