{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,5]],"date-time":"2025-11-05T20:38:11Z","timestamp":1762375091074},"reference-count":53,"publisher":"American Association for Cancer Research (AACR)","issue":"12","content-domain":{"domain":["aacrjournals.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2006,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Defective expression of HLA class I molecules is common in tumor cells and may allow escape from CTL-mediated immunity. We here investigate alterations in expression of HLA class I and their underlying molecular mechanisms in ovarian cancer patients. The HLA class I and HLA-A2 expression levels on noncultured tumor cells of 12 patients diagnosed with ovarian carcinoma were investigated by flow cytometry. Molecular analyses of antigen-processing machinery (APM) components were done in metastatic cancer cells, and the HLA genotype was determined in both these and the primary tumor. HER-2\/neu-specific immunity was evaluated by enzyme-linked immunospot assays. The metastatic tumor cells from all patients expressed low levels of HLA class I surface antigens. In six of nine HLA-A2+ patients, HLA-A2 expression was heterogeneous with a subpopulation of tumor cells exhibiting decreased or absent HLA-A2 expression. One patient-derived tumor cell line completely lacked HLA-A2 but exhibited constitutive expression of APM components and high HLA class I expression that was further inducible by IFN-\u03b3 treatment. Genotyping showed a haplotype loss in the metastatic tumor cells, whereas tumor tissue microdissected from the primary tumor exhibited an intact HLA gene complex. Interestingly, HLA-A2-restricted HER-2\/neu-specific T-cell responses were evident among the lymphocytes of this patient. Abnormalities in HLA class I antigen expression are common features during the progression of ovarian cancer, and haplotype loss was, for the first time, described as an underlying mechanism. (Cancer Res 2006; 66(12): 6387-94)<\/jats:p>","DOI":"10.1158\/0008-5472.can-06-0029","type":"journal-article","created":{"date-parts":[[2006,6,15]],"date-time":"2006-06-15T21:49:25Z","timestamp":1150408165000},"page":"6387-6394","update-policy":"http:\/\/dx.doi.org\/10.1158\/crossmark_policy","source":"Crossref","is-referenced-by-count":55,"title":["Frequent Loss of HLA-A2 Expression in Metastasizing Ovarian Carcinomas Associated with Genomic Haplotype Loss and HLA-A2-Restricted HER-2\/<i>neu<\/i>-Specific Immunity"],"prefix":"10.1158","volume":"66","author":[{"given":"Ha\u030akan","family":"Norell","sequence":"first","affiliation":[{"name":"1Department of Oncology and Pathology, Immune and Gene Therapy Laboratory, Cancer Center Karolinska, Karolinska Institutet, Karolinska University Hospital;"}]},{"given":"Mattias","family":"Carlsten","sequence":"additional","affiliation":[{"name":"1Department of Oncology and Pathology, Immune and Gene Therapy Laboratory, Cancer Center Karolinska, Karolinska Institutet, Karolinska University Hospital;"},{"name":"2Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge;"}]},{"given":"Tomas","family":"Ohlum","sequence":"additional","affiliation":[{"name":"1Department of Oncology and Pathology, Immune and Gene Therapy Laboratory, Cancer Center Karolinska, Karolinska Institutet, Karolinska University Hospital;"}]},{"given":"Karl-Johan","family":"Malmberg","sequence":"additional","affiliation":[{"name":"2Department of Medicine, Center for Infectious Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge;"}]},{"given":"Giuseppe","family":"Masucci","sequence":"additional","affiliation":[{"name":"1Department of Oncology and Pathology, Immune and Gene Therapy Laboratory, Cancer Center Karolinska, Karolinska Institutet, Karolinska University Hospital;"}]},{"given":"Kjell","family":"Schedvins","sequence":"additional","affiliation":[{"name":"3Department of Obstetrics and Gynecology, Karolinska University Hospital, Stockholm, Sweden;"}]},{"given":"Wolfgang","family":"Altermann","sequence":"additional","affiliation":[{"name":"4Institute of Medical Immunology, Martin-Luther University, Halle, Germany; and"}]},{"given":"Diana","family":"Handke","sequence":"additional","affiliation":[{"name":"4Institute of Medical Immunology, Martin-Luther University, Halle, Germany; and"}]},{"given":"Derek","family":"Atkins","sequence":"additional","affiliation":[{"name":"5Institute of Pathology, University of Witten\/Herdecke, Witten\/Herdecke, Germany"}]},{"given":"Barbara","family":"Seliger","sequence":"additional","affiliation":[{"name":"4Institute of Medical Immunology, Martin-Luther University, Halle, Germany; and"}]},{"given":"Rolf","family":"Kiessling","sequence":"additional","affiliation":[{"name":"1Department of Oncology and Pathology, Immune and Gene Therapy Laboratory, Cancer Center Karolinska, Karolinska Institutet, Karolinska University Hospital;"}]}],"member":"1086","published-online":{"date-parts":[[2006,6,15]]},"reference":[{"key":"2022061621203548500_B1","doi-asserted-by":"crossref","unstructured":"Jemal A, Murray T, Ward E, et al. 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