Mutace BRAF: nový přístup k cílené léčbě melanomu
[BRAF mutation: a novel approach in targeted melanoma therapy]
Language Czech Country Czech Republic Media print
Document type Journal Article, Review
PubMed
23102192
PII: 38972
- MeSH
- Molecular Targeted Therapy * MeSH
- Indoles adverse effects therapeutic use MeSH
- Humans MeSH
- Melanoma immunology secondary therapy MeSH
- Mutation * MeSH
- Skin Neoplasms immunology therapy MeSH
- Phosphatidylethanolamine Binding Protein adverse effects therapeutic use MeSH
- Antineoplastic Combined Chemotherapy Protocols therapeutic use MeSH
- Proto-Oncogene Proteins B-raf antagonists & inhibitors genetics MeSH
- Sulfonamides adverse effects therapeutic use MeSH
- Vemurafenib MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Review MeSH
- Names of Substances
- BRAF protein, human MeSH Browser
- Indoles MeSH
- Phosphatidylethanolamine Binding Protein MeSH
- Proto-Oncogene Proteins B-raf MeSH
- Sulfonamides MeSH
- Vemurafenib MeSH
The incidence of malignant melanoma is increasing worldwide, despite our best efforts in prevention and early detection. The locally advanced disease may be treated surgically with good results, however, metastatic melanoma is considered to be one of the most therapeutically challenging malignancies. The increasing knowledge of molecular changes in melanoma may change this picture. Malignant melanoma is not a singular, homogeneous disease but rather a mixture of subtypes characterized by specific mutations. Tumors with C-KIT mutation respond to therapy with C-KIT kinase inhibitor imatinib and the ones characterized by BRAF mutations respond to BRAF kinase inhibitor vemurafenib. Vemurafenib was approved by US FDA in 2011 and EMA in 2012 for therapy of patients with advanced melanoma, harboring mutation in BRAFV600E gene. Ipilimumab, an antibody to cytotoxic T-lymphocyte antigen 4 (CTLA-4), was registered in 2011 by both US FDA and European Medicines Agency for treatment of metastatic melanoma. This therapy promotes the anti-tumor T-cell activity by blocking a CTLA-4 antigen, a key negative regulator of immune response.