Clinical Features and Outcome of Patients With  Non–Small-Cell Lung Cancer Harboring <i>BRAF</i> Mutations

Marchetti, Antonio; Felicioni, Lara; Malatesta, Sara; Sciarrotta, Maria Grazia; Guetti, Luigi; Chella, Antonio; Viola, Patrizia; Pullara, Carmela; Mucilli, Felice; Buttitta, Fiamma

doi:10.1200/jco.2011.35.9638

Cited by 509 publications

(472 citation statements)

References 33 publications

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“…BRAF p.V600E mutation is more frequent in females 52,54 and never smokers 54 in some studies, but several studies failed to show these associations. 49,50,53,58 One distinction between BRAF mutations and other Figure 1 Forest plot of sensitivity and specificity for immunohistochemistry (IHC)-based determination of ROS1 rearrangement positivity compared with fluorescence in situ hybridization.…”

Section: Expert Consensus Opinionmentioning

confidence: 99%

“…49e52, 54 In lung cancer, data from a 2016 phase II single-arm clinical trial 56 showed that single-agent dabrafenib given in second line to stage IV BRAF p.V600E mutant NSCLC had a partial response rate of 33% and disease control rate of 58% and combination dabrafenibtrametinib therapy given in second line to stage IV BRAF p.V600E mutant lung adenocarcinoma had a partial response rate of 63% and disease control rate of 75%.…”

Section: Expert Consensus Opinionmentioning

confidence: 99%

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Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Aung

Donald

Ellison

et al. 2014

The Journal of Molecular Diagnostics

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Context: In 2013, an evidence-based guideline was published by the College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology to set standards for the molecular analysis of lung cancers to guide treatment decisions with targeted inhibitors. New evidence has prompted an evaluation of additional laboratory technologies, targetable genes, patient populations, and tumor types for testing. Objective: To systematically review and update the 2013 guideline to affirm its validity; to assess the evidence of new genetic discoveries, technologies, and therapies; and to issue an evidence-based update. Design: The College of American Pathologists, the International Association for the Study of Lung Cancer, and the Association for Molecular Pathology convened an expert panel to develop an evidence-based guideline to help define the key questions and literature search terms, review abstracts and full articles, and draft recommendations. Results: Eighteen new recommendations were drafted. The panel also updated 3 recommendations from the 2013 guideline. Conclusions: The 2013 guideline was largely reaffirmed with updated recommendations to allow testing of cytology samples, require improved assay sensitivity, and recommend against the use of

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Section: Expert Consensus Opinionmentioning

confidence: 99%

Section: Expert Consensus Opinionmentioning

confidence: 99%

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Aung

Donald

Ellison

et al. 2014

The Journal of Molecular Diagnostics

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“…Litvak, et al observed that among patients with advanced stage NSCLC harboring B-Raf mutations, those with V600 mutations had a longer 3-year overall survival rate compared with patients with non-V600 mutations (24% versus 0%; p < 0.001) (Litvak et al, 2014). On the contrary, the study published by Marchetti et al involving 1046 patents (37 harboring B-Raf mutations) found the V600E mutation as a negative prognostic factor, significantly associated with shorter overall survival on multivariate analyses (HR for death: 2.18; P = .014) (Marchetti et al, 2011).…”

Section: Mutationmentioning

confidence: 87%

BRAF mutations in non-small cell lung cancer: has finally Janus opened the door?

Caparica

Castro

Gil-Bazo

et al. 2016

Critical Reviews in Oncology/Hematology

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“…Mutations in BRAF are seen in approximately one-half of melanomas, in which BRAF V600E is a driver mutation that can be effectively targeted with selective BRAF and/or MEK inhibitors. Mutations in BRAF are also detected in 2 to 4% of NSCLCs (27)(28)(29). The mutations found in NSCLC are distinct from the melanoma setting: whereas BRAF-mutated melanomas harbor a V600E amino acid substitution in more than 80% of cases, lung adenocarcinomas harbor non-V600E mutations in 40 to 50% of cases.…”

Section: Braf Mutationsmentioning

confidence: 95%

The Impact of Genomic Changes on Treatment of Lung Cancer

Cardarella

Johnson

2013

Am J Respir Crit Care Med

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The remarkable success of epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitors in patients with EGFR mutations and ALK rearrangements, respectively, introduced the era of targeted therapy in advanced non-small cell lung cancer (NSCLC), shifting treatment from platinum-based combination chemotherapy to molecularly tailored therapy. Recent genomic studies in lung adenocarcinoma identified other potential therapeutic targets, including ROS1 rearrangements, RET fusions, MET amplification, and activating mutations in BRAF, HER2, and KRAS in frequencies exceeding 1%. Lung cancers that harbor these genomic changes can potentially be targeted with agents approved for other indications or under clinical development. The need to generate increasing amounts of genomic information should prompt health-care providers to be mindful of the amounts of tissue needed for these assays when planning diagnostic procedures. In this review, we summarize oncogenic drivers in NSCLC that can be currently detected, highlight their potential therapeutic implications, and discuss practical considerations for successful application of tumor genotyping in clinical decision making.Keywords: lung cancer; cancer genomics; molecular targeted therapy Lung cancer remains the leading cause of cancer-related mortality in the United States and worldwide. Approximately 85% of patients are diagnosed with non-small cell lung cancer (NSCLC), and most present with advanced disease that is not amenable to curative therapy. For these patients, cytotoxic chemotherapy offers modest prolongation in survival. Over the past 2 decades, modifications of chemotherapy combinations, the addition of monoclonal antibodies, including bevacizumab and cetuximab, and the incorporation of histologic subtype into treatment decisions have added incrementally to the survival of patients with advanced NSCLC. However, therapeutic outcomes appear to have reached a plateau, with response rates of 20 to 35% and median survival of 8 to 12 months (1-3). Recently, clinical and laboratory research have led to a better understanding of the molecular pathogenesis that causes lung cancer. The ongoing research of patients with NSCLC and their tumors has demonstrated that NSCLC can be further defined at the molecular level by the identification and characterization of oncogenic drivers that occur in genes critical to cellular proliferation and survival, leading to aberrant activation of signaling proteins that induce sustained growth of the lung cancer cells. These advances in the molecular pathogenesis of NSCLC have prompted investigators to systematically characterize lung cancers for these oncogenic drivers and treat with appropriate targeted therapies. A cohort of patients can now be prospectively identified who have significantly improved outcomes with such therapies, with median survival in excess of 2 years, necessitating the routine identification of these genomically defined patient subsets. In this perspective, we review oncogenic ...

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Clinical Features and Outcome of Patients With Non–Small-Cell Lung Cancer Harboring BRAF Mutations

Cited by 509 publications

References 33 publications

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

Analytical Validation of BRAF Mutation Testing from Circulating Free DNA Using the Amplification Refractory Mutation Testing System

BRAF mutations in non-small cell lung cancer: has finally Janus opened the door?

The Impact of Genomic Changes on Treatment of Lung Cancer

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