Merkel cell carcinoma induces lymphatic microvessel formation

• Verfasst von: Werchau, Siegfried Arthur [VerfasserIn]
• Verfasst von: Toberer, Ferdinand [VerfasserIn]
• Verfasst von: Enk, Alexander [VerfasserIn]
• Verfasst von: Helmbold, Peter [VerfasserIn]
• Titel: Merkel cell carcinoma induces lymphatic microvessel formation
• Verf.angabe: Siegfried Werchau, Ferdinand Toberer, Alexander Enk, Reinhard Dammann, and Peter Helmbold
• E-Jahr: 2012
• Jahr: August 2012
• Umfang: 11 S.
• Fussnoten: Published online: September 4, 2011 ; Gesehen am 26.11.2018
• Titel Quelle: Enthalten in: American Academy of DermatologyJournal of the American Academy of Dermatology
• Ort Quelle: Amsterdam [u.a.] : Elsevier, 1979
• Jahr Quelle: 2012
• Band/Heft Quelle: 67(2012), 2, Seite 215-225
• ISSN Quelle: 1097-6787
• DOI: doi:10.1016/j.jaad.2011.09.002
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: lymphangiogenesis
• Sach-SW: lymphatic microvessel density
• Sach-SW: lymphatic vessel
• Sach-SW: Merkel cell carcinoma
• Sach-SW: Merkel cell polyomavirus
• Sach-SW: tumor-associated macrophages
• K10plus-PPN: 1584421088

Abstract

Background: Merkel cell carcinoma (MCC) is a rare, highly malignant neuroendocrine tumor of the skin characterized by frequent lymphatic metastasis. Objective: We sought to identify lymphovascular anatomy and expression profiles of lymphangiogenic cytokines to give an opinion on lymphangiogenesis in MCC. Methods: We studied lymphatic microanatomy and lymphangiogenic cytokines in 27 MCC by immunohistology or immunofluorescence (D2-40, lymphatic vessel endothelial hyaluronan receptor [LYVE-1], vascular endothelial growth factor [VEGF] receptor-3, VEGF-C, VEGF-D, Ki67/MiB-1, CD68/PG-M1, CD68/KP1, CD163), Merkel cell polyomavirus-specific polymerase chain reaction, and coanalysis with clinical and histologic data. Results: We found a more than 3-fold increase in the mean density of absolute numbers of small lymphatic capillaries (diameter <10 μm) and a more than 8-fold increase in the median ratio of the number of small to large lymphatics (<10/≥10 μm) paratumorally compared with intraindividual controls. VEGF-C+CD68+ CD163+ cells (interpreted as M2 macrophages) could be identified as an important potentially lymphangiogenesis-inducing cell type. Limitations: Partially lacking follow-up data limited the analysis of the prognostic impact. Conclusions: Our findings strongly indicate lymphangiogenesis in MCC driven by VEGF-C+CD68+ CD163+ M2 macrophages.