Bevacizumab-based treatment in colorectal cancer with a NRAS Q61K mutation. Target Oncol 2013 Sep;8(3):183-188
Date
02/13/2013Pubmed ID
23400451Pubmed Central ID
PMC3766504DOI
10.1007/s11523-013-0266-9Scopus ID
2-s2.0-84884287113 (requires institutional sign-in at Scopus site) 5 CitationsAbstract
Despite development of new therapies, metastatic colorectal cancer (mCRC) largely remains an incurable disease. Approximately 2-6% of colorectal cancers harbor NRAS mutations. The anti-VEGF antibody bevacizumab is a backbone of most therapeutic regimens; however, biomarkers predicting its activity are not known. We report two cases of mCRC with a Q61K NRAS mutation that had a favorable response to bevacizumab and the histone deacetylase inhibitor valproic acid. In contrast, none of ten patients with wild-type NRAS or unknown NRAS status and mutated KRAS (NRAS and KRAS mutations are mutually exclusive) responded to the same regimen. These results suggest that NRAS mutation merits further investigation as a potential biomarker predicting the efficacy of bevacizumab-based treatment.
Author List
Janku F, Wheler JJ, Hong DS, Kurzrock RAuthor
Razelle Kurzrock MD Center Associate Director, Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AdultAntibodies, Monoclonal, Humanized
Antineoplastic Combined Chemotherapy Protocols
Bevacizumab
Biomarkers, Tumor
Colorectal Neoplasms
GTP Phosphohydrolases
Humans
Male
Membrane Proteins
Middle Aged
Mutation
Treatment Outcome
