英国科学家近日研究发现，大约70%的皮肤癌（黑素瘤）可能都是由同一种突变基因所诱发，在过多的日晒情况下，该基因会导致细胞癌变。这一发现将导致对于恶性皮肤癌更好的疗法。相关论文4月7日发表在《癌细胞》（Cancer Cell）上。
该基因名为BRAF，科学家早已知道，黑素瘤患者体内的BRAF基因经常遭到破坏，但一直不清楚这是诱发黑素瘤的原因还是其导致的结果。
论文通讯作者、英国癌症研究所的Richard Marais说：“我们的研究显示，BRAF的遗传损伤是皮肤癌发展的第一步。理解这一过程将帮助我们开发更有效的疗法。”
研究人员希望，通过理解皮肤癌背后的遗传机制来开发出相关的靶标药物，从而能够修补不完善的遗传机制。（生物谷Bioon.com）
生物谷推荐原始出处：
Cancer Cell, 7 April 2009 doi:10.1016/j.ccr.2009.02.022
Oncogenic Braf Induces Melanocyte Senescence and Melanoma in Mice
Nathalie Dhomen1,5,Jorge S. Reis-Filho2,5,Silvy da Rocha Dias1,5,Robert Hayward1,Kay Savage2,Veronique Delmas3,Lionel Larue3,Catrin Pritchard4andRichard Marais1,,
1 Signal Transduction Team, Cancer Research UK Centre for Cell and Molecular Biology, The Institute of Cancer Research, London SW3 6JB, UK
2 Breakthrough Breast Cancer Research Centre, The Institute of Cancer Research, London SW3 6JB, UK
3 Institut Curie, UMR146 CNRS, 91405 Orsay, France
4 Department of Biochemistry, University of Leicester, Leicester LE1 7RH, UK
5 These authors contributed equally to this work
We show here that inducible expression of BrafV600E off the endogenous Braf gene in mouse melanocytes stimulates skin hyperpigmentation and the appearance of nevi harboring senescent melanocytes. Additionally, approximately 70% of BrafV600E mice develop melanomas that reproduce many of the cardinal histological and molecular features of human melanoma and whose cells can colonize the lungs of nude mice. We show that the tumor suppressor p16INK4a is not required to induce melanocyte senescence and that its loss is not required for tumor progression, although it does regulate tumor penetrance and latency. Thus, we have developed a mouse model of melanoma driven by BrafV600E expressed at physiological levels that reflects the genetics and pathology of the human disease.
