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A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
Published on: April 6, 2016
BRAF in non-small cell lung cancer: From molecular mechanisms to clinical practice
Claudia Parisi1,2,3, David Planchard1,2
1Thoracic Cancer Group, Department of Medical Oncology, Gustave Roussy and International Center for Thoracic Cancers, Villejuif, France.
Abstract:
V-Raf murine sarcoma viral oncogene homolog B (BRAF) mutations are found in up to 4% of patients with non-small cell lung cancer (NSCLC). Approximately 2% of advanced NSCLC cases harbor a BRAF V600E (class I) mutation. Because targeted therapies inhibiting BRAF (e.g., dabrafenib and encorafenib) and MEK (trametinib and binimetinib) are associated with improved outcomes as first- or second-line treatment for BRAF V600E-mutant NSCLC, both European Society for Medical Oncology and National Comprehensive Cancer Network guidelines recommend testing for the BRAF V600E oncogenic driver at the time of diagnosis. In recent years, the treatment landscape of this molecular subgroup has seen great development. Different therapeutic strategies including anti-programmed death ligand 1 antibodies and kinase inhibitors have been assessed thus far, with novel agents (e.g., pan-BRAF inhibitors) and therapeutic associations underway in preclinical and clinical trials. This review describes the current understanding of the BRAF clinicopathologic role in NSCLC, with a special focus on published trials assessing currently approved therapies. Mechanisms of drug resistance and future perspectives on the therapeutic approach of BRAF-deregulated NSCLC are also summarized.
Insights
BRAF V600E mutations in non-small cell lung cancer (NSCLC) are treatable with targeted therapies. This review covers approved treatments, resistance mechanisms, and future BRAF-directed strategies for NSCLC.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- BRAF mutations, particularly V600E, occur in 2% of advanced non-small cell lung cancer (NSCLC).
- Targeted therapies like BRAF and MEK inhibitors show improved outcomes in BRAF V600E-mutant NSCLC.
- Guidelines recommend BRAF V600E testing at diagnosis for NSCLC patients.
Purpose of the Study:
- To review the clinicopathologic role of BRAF in NSCLC.
- To summarize published trials of approved therapies for BRAF-mutant NSCLC.
- To discuss drug resistance mechanisms and future therapeutic perspectives.
Main Methods:
- Literature review of published clinical trials and preclinical studies.
- Focus on approved targeted therapies and emerging agents for BRAF-deregulated NSCLC.
- Analysis of treatment strategies, including kinase inhibitors and immunotherapies.
Main Results:
- BRAF and MEK inhibitors offer improved outcomes for BRAF V600E-mutant NSCLC.
- Various therapeutic strategies, including anti-PD-L1 antibodies, are under investigation.
- Novel agents and combinations are in clinical development.
Conclusions:
- BRAF V600E testing is crucial for guiding NSCLC treatment.
- The therapeutic landscape for BRAF-mutant NSCLC is rapidly evolving.
- Future research focuses on overcoming drug resistance and exploring novel therapeutic combinations.
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