BRAF mutations in non-small cell lung cancer: has finally Janus opened the door?
Caparica R (1), de Castro G Jr (1), Gil-Bazo I (2), Caglevic C (3), Calogero R (4), Giallombardo M (5), Santos ES (6), Raez LE (7), Rolfo C (8).
(1) Instituto do Câncer do Estado de São Paulo, Faculdade de Medicina da USP, São Paulo, Brazil.
(2) Oncology Department, Clínica Universidad de Navarra, Center for Applied Medical Research (CIMA), Pamplona, Spain.
(3) Oncology Department, Fundación Arturo Lopez Pérez, Santiago, Chile.
(4) Department of Molecular Biotechnology and Health Sciences, University of Torino, Italy.
(5) Biopathology and Medical Biotechnology Department, Biology section, University of Palermo, Italy; Phase I - Early Clinical Trials Unit, Oncology Department, Antwerp University Hospital & Center for Oncological Research (CORE), Antwerp University, Belgium.
(6) Lynn Cancer Institute, Thoracic and Head/Neck Cancer Programs, Florida Atlantic University, Boca Raton, FL, USA.
(7) Memorial Cancer Institute, Memorial Health Care System, Florida International University, Miami, FL, USA.
(8) Phase I - Early Clinical Trials Unit, Oncology Department, Antwerp University Hospital & Center for Oncological Research (CORE), Antwerp University, Belgium
B-Raf mutations occur in about 1-2% of non-small cell lung cancers (NSCLC). These mutations generate a permanent activation of the mitogen activated protein kinase (MAPK) pathway, which promotes tumor growth and proliferation.
In the present review, we discuss B-Raf mutation epidemiology, diagnostic methods to detect B-Raf mutations, the role of B-Raf as a driver mutation and a potential therapeutic target in NSCLC.
The results of clinical trials involving B-Raf or MAPK pathway inhibitors for the treatment of NSCLC are also discussed. Clinical trials evaluating B-Raf inhibitors in BRAF mutated NSCLC patients have shown promising results, and larger prospective studies are warranted to validate these findings. Enrollment of these patients in clinical trials is an interesting strategy to offer a potentially more effective and less toxic targeted therapy.
CITATION Crit Rev Oncol Hematol. 2016 Feb 27. pii: S1040-8428(16)30036-1. doi: 10.1016/j.critrevonc.2016.02.012