期刊
CURRENT OPINION IN VIROLOGY
卷 2, 期 4, 页码 489-498出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.coviro.2012.05.007
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- NCI NIH HHS [R01 CA136363, R01 CA136806] Funding Source: Medline
Merkel cell polyomavirus (MCV), discovered in 2008, is clonally integrated in similar to 80% Merkel cell carcinoma (MCC). MCV is a common skin flora and initiates cancer in susceptible hosts only after it acquires a precise set of mutations that render it replication incompetent. Both MCV large and small T proteins promote cancer cell survival and proliferation. Large T targets pocket proteins regulating cell cycle transit while small T activates cap-dependent translation critical for cancer cell growth. These findings already have led to new diagnostics and clinical trials to target MCV-induced survivin and to promote antitumor immunity. In four years, the cause, diagnosis and therapy for an intractable cancer has been changed due to the molecular discovery of MCV.
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