V599E BRAF mutation was uncommon in Japanese lung cancer.

lung adenocarcinoma of mixed type with a high incidence of papillary and lepidic growth may be worthwhile investigating for BRAF-V600E mutation as more genetically oriented drug therapies emerge.

K-ras, EGFR, and BRAF mutations are disproportionately seen in adenocarcinomas of lung with a dominant micropapillary growth pattern compared with conventional adenocarcinoma in our institutional experience.

Ablation of B-Raf had no significant effect on development of K-Ras oncogene-driven non-small cell lung carcinoma.

study reports that V600E and non-V600E BRAF mutations affect different patients with non-small-cell lung cancer; V600E mutations are significantly associated with female sex and represent a negative prognostic factor

analysis of BRAF gene mutations in non-small cell lung cancer

Article reviews the current understanding of BRAF gene, its structure, expression, and signal pathway in non-small cell lung cancer. [Review]

The prevalence of EGFR, KRAS, BRAF and PIK3CA somatic mutations in 861 randomly selected Chinese patients with non-small cell lung cancer

BRAF V600E mutation is associated with response to vemurafenib in lung adenocarcinoma.

lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1.

The detected Merkel cell polyomavirus prevalence in non-small cell lung cancer in combination with the deregulated expression of BRAF and Bcl-2 genes suggests that these events are likely to contribute to the pathogenesis of non-small cell lung cancer.

The role of BRAF V600E as targetable driver mutation in lung adenocarcinoma is strengthened by finding that in vivo expression of V600E in mice leads to development of invasive adenocarcinoma, a phenotype that is reversed when V600E expression is stopped.

The mutations of EGFR and BRAF genes were not found in HER2-mutated patients with brain metastasis from non-small cell lung cancer.

BRAF mutations are associated with lung cancer.

BRAF mutations are found in 2 to 4% of non-small cell lung cancers. The mutations harbor non-V600E mutations in 40 to 50% of cases. A phase 2 trial of dabrafenib described 8 responses of 20 patients with BRAF V600E mutant NSCLC

Nonsmall cell lung cancer cells with BRAF-V600E, but not other BRAF mutations, initially are sensitive to BRAF-inhibitor treatment, but rapidly acquire resistance to BRAF inhibition.

BRAF mutations occurred in 2.2% of advanced-stage lung adenocarcinomas, were most commonly V600E, and were associated with distinct clinicopathologic features in comparison with other genomic subtypes and with a high mutation rate in more than 1 gene.

mutated KRAS and mutated BRAF seem to be prognostic factors in patients with Colorectal cancer who undergo lung metastasectomy.

BRAF mutations in Non-small cell lung cancer are more likely in Adenocarcinoma, and BRAF V600E mutations are more frequent in women and never smokers.

findings suggest that the BRAF(V600E) mutation can be detected using a PNA clamp real-time PCR in the blood of PTC[ papillary thyroid carcinoma ] patients with lung metastasis

Case Report: BRAFV600 mutant non-small-cell lung cancer which progressed on vemurafenib therapy.

Given the high prevalence of lung cancer and the availability of targeted therapy, Chinese lung ADC patients without EGFR and KRAS mutations are recommended for HER2 and BRAF mutations detection, especially for those never smokers

BRAF mutations are associated with lung Adenocarcinoma.

BRAF V600 appears to be a targetable oncogene in some, but not all, nonmelanoma cancers. Preliminary vemurafenib activity was observed in non-small-cell lung cancer and in Erdheim-Chester disease and Langerhans'-cell histiocytosis.

Data show that dasatinib induced DNA damage and activated DNA repair pathways leading to senescence only in the kinase-inactivating BRAF kinase (BRAF) mutations (KIBRAF) non-small cell lung cancer (NSCLC) cells.

Clinical data suggest that BRAF mutations define specific subsets of patients with NSCLC; while their oncogenic nature is yet to be established in lung cancer, especially for non-V600E mutations, the value of BRAF mutations to predict the efficacy of targeted agents remains unclear.

BRAF mutation is associated with response to chemotherapy in lung cancer.

For patients with non-small cell lung cancer with a EGFR mutation and an anaplastic lymphoma kinase mutation(ALK) with brain metastases, several agents have shown intracranial activity. Lapatinib has been tested for patients with brain metastases from breast cancer harboring a HER2 mutation. molecular targeted therapies have shown efficacy in BRAF-positive melanoma brain metastasis

BRAF(V600E)-mutation is associated with metastatic non-small cell lung cancer.

Study of four cases confirms BRAF V600E mutation as a probable driver in a subset of ciliated muconodular papillary tumors (CMPT) of the lung, along with AKT1 mutation, which further supports that CMPT are indolent pulmonary neoplasms.

Acquired BRAF V600E mutation is associated with resistance to osimertinib in lung cancer.

Study identified BRAF mutations in 1.7% of Chinese patients with non-small-cell lung cancer and seems associated with adenocarcinoma.

BRAFV600E mutation significantly associated with nonsmall cell lung cancer in females and nonsmokers [meta-analysis]

We have found a higher incidence of axLN metastases in BRAF mutated NSCLC patients than described in non-BRAF mutated NSCLC patients. Examination of the axilla should be a routine part of physical examination in this genetically distinct subgroup of lung cancer patients.

This study demonstrates that idiopathic pulmonary fibrosis-associated lung cancer (IPF-LC) is genetically characterized by the presence of somatic mutations reflecting a variety of environmental exposures on the background of specific germline mutations, and is associated with potentially targetable alterations such as BRAF mutations.

The diesel exhaust fumes-exposed patients were diagnosed with a BRAF mutation in 25% of all cases. Given its minimal effects in the subgroups, we conclude that occupational exposure slightly affects the molecular pattern of lung cancers in never-smokers.

In lung adenocarcinomas, BRAF mutations tended to occur in former or current smokers, and BRAF V600E mutations are more common in females. The histologic grade and architecture of these tumors varied significantly in both cytology and histology material, from well to poorly differentiated.

BRAF-mutant non-small cell lung cancer is a heterogeneous disease that encompasses 3 distinct functional classes. Classes II and III have more aggressive clinical features leading to less favorable outcomes.

Outcomes in patients with stage iv non-small-cell lung cancer (nsclc) harboring BRAF V600E mutations (n = 32) did not differ significantly from those of patients with other BRAF mutations. Most nsclc patients with a BRAF mutation were men and current or former smokers. Survival appears to be better in these BRAF-mutated patients than in nsclc patients without an oncogenic driver.

Epidermal growth factor receptor (EGFR), KRAS, and BRAF mutations in lung adenocarcinomas: A study from India.

This study revealed a 2.8% BRAF mutation rate in Chinese non-small cell lung cancer patients.

The BRAF G469A-activating mutation is a potential mechanism of acquired resistance to osimertinib treatment in non-small cell lung cancer cell lines .

BRAF mutation is associated with lung cancer risk.

Outcome of patients with colorectal cancer undergoing lung metastases resection: a single-institution retrospective analysis.

A PCR-Based Approach for Driver mutation Analysis of EGFR, KRAS, and BRAF Genes in lung cancer Tissue Sections.

Oncogenic BRaf (V600E) induces benign lung adenomas that progress to malignant lung cancer in cooperation with silencing of either Trp53 or Cdk2n2a in mouse models

LKB1 haploinsufficiency as a risk factor for tumor progression of BRAF(V600E) mutated lung adenomas in human cancer patients

MYC inactivation restores BRAF(V600E)-induced senescence in lung tumors in mice.

Braf(V600E) expression, coupled with simultaneous p53 ablation, permits bypass of senescence and progression to lung adenocarcinoma.

expression of an endogenous Braf(D631A) kinase-inactive isoform in mice (corresponding to the human BRAF(D594A) mutation) triggers lung adenocarcinoma in vivo, indicating that BRAF-inactivating mutations are initiating events in lung oncogenesis