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Characterization of antigen processing machinery and Survivin expression in tonsillar squamous cell carcinoma
Author(s) -
Weinman Eric C.,
Roche Patrick C.,
Kasperbauer Jan L.,
Cha Steve S.,
Sargent Dan J.,
Cheville John,
Murphy Linda M.,
Chen Lieping,
Wettstein Peter J.,
Gostout Bobbie,
Ferrone Soldano,
Strome Scott E.
Publication year - 2003
Publication title -
cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.052
H-Index - 304
eISSN - 1097-0142
pISSN - 0008-543X
DOI - 10.1002/cncr.11311
Subject(s) - survivin , antigen , human leukocyte antigen , medicine , cancer research , tissue microarray , pathology , immunoperoxidase , antigen processing , immunology , immunohistochemistry , cancer , mhc class i , antibody , major histocompatibility complex , monoclonal antibody
BACKGROUND There is a statistically significant association between human leukocyte antigen (HLA) Class I antigen expression and improved prognosis for some patients. This association reflects the control of tumor growth by HLA Class I antigen‐restricted, tumor‐associated antigen‐specific cytolytic T cells. However, progression of other malignant diseases is not associated with the loss of HLA expression. These observations show that the poor prognosis of a subset of tumors, despite high HLA Class I antigen expression, may reflect the development of alternative mechanisms utilized by tumor cells to escape from immune recognition and destruction. METHODS The authors evaluated the possible correlation between the expression of the antiapoptosis gene, Survivin , HLA Class I, and progression of tonsillar squamous cell carcinomas (TSCC) lesions. Tissue microarrays were constructed from primary TSCC, metastatically involved lymph nodes, adjacent normal mucosa, and tonsillar parenchyma excised for nonmalignant conditions. RESULTS Immunoperoxidase staining of tissue sections demonstrated that Survivin expression is significantly higher ( P < 0.001) in malignant tumors than in normal tissue samples. In addition, Survivin expression is significantly higher ( P = 0.05) in metastatic than in primary lesions. Survivin expression in primary lesions correlated positively with delta ( P = 0.025), tapasin ( P = 0.028), and HLA Class I antigen ( P = 0.006) expression. The expression patterns of delta, tapasin, HLA Class I antigen, β‐2‐microglobulin, and Survivin did not demonstrate any significant association with the clinical course of disease. CONCLUSIONS For TSCC that maintain the expression of HLA Class I antigen, overexpression of Survivin may provide an alternative explanation for tumor progression. Cancer 2003;97:2203–11. © 2003 American Cancer Society. DOI 10.1002/cncr.11311