Merkel Cell Polyomavirus Is More Frequently Present in North American than Australian Merkel Cell Carcinoma Tumors

Garneski, Kelly M.; Warcola, Ashley H.; Feng, Qinghua; Kiviat, Nancy B.; Leonard, J. Helen; Nghiem, Paul

doi:10.1038/jid.2008.229

Cited by 297 publications

(298 citation statements)

References 3 publications

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“…2 The virus, provisionally designed Merkel cell polyomavirus, was indicated to be the aetiological agent of Merkel cell carcinoma. [19][20][21][22][23] Accordingly, presence of Merkel cell polyomavirus DNA sequences was observed in 86% of our case series, together with significant expression levels of transforming viral sequences.…”

Section: Discussionmentioning

confidence: 57%

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Expression of p63 is the sole independent marker of aggressiveness in localised (stage I–II) Merkel cell carcinomas

et al. 2011

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Merkel cell carcinoma of the skin is a malignant neuroendocrine tumour, whose prognostic criteria are a matter of dispute. Specifically, no predictor is presently available in stage I-II tumours. We collected clinical and follow-up data from 70 Merkel cell carcinomas of the skin. The same cases were studied for p63 expression by immunohistochemistry, by reverse-transcription PCR (RT-PCR) and TP63 gene status by FISH and for presence of Merkel cell polyomavirus by PCR. Stage emerged as a significant prognostic parameter (P ¼ 0.008). p63 expression, detected in 61% (43/70) of cases by immunohistochemistry, was associated with both decreased overall survival (Po0.0001) and disease-free survival (Po0.0001). Variable expression patterns of the different p63 isoforms were found only in cases immunoreactive for p63. In these latter lesions, at least one of the N-terminal p63 isoforms was detected and TAp63a was the most frequently expressed isoform. TP63 gene amplification was observed by FISH in only one case. Presence of Merkel cell polyomavirus DNA sequences was detected in 86% (60/70) of Merkel cell carcinomas and did not emerge as a significant prognostic parameter. Merkel cell carcinoma cases at low stage (stage I-II) represented over half (40/70 cases, 57%) of cases, and the clinical course was uneventful in 25 of 40 cases while 15 cases died of tumour (10/40 cases) within 34 months or were alive with disease (5/40 cases) within 20 months. Interestingly, a very strict correlation was found between evolution and p63 expression (Po0.0001). The present data indicate that p63 expression is associated with a worse prognosis in patients with Merkel cell carcinoma, and in localised tumours it represents the single independent predictor of clinical evolution.

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Section: Discussionmentioning

confidence: 57%

“…For four patients (n. 2,8,20,40), multiple distant metastases (lymph nodal and brain metastases) specimens were also available. Institutional Review Board permission was obtained for the study.…”

Section: Specimensmentioning

confidence: 99%

Expression of p63 is the sole independent marker of aggressiveness in localised (stage I–II) Merkel cell carcinomas

et al. 2011

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“…In line with this, MCPyV DNA was recently found to be present only rarely and at low concentrations in human haematological malignancies (Shuda et al, 2009). The rates of MCPyV infection may also vary in different populations (Garneski et al, 2009), which may influence the frequency of MCC in patients diagnosed with CLL.…”

Section: Discussionmentioning

confidence: 78%

Chronic lymphocytic leukaemia patients have a high risk of Merkel-cell polyomavirus DNA-positive Merkel-cell carcinoma

et al. 2009

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BACKGROUND: Immunosuppression and Merkel-cell polyomavirus (MCPyV) infection may have a role in the pathogenesis of Merkelcell carcinoma (MCC), a rare neuroendocrine carcinoma of the skin. METHODS: We studied incidence of chronic lymphocytic leukaemia (CLL) and MCC from the files of the Finnish Cancer Registry and the largest hospital of Finland, Helsinki University Central Hospital, from 1979 to 2006. Presence of MCPyV DNA in MCCs was investigated by quantitative PCR. RESULTS: We identified 4164 patients diagnosed with CLL and 172 diagnosed with MCC. Six patients diagnosed with both diseases were found; CLL was the first diagnosis in four cases and MCC in two. The standardised incidence ratio (SIR) for CLL after the diagnosis of MCC was highly elevated, 17.9 (95% confidence interval (CI), 2.2 -64.6; Po0.001), and the SIR for MCC after the diagnosis of CLL was also elevated, 15.7 (3.2 -46.0, Po0.01). Merkel-cell polyomavirus DNA was present in all five MCCs with tumour tissue available for analysis. CONCLUSIONS: We conclude that patients diagnosed with CLL have a substantially increased risk for MCC, and vice versa. Merkel-cell polyomavirus DNA is frequently present in MCCs that occur in CLL patients. Immunosuppression related with CLL and viral infection might explain the association between CLL and MCC.

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“…MCPyV DNA has been detected in 59-100% of MCCs (1,8,21,25,32,53,82,(89)(90)(91)(92)(93)(94). Viral loads of 0.1 to thousands of copies per cell have been observed in about 80% of MCCs.…”

Section: Mcpyv Viral Markers In MCC Patientsmentioning

confidence: 99%

Human Merkel cell polyomavirus: virological background and clinical implications

Coursaget

Samimi

Nicol

et al. 2013

APMIS

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The Merkel cell polyomavirus (MCPyV), identified in humans in 2008, is associated with a relatively rare but aggressive neuroendocrine skin cancer, the Merkel cell carcinoma (MCC). MCC incidence is increasing due to the advancing age of the population, the increase in damaging sun exposure and in the number of immunocompromised individuals. MCPyV must be considered as the etiological agent of MCC and thus is the first example of a human oncogenic polyomavirus. MCPyV infection is common, and seroprevalence studies indicate that widespread exposure begins early in life. The majority of adults have anti-MCPyV antibodies and there is a growing body of evidence that healthy human skin harbors resident or transient MCPyV suggesting that MCPyV infection persists throughout life. However, the mode of transmission, the host cells, and the latency characteristics of this virus remain to be elucidated. In addition, it is still not clear whether MCPyV is associated with diseases or lesions other than Merkel cell carcinoma. The etiologic role of MCPyV in MCC opens up opportunities to improve the understanding of this cancer and to potentially improve its treatment.

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Merkel Cell Polyomavirus Is More Frequently Present in North American than Australian Merkel Cell Carcinoma Tumors

Cited by 297 publications

References 3 publications

Expression of p63 is the sole independent marker of aggressiveness in localised (stage I–II) Merkel cell carcinomas

Expression of p63 is the sole independent marker of aggressiveness in localised (stage I–II) Merkel cell carcinomas

Chronic lymphocytic leukaemia patients have a high risk of Merkel-cell polyomavirus DNA-positive Merkel-cell carcinoma

Human Merkel cell polyomavirus: virological background and clinical implications

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