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Melanoma / Skin Cancer News

Polyomavirus Infection In Merkel Cell Carcinoma Is Associated With Better Outcomes

Main Category: Melanoma / Skin Cancer
Also Included In: Dermatology;  Cancer / Oncology
Article Date: 19 Jun 2009 - 0:00 PDT

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A polyomavirus known as MCPyV is associated with clinical outcomes, including fewer metastases and better survival, in patients with a rare form of skin cancer called Merkel cell carcinoma, according to a new study published online June 17 in the JNCI.

Integration of the Merkel cell carcinoma polyomavirus (MCPyV) genome into the tumor genome was recently found to be frequent in skin cancers, but the clinical consequences of MVPyV genomic integration was unclear.

To examine the consequences of viral DNA integration, Heikki Joensuu, M.D., of the Department of Oncology at Helsinki University Central Hospital, and colleagues, conducted histopathologic and molecular biological analyses of tumor tissue and DNA from 109 Finnish patients who were diagnosed with Merkel cell carcinoma from 1979 to 2004.

Approximately 50% of the tumors were positive for MCPyV DNA. These cancers tended to be located in a limb, to have less frequent nodal or distant metastases at the time of diagnosis, and to be associated with better survival compared with MCPyV DNA-negative cancers.

"Identification of MCPyV as a contributing factor to the pathogenesis of Merkel cell carcinoma might provide novel choices for future therapeutic strategies," the authors write.

In an accompanying editorial, James A. DeCaprio, M.D., of the Dana-Farber Cancer Institute in Boston, points out parallels between MCPyV infection in Merkel cell carcinoma and human papillomavirus infection in head and neck cancers, suggesting reasons that the presence of these viruses would predict a better prognosis.

"Perhaps expression of the viral oncogenes can induce or promote the development of cancers that have fewer host cell chromosomal abnormalities, which may result in tumors with simpler genomic abnormalities," the editorialist writes. "Alternatively, the viral oncogenes may specifically perturb host signaling pathways, including immune surveillance, that render them less aggressive or lethal."

Author:
Joensuu Heikki

Source:
Steve Graff
Journal of the National Cancer Institute




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