SHP2 Drives Adaptive Resistance to ERK Signaling Inhibition in Molecularly Defined Subsets of ERK-Dependent Tumors-Reference-Cited by-同舟云学术

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SHP2 Drives Adaptive Resistance to ERK Signaling Inhibition in Molecularly Defined Subsets of ERK-Dependent Tumors

Published:2019-01 Issue:1 Volume:26 Page:65-78.e5
ISSN:2211-1247
Container-title:Cell Reports
language:en
Short-container-title:Cell Reports

Author:

Ahmed Tamer A.,Adamopoulos Christos,Karoulia Zoi,Wu Xuewei,Sachidanandam Ravi,Aaronson Stuart A.,Poulikakos Poulikos I.

Funder

Dermatology Foundation

Melanoma Research Foundation

Melanoma Research Alliance

Sidney Kimmel Foundation for Cancer Research

TCI

NIH/NCI

Breast Cancer Research Foundation

Robin Chemers Neustein Postdoctoral Fellowship

Publisher

Elsevier BV

Subject

General Biochemistry, Genetics and Molecular Biology

Reference49 articles.

1. Molecular mechanism for a role of SHP2 in epidermal growth factor receptor signaling;Agazie;Mol. Cell. Biol.,2003

2. Tyrosyl phosphorylation of Shp2 is required for normal ERK activation in response to some, but not all, growth factors;Araki;J. Biol. Chem.,2003

3. Inhibition of Ras for cancer treatment: the search continues;Baines;Future Med. Chem.,2011

4. Protein-tyrosine-phosphatase SHPTP2 couples platelet-derived growth factor receptor beta to Ras;Bennett;Proc. Natl. Acad. Sci. USA,1994

5. Triple-negative breast cancer: challenges and opportunities of a heterogeneous disease;Bianchini;Nat. Rev. Clin. Oncol.,2016

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