Cytoplasmic melanoma-associated antigen (CYT-MAA) serum level in patients with melanoma: A potential marker of response to immunotherapy?

✍ Scribed by Sandra R. Reynolds; Irene J. Vergilis; Michael Szarek; Soldano Ferrone; Jean-Claude Bystryn

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: French
• Weight: 135 KB
• Volume: 119
• Category: Article
• ISSN: 0020-7136
• DOI: 10.1002/ijc.21820

✦ Synopsis

Abstract

Simple, noninvasive methods are needed to follow effectiveness of new treatments in patients with melanoma. In our study, we examined cytoplasmic melanoma‐associated antigen (CYT‐MAA) serum level in melanoma patients during immunotherapy. Sera of 117 patients were assayed for CYT‐MAA by double‐sandwich ELISA before and during treatment with a polyvalent, shed antigen, melanoma vaccine. Vaccine‐treated patients included 30 with American Joint Committee on Cancer (AJCC) stage IIb or IIIa, 30 with stage IIc, IIIb or IIIc, 30 with resected stage IV and 27 with measurable stage IV disease. Prior to vaccine therapy, 63% of patients had elevated serum CYT‐MAA with high levels of antigen in all disease stages. After initiation of therapy, the level declined in more than 90% of the positive patients and fell below the positive cut‐off in 56% of these patients within 5 months. By contrast, there was no decline in CYT‐MAA serum level in 11 patients who served as untreated controls with melanoma. Multivariate analysis of the treated patients using accelerated failure time Weibull models adjusted for stage and age showed that patients whose CYT‐MAA serum level remained elevated during treatment were ∼3 times more likely to recur or progress than patients who were consistently below the positive cut‐off (hazard ratio = 3.42, 95% CI [1.38, 8.47], p = 0.0079). Measurement of CYT‐MAA serum level appears to show potential as an early marker of prognosis in patients with stages IIb to IV melanoma. Measurement of CYT‐MAA serum level during therapy could provide an intermediate marker of response in these patients. © 2006 Wiley‐Liss, Inc.