By Ryan J. Sullivan
This quantity encompasses a selection of writings from the leaders within the fields of Molecular Biology and cancer examine for you to start to inform the ever-expanding tale of the latest findings, discoveries, and strength of BRAF-directed goals in cancer. contemporary learn has proven that BRAF inhibitors are powerful for a quick time period, yet there's little wish that this medicinal drugs as unmarried brokers will bring about sturdy profit in a majority of sufferers. between scientists and researchers who paintings in drug discovery, there's a lot of curiosity within the improvement of molecularly special carcinogens. specifically, the identity of a molecular objective, the choice of molecules which successfully inhibit this goal. what's starkly assorted concerning the improvement of this type of compounds, despite the fact that, is that the mechanism of motion of those brokers aren't as trouble-free as was formerly assumed and the mechanisms of resistance that tumor cells hire to stay away from whole destruction are in contrast to any which have been defined earlier than. those discoveries as well as usage of contemporary molecular biology options have resulted in a sequence of hypotheses concerning which different different types of molecules will be utilized in mixture with BRAF-inhibitors in hopes of revolutionizing the possibility of therapeutics in melanoma.
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Hum Mutat. 2005;25:6–17. 74. Yang G, Rajadurai A, Tsao H. Recurrent patterns of dual RB and p53 pathway inactivation in melanoma. J Invest Dermatol. 2005;125:1242–51. 75. Kamijo T, Weber JD, Zambetti G, Zindy F, Roussel MF, Sherr CJ. Functional and physical interactions of the ARF tumor suppressor with p53 and Mdm2. Proc Natl Acad Sci U S A. 1998;95:8292–7. 76. Stott FJ, Bates S, James MC, McConnell BB, Starborg M, Brookes S, Palmero I, Ryan K, Hara E, Vousden KH, Peters G. The alternative product from the human CDKN2A locus, p14(ARF), participates in a regulatory feedback loop with p53 and MDM2.
Modeling genomic diversity and tumor dependency in malignant melanoma. Cancer Res. 2008;68:664–73. 43. Zhou XP, Gimm O, Hampel H, Niemann T, Walker MJ, Eng C. Epigenetic PTEN silencing in malignant melanomas without PTEN mutation. Am J Pathol. 2000;157:1123–8. 44. Bastian BC. Understanding the progression of melanocytic neoplasia using genomic analysis: from fields to cancer. Oncogene. 2003;22:3081–6 45. Dankort D, Curley DP, Cartlidge RA, Nelson B, Karnezis AN, Damsky WE, You MJ, DePinho RA, McMahon M, Bosenberg M.
MAPK signaling is constitutively activated in almost all melanomas. The vraf murine sarcoma viral oncogene homolog B1 (BRAF) is the dominant genetic target in this pathway, with 40–50 % of melanomas carrying a somatic mutation [19–22]. To a lesser extent, BRAF mutations are also observed in other cancers [23, 24]. BRAF is a serine/threonine kinase directly activated by RAS and is highly expressed in melanocytes, neuronal tissues, testis, and haematopoietic cells. Unlike 28 J. A. Lo and D. E. Fisher ^& ĐͲ