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Up‐regulation of ephrin‐a1 during melanoma progression
Author(s) -
Easty David J.,
Hill Simon P.,
Hsu MeiYu,
Fallowfield Mary E.,
Flørenes Vivi Ann,
Herlyn Meenhard,
Bennett Dorothy C.
Publication year - 1999
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/(sici)1097-0215(19991022)84:5<494::aid-ijc8>3.0.co;2-o
Subject(s) - melanoma , erythropoietin producing hepatocellular (eph) receptor , ephrin , pathology , medicine , cancer research , receptor , tumor progression , metastasis , cancer , biology , receptor tyrosine kinase
Ephrin‐A1, formerly called B61, is a new melanoma growth factor; it is angiogenic and chemoattractant for endothelial cells. EPH‐A2, or ECK (a receptor for ephrin‐A1), is ectopically expressed in most melanoma cell lines; the pathology where this expression is first manifested and the possible role of the receptor in tumor progression are unknown. To determine these, we studied the expression of this ligand and receptor in biopsies of benign and malignant melanocytic lesions. EPH‐A2 was not detected in normal melanocytes, benign compound nevi or advanced melanomas, though it was found in 2 of 9 biopsies of malignant melanoma in situ. Ephrin‐A1 was present in occasional early lesions and in advanced primary melanomas (43%) and metastatic melanomas (67%). Expression of ephrin‐A1 was induced in melanoma cells by pro‐inflammatory cytokines. Our findings are consistent with 2 possible roles for ephrin‐A1 in melanoma development: it may promote melanocytic cell growth or survival and induce vascularization in advanced melanomas. Both effects may be potentiated by inflammatory responses. Our data are consistent with earlier observations that an inflammatory infiltrate is associated with poor prognosis in thin primary melanomas. Int. J. Cancer (Pred. Oncol.) 84:494–501, 1999. © 1999 Wiley‐Liss, Inc.