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PMID: 19161534 Published · ppublish English

Immunohistochemical analysis of Fas and FLIP in prostate cancers.

Kim Su Young, Song Sang Yong, Kim Min Sung, Lee Ji Youl, Lee Hyun Moo, Choi Han Yong, Yoo Nam Jin, Lee Sug Hyung

Abstract

Fas-mediated apoptosis is considered a principal pathway for apoptosis induction in normal and cancer cells. Expression of Fas has been reported in prostate tissues several times, but the data were not consistent. Expression of FLICE-like inhibitory protein (FLIP), an inhibitor of Fas-mediated apoptosis, has not been studied by immunohistochemistry in prostate tissues. The aim of this study is to explore whether alterations of Fas and FLIP expression occur in prostate cancer tissues. We analyzed the expression of Fas and FLIP in 107 prostate adenocarcinoma tissues by immunohistochemistry using a tissue microarray approach. Normal glandular cells of the prostates strongly expressed both Fas and FLIP proteins. Prostate intraepithelial neoplasm also showed a strong Fas immunoreactivity. Fas expression was strongly positive in 60 cancers (56.1%), but the remaining 47 cancers showed no (6.5%) or markedly decreased (37.4%) Fas immunostaining compared with the normal glandular cells of the same patients. By contrast, FLIP expression was strong in most (103/107; 96.3%) of the cancers, and only four cancers (3.7%) showed decreased immunoreactivities compared with the normal cells. The decreased expression of Fas was not associated with pathologic characteristics, including FLIP expression, size of the cancers, age, Gleason score and stage. The decreased expression of Fas in a large fraction of prostate cancers compared with their normal cells suggested that loss of Fas expression might play a role in tumorigenesis in some prostate cancers possibly by inhibiting apoptosis mediated by Fas.

Article Info
Journal
APMIS : acta pathologica, microbiologica, et immunologica Scandinavica
Abbr.
APMIS
Published
2009-03-16
Indexed
2009-01-23
Updated
2009-01-23
Language
English
Country/Region
Denmark
NLM ID
8803400
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