ADAM-17: A target to increase chemotherapeutic efficacy in colorectal cancer?

Adam M. Lee; Robert B. Diasio

doi:10.1158/1078-0432.CCR-10-1059

ADAM-17: A target to increase chemotherapeutic efficacy in colorectal cancer?

Adam M. Lee, Robert B. Diasio

Pharmacology

Research output: Contribution to journal › Comment/debate › peer-review

3 Scopus citations

Abstract

Chemotherapy-induced activation of ADAM-17 results in increased growth factor shedding and activation of growth factor receptor-mediated pro-survival response. Enhanced ADAM-17 activity and HER ligand shedding results in resistance to chemotherapy in CRC. Therapies that decrease ADAM-17 activity in conjunction with current treatments may enhance response rates in advanced CRC patients.

Original language	English (US)
Pages (from-to)	3319-3321
Number of pages	3
Journal	Clinical Cancer Research
Volume	16
Issue number	13
DOIs	https://doi.org/10.1158/1078-0432.CCR-10-1059
State	Published - Jul 1 2010

ASJC Scopus subject areas

Oncology
Cancer Research

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10.1158/1078-0432.CCR-10-1059

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title = "ADAM-17: A target to increase chemotherapeutic efficacy in colorectal cancer?",

abstract = "Chemotherapy-induced activation of ADAM-17 results in increased growth factor shedding and activation of growth factor receptor-mediated pro-survival response. Enhanced ADAM-17 activity and HER ligand shedding results in resistance to chemotherapy in CRC. Therapies that decrease ADAM-17 activity in conjunction with current treatments may enhance response rates in advanced CRC patients.",

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T2 - A target to increase chemotherapeutic efficacy in colorectal cancer?

AU - Lee, Adam M.

AU - Diasio, Robert B.

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N2 - Chemotherapy-induced activation of ADAM-17 results in increased growth factor shedding and activation of growth factor receptor-mediated pro-survival response. Enhanced ADAM-17 activity and HER ligand shedding results in resistance to chemotherapy in CRC. Therapies that decrease ADAM-17 activity in conjunction with current treatments may enhance response rates in advanced CRC patients.

AB - Chemotherapy-induced activation of ADAM-17 results in increased growth factor shedding and activation of growth factor receptor-mediated pro-survival response. Enhanced ADAM-17 activity and HER ligand shedding results in resistance to chemotherapy in CRC. Therapies that decrease ADAM-17 activity in conjunction with current treatments may enhance response rates in advanced CRC patients.

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ADAM-17: A target to increase chemotherapeutic efficacy in colorectal cancer?

Abstract

ASJC Scopus subject areas

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