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Threshold levels of gene expression of the melanoma antigen gp100 correlate with tumor cell recognition by cytotoxic T lymphocytes
Author(s) -
Riker Adam I.,
Kammula Udai S.,
Panelli Monica C.,
Wang Ena,
Ohnmacht Galen A.,
Steinberg Seth M.,
Rosenberg Steven A.,
Marincola Francesco M.
Publication year - 2000
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(20000615)86:6<818::aid-ijc10>3.0.co;2-w
Subject(s) - cytotoxic t cell , melanoma , antigen , gene , immunology , cancer research , biology , gene expression , t lymphocyte , genetics , in vitro
The level of expression of melanoma antigens (MA) may modulate the host immunologic response. Thus, the accurate measurement of MA expression may allow proper patient selection for antigen‐specific therapies and yield important information for the evaluation of clinical results. In this study, we measured the absolute levels of MA messenger ribonucleic acid (mRNA) in tumor cell lines utilizing real‐time quantitative reverse transcriptase‐polymerase chain reaction (qRT‐PCR). mRNA levels of MART‐1, gp100, tyrosinase, TRP‐1 and TRP‐2 melanoma differentiation antigens and MAGE‐1, MAGE‐3 and ESO‐1 cancer testis (CT) antigens were compared in 24 early‐passage (<5 passages in culture) and 12 archival melanoma cell lines. MA mRNA expression was extremely variable among cell lines, occasionally reaching levels comparable to ribosomal RNA (rRNA). gp100 and MART‐1 mRNA levels correlated with protein expression measurement obtained by FACS analysis. More significantly, a threshold of gp100 mRNA expression required for T‐cell stimulation and target‐cell killing was identified. This threshold level corresponded to approximately 500 mRNA copies per 10 8 copies of rRNA. Our results suggest that the measurements of MA mRNA levels may yield useful information relevant to the interpretation of clinical outcome during antigen‐specific treatments. Int. J. Cancer 86:818–826, 2000. © 2000 Wiley‐Liss, Inc.