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Lamin subtype expression in Merkel-cell carcinoma: its relation to polyomavirus infection and tumor metastasis

Merel Stiekema; Monique Ummelen; Moritz Jesinghaus; Corinna U. Keber; Viktoria Wischmann; Ingrid Moll; Jack Cleutjens; Marc A. M. J. van Zandvoort; Jos L. V. Broers; Frans C. S. Ramaekers; Roland Moll
Histochemistry and Cell Biology · Vol. 164, Issue 1 · 2026

Abstract

Merkel-cell carcinoma (MCC) is known for its high metastatic potential. Studies in several tumor types have proposed a role for up- or downregulation of nuclear A- and B-type lamins in facilitating the process of invasion and metastasis, but such studies are lacking for MCC. Therefore, lamin expression levels were examined in 38 tissue samples from 28 patients with MCC using immunohistochemistry. The series comprised primary tumors and different metastases and both Merkel cell polyomavirus (MCPyV) positive and MCPyV-negative cases. This study revealed that primary MCC tumors express variable, but mostly low levels of A-type lamins, while the B-type lamins are overall highly expressed. No obvious differences in lamin expression were observed between the MCPyV-positive and MCPyV-negative cases. A generally higher A-type lamin expression was detected in MCC metastases, although comparison of primary tumors versus metastases from the same patients showed either no change or up- or downregulation of A-type lamins. Normal Merkel cells were found to express both A- and B-type lamins. Conclusively, our data suggest a flexible A-type lamin expression in the process of MCC carcinogenesis and metastasis, which is an important finding regarding the aggressiveness of MCC and in the debate about the cellular origin of MCC.

Bibliographic Information

JournalHistochemistry and Cell Biology
PublisherSpringer
Publication Date2026-08-27
Publication Year2026
Volume164
Issue1
Document TypeJournal Article
eISSN1432-119X
DOI10.1007/s00418-026-02526-1

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NARA Access Coverage1958-01-01~Current
Journal Homepagehttps://www.springer.com/journal/418
Publisher PageOpen Publisher Page
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