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Lateral distribution of Merkel cell carcinoma in a nationwide cohort
Author(s) -
Koljonen V.,
Kluger N.,
Sihto H.,
Böhling T.
Publication year - 2013
Publication title -
journal of the european academy of dermatology and venereology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.655
H-Index - 107
eISSN - 1468-3083
pISSN - 0926-9959
DOI - 10.1111/j.1468-3083.2012.04600.x
Subject(s) - medicine , merkel cell carcinoma , cohort , distribution (mathematics) , oncology , dermatology , carcinoma , mathematical analysis , mathematics
Background  The asymmetric laterality of UV‐linked skin cancer, including melanoma and non‐ melanoma skin cancers has been identified. However, there seems to be a paucity in the data correlating the laterality and presence of Merkel cell polyoma virus (MCPyV) DNA as an aetiological factor for this phenomenon. Objective  To study the laterality in Finnish primary Merkel cell carcinoma (MCC) patients, and compare statistically clinicopathological variables with lateral distribution. Methods  Data on 171 primary MCC patients and tumour characteristics; and the presence of MCPyV DNA or large T antigen in the tumour tissue, MCPyV copy number and MCC specific mortality were compared statistically against left, right or midline presentation. Results  Fiftysix percentage of tumours presented on the left, 37% on the right and 7% in the midline. Excluding the latter category, the left‐sided excess was 60%. The excess of left‐sided tumours was noted in head and neck with left‐right ratio 3.22, face 1.5, forearm and hand 4.0 and the leg and foot 2.4. On the trunk, tumours occurred equally on both sides. Statistically significant difference was noted for smaller midline tumours ( P  < 0.0065). Left‐sided tumours associated with lower median Merkel cell polyoma virus copy number ( P  < 0.042) although the trend vanished when comparing the groups separately. Conclusion  We confirmed left‐sided asymmetry in MCC distribution. In areas commonly hidden form solar exposure, the occurrence was symmetrical. Detailed aetiology of these findings remains unclear, plausible explanations include biology of viral associated tumours or alterations in Nodal transcription factor pathway.

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