Braf V600E mutation in melanoma: translational current scenario

被引：18

作者：

Guadarrama-Orozco, J. A. ^{[1
]}

Ortega-Gomez, A. ^{[1
]}

Ruiz-Garcia, E. B. ^{[1
]}

Astudillo-de la Vega, H. ^{[2
]}

Meneses-Garcia, A. ^{[3
]}

Lopez-Camarillo, C. ^{[4
]}

机构：

[1] Natl Canc Inst, Translat Med Lab, San Fernando N-22, Mexico City 14080, DF, Mexico

[2] Med Ctr Siglo XXI, Oncol Hosp, Lab Translat Canc Res & Cellular Therapy, Mexico City, DF, Mexico

[3] Natl Canc Inst, Mexico City, DF, Mexico

[4] Autonomous Univ Mexico City, Genom Sci Program, Mexico City, DF, Mexico

来源：

CLINICAL & TRANSLATIONAL ONCOLOGY | 2016年 / 18卷 / 09期

关键词：

Melanoma; BRAF; V600E; Inhibitor resistance; METASTATIC MELANOMA; INHIBITOR RESISTANCE; ACQUIRED-RESISTANCE; MALIGNANT-MELANOMA; TUMOR PROGRESSION; PD-L1; EXPRESSION; MEK INHIBITORS; OPEN-LABEL; B-RAF; NRAS;

D O I：

10.1007/s12094-015-1469-6

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Melanoma was one of the translational cancer examples in clinic, including target therapy related to specific biomarkers impacting in the outcome of melanoma patients. Melanomagenesis involved a wide variety of mutations during his evolution; many of these mutated proteins have a kinase activity. One of the most cited proteins in melanoma is BRAF (about 50-60 % of melanomas harbors activating BRAF mutations), for these the most common is a substitution of valine to glutamic acid at codon 600 (p.V600E). Therefore, the precise identification of this underlying somatic mutation is essential; knowing the translational implications has opened a wide view of melanoma biology and therapy.

引用

页码：863 / 871

页数：9

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