Current best practices and rationalistic perspectives in causation-based prevention, early detection and multidisciplinary treatment of breast and gastric cancer

Gastric & Breast Cancer e-journal
DOI: 10.2122/gbc.2012.0251

PERSPECTIVE

Trametinib plus dabrafenib : Targeting RAS-MAPK pathway for BRAF V600-mutant melanoma.

Chee-Seng Ku, MD, PhD.

Affiliation: Chee-Seng Ku, Cancer Science Institute of Singapore, National University of Singapore, Singapore.

E-mail: csikcs@nus.edu.sg

Abstract
Genetic and epigenetic changes and signalling pathways activation drive carcinogenesis, tumor growth and metastasis. One of several signalling pathways involved in ~ 20% of cancers is the RAF-MEK-ERK pathway that is activated through RAS oncoproteins or mutations in these genes [1]. In 66% of melanomas and in lower frequency for other cancer types, activating mutations in BRAF have been found. Despite progression-free survival and overall survival benefit with vemurafenib and dabrafenib that are BRAF and MEK inhibitors of BRAFV600-mutant advanced melanomas respectively [2,3], resistance occurs in more than 50% of patients. In a more recent phase 1 and 2 study, the BRAF-MEK complex of dabrafenib plus trametinib inhibitors has been evaluated for metastatic melanoma patients with BRAF V600 mutations [4]. Can this combined treatment decrease resistance for improving survival of these patients?

(Citation: Gastric & Breast Cancer 2012; 11(4): 208-210)

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last update: 31 October 2012