| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2473389 | Current Opinion in Virology | 2012 | 10 Pages |
Merkel cell polyomavirus (MCV), discovered in 2008, is clonally integrated in ∼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.
► MCV was discovered in 2008 by digital transcriptome subtraction and is one of seven new human polyomaviruses described in the past five years. ► Merkel cell polyomavirus (MCV), a new human polyomavirus, is clonally integrated in 70–80% of Merkel cell carcinoma (MCC) tumors. ► MCV is part of the normal, healthy skin flora but causes cancer after viral genome mutations eliminate its replication capacity. ► While similar to known polyomaviruses, MCV oncogenes act in new ways, such as activation of the survivin oncoprotein and PP2A-independent targeting of cap-dependent translation. ► In four years, the diagnosis and treatment potential for an intractable and enigmatic cancer has dramatically changed through discovery of the viral cause of MCC.
