دورية أكاديمية
Pathways and targeting avenues of BRAF in non-small cell lung cancer.
العنوان: | Pathways and targeting avenues of BRAF in non-small cell lung cancer. |
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المؤلفون: | Imyanitov EN; Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, Russia.; Department of Medical Genetics, St.-Petersburg Pediatric Medical University, St.-Petersburg, Russia., Mitiushkina NV; Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, Russia., Kuligina ES; Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, Russia., Tiurin VI; Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, Russia., Venina AR; Department of Tumor Growth Biology, N.N. Petrov Institute of Oncology, St.-Petersburg, Russia. |
المصدر: | Expert opinion on therapeutic targets [Expert Opin Ther Targets] 2024 Jul; Vol. 28 (7), pp. 613-622. Date of Electronic Publication: 2024 Jul 04. |
نوع المنشور: | Journal Article; Review |
اللغة: | English |
بيانات الدورية: | Publisher: Informa Healthcare Country of Publication: England NLM ID: 101127833 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1744-7631 (Electronic) Linking ISSN: 14728222 NLM ISO Abbreviation: Expert Opin Ther Targets Subsets: MEDLINE |
أسماء مطبوعة: | Publication: London : Informa Healthcare Original Publication: London : Ashley Publications, c2001- |
مواضيع طبية MeSH: | Carcinoma, Non-Small-Cell Lung*/drug therapy , Carcinoma, Non-Small-Cell Lung*/genetics , Carcinoma, Non-Small-Cell Lung*/pathology , Proto-Oncogene Proteins B-raf*/genetics , Lung Neoplasms*/drug therapy , Lung Neoplasms*/genetics , Lung Neoplasms*/pathology , Mutation* , Protein Kinase Inhibitors*/pharmacology , Molecular Targeted Therapy* , Drug Resistance, Neoplasm* , Antineoplastic Agents*/pharmacology, Humans ; Animals ; MAP Kinase Signaling System/drug effects |
مستخلص: | Introduction: BRAF is a serine-threonine kinase implicated in the regulation of MAPK signaling cascade. BRAF mutation-driven activation occurs in approximately 2-4% of treatment-naive non-small cell carcinomas (NSCLCs). BRAF upregulation is also often observed in tumors with acquired resistance to receptor tyrosine kinase inhibitors (TKIs). Areas Covered: This review describes the spectrum of BRAF mutations and their functional roles, discusses treatment options available for BRAF p.V600 and non-V600 mutated NSCLCs, and identifies some gaps in the current knowledge. Expert Opinion: Administration of combined BRAF/MEK inhibitors usually produces significant, although often a short-term, benefit to NSCLC patients with BRAF V600 (class 1) mutations. There are no established treatments for BRAF class 2 (L597, K601, G464, G469A/V/R/S, fusions, etc.) and class 3 (D594, G596, G466, etc.) mutants, which account for up to two-thirds of BRAF -driven NSCLCs. Many important issues related to the use of immune therapy for the management of BRAF -mutated NSCLC deserve further investigation. The rare occurrence of BRAF mutations in NSCLC is compensated by high overall incidence of lung cancer disease; therefore, clinical studies on BRAF -associated NSCLC are feasible. |
فهرسة مساهمة: | Keywords: BRAF; acquired resistance; immunotherapy; mutation; non-small cell lung cancer; targeted therapy |
المشرفين على المادة: | EC 2.7.11.1 (Proto-Oncogene Proteins B-raf) EC 2.7.11.1 (BRAF protein, human) 0 (Protein Kinase Inhibitors) 0 (Antineoplastic Agents) |
تواريخ الأحداث: | Date Created: 20240628 Date Completed: 20240801 Latest Revision: 20240801 |
رمز التحديث: | 20240801 |
DOI: | 10.1080/14728222.2024.2374742 |
PMID: | 38941191 |
قاعدة البيانات: | MEDLINE |
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