期刊
MOLECULAR CANCER THERAPEUTICS
卷 11, 期 12, 页码 2704-2708出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/1535-7163.MCT-12-0530
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资金
- Roche
- Cancer Institute New South Wales Fellowship program
- Cancer Institute New South Wales Research Fellowship
- NHMRC Senior Research Fellowship
- National Health and Medical Research Council of Australia (NHMRC) [402761]
- Translational Research Program of the Cancer Institute New SouthWales (NSW) [05/TPG/1-01]
- Health Department of NSW through Sydney West Area Health Service
- Australian Cancer Research Foundation
Targeted therapies are increasingly being used to treat a variety of cancers. Their efficacy depends upon the accurate detection and targeting of a specific mutation or aberration in the tumor. All cancers, such as melanoma, are molecularly heterogeneous, with drug-resistant subclones present before the treatment or emerging as a result of targeted therapies. Here, we show intralesional molecular heterogeneity in a progressing V600E BRAF-mutant melanoma metastasis from a patient treated for 7 months with the BRAF inhibitor vemurafenib. In the single metastasis, two distinct subclones were observed, both V600E BRAF-mutant and only one with an additional G13R NRAS mutation. Molecular heterogeneity even at the intralesional level shows that personalizing or adjusting therapies based on genotyping of a portion of a single lesion may not accurately depict the molecular profile or drivers of oncogenesis across the entire patient's melanoma. Mol Cancer Ther; 11(12); 2704-8. (C)2012 AACR.
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