Document Detail


Resistance to EGFR blockade in colorectal cancer: liquid biopsies and latent subclones.
MedLine Citation:
PMID:  22847744     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Two recent papers identify KRAS activation as a mechanism of acquired resistance to EGFR blockade in colorectal cancer. In doing so, they suggest that resistance to single-agent EGFR blockade will be unavoidable because these alterations exist as latent subclones within the tumor even prior to the initiation of therapy.
Authors:
David J Konieczkowski; Levi A Garraway
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Publication Detail:
Type:  Journal Article     Date:  2012-07-31
Journal Detail:
Title:  Cell research     Volume:  23     ISSN:  1748-7838     ISO Abbreviation:  Cell Res.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-03     Completed Date:  2013-06-18     Revised Date:  2014-03-19    
Medline Journal Info:
Nlm Unique ID:  9425763     Medline TA:  Cell Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  13-4     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Antibodies, Monoclonal / therapeutic use*
Antibodies, Monoclonal, Humanized / pharmacology
Antineoplastic Agents / pharmacology,  therapeutic use*
Cell Line, Tumor
Colorectal Neoplasms / drug therapy*,  metabolism,  pathology
DNA, Neoplasm / blood
Drug Resistance, Neoplasm / drug effects*
Humans
Mutation
Receptor, Epidermal Growth Factor / antagonists & inhibitors*,  metabolism
ras Proteins / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
T32 GM007753/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antibodies, Monoclonal, Humanized; 0/Antineoplastic Agents; 0/DNA, Neoplasm; 0/panitumumab; EC 2.7.10.1/Receptor, Epidermal Growth Factor; EC 3.6.5.2/ras Proteins; PQX0D8J21J/cetuximab
Comments/Corrections

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