Switch to an invasive growth phase in melanoma is associated with tenascin‐C, fibronectin, and procollagen‐I forming specific channel structures for invasion

• DOI: 10.1002/path.2045
• Publication Date: 2006-08-21T13:46:40Z
• Authors: E Kääriäinen; P Nummela; J Soikkeli; M Yin; M Lukk; T Jahkola; S Virolainen; A Ora; E Ukkonen; O Saksela; E Hölttä
• Keywords: Tenascin C; Tissue microarray

Abstract Malignant melanomas are characterized by their high propensity to invade and metastasize, but the molecular mechanisms of these traits have remained elusive. Our DNA microarray analyses benign nevi melanoma tissue specimens revealed that genes encoding extracellular matrix proteins tenascin‐C (TN‐C), fibronectin (FN), procollagen‐I (PCOL‐I) highly upregulated in invasive metastatic melanomas. The expression distribution were further studied immunohistochemistry nevi, radially vertically growing melanomas, sentinel node micrometastases, macrometastases. TN‐C was increased all tumours metastases, especially at invasion fronts, not or non‐invasive Significantly, intensity staining correlated with metastasis lymph nodes, better than tumour thickness (Breslow). Moreover, TN‐C, FN, PCOL‐I appeared co‐localize form tubular meshworks channels ensheathing cells. data suggest is associated formation special channel‐like structures, providing a new concept, structured cell spreading. Altogether, provide potential prognostic markers therapeutic targets/strategies for preventing dissemination. Copyright © 2006 Pathological Society Great Britain Ireland. Published John Wiley & Sons, Ltd.