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Angiogenesis, Metastasis, and the Cellular Microenvironment

Induction of "Antigen Silencing" in Melanomas by Oncostatin M: Down-Modulation of Melanocyte Antigen Expression¹

¹ Department of Pathology, Massachusetts General Hospital, Boston, MA;
² CytoCure LLC, Beverly, MA;
³ The Boston Biomedical Research Institute, Watertown, MA;
⁴ The Institute for Immunology and Allergy Research, ICPMR and ⁵ Department of Immunopathology, Westmead Hospital, Westmead, New South Wales, Australia; and
⁶ Catholic University, Largo A. Gemelli, Rome, Italy

Requests for reprints: Paul J. Durda, Department of Pathology, Massachusetts General Hospital, Warren 508, 100 Blossom St., Boston, MA 02114. Phone: (617) 724-1613; Fax: (617) 726-2365. E-mail: pdurda{at}partners.org

We previously reported that antigen expression in melanoma cell lines is down-regulated by proteins secreted by antigen-negative melanoma cells. Here we report the purification and characterization of one of these down-regulatory factors, the cytokine, oncostatin M (OSM), which transmits its signal via the gp130 cell surface receptor, resulting in the selective down-modulation of the melanocyte lineage antigens: Melan-A/MART-1, gp100, tyrosinase, tyrosinase-related proteins 1 and 2, and the M isoform of microphthalmia transcription factor. Furthermore, we have found that some melanoma cell lines produce as yet uncharacterized factors distinct from OSM which also down-modulate antigen expression via signaling pathways different from that employed by OSM. These data indicate that there may be several regulatory pathways and molecules involved in the antigen-silencing process which may be related to the state of differentiation of the tumor cell and may affect the outcome of antitumor vaccine immunotherapies.

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