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Prognostic significance of p27 Kip1 expression in colorectal cancer: a clinico‐pathological characterization
Author(s) -
Palmqvist Richard,
Stenling Roger,
Öberg Åke,
Landberg Göran
Publication year - 1999
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/(sici)1096-9896(199905)188:1<18::aid-path311>3.0.co;2-t
Subject(s) - immunohistochemistry , retinoblastoma protein , colorectal cancer , pathological , retinoblastoma , cyclin d1 , cancer research , pathology , tissue microarray , cyclin e , oncology , cell growth , medicine , cell cycle , biology , cancer , gene , biochemistry , genetics
This study has evaluated the expression of the cyclin‐dependent kinase inhibitor p27 Kip1 in 89 colorectal cancers (CRCs) using immunohistochemistry and has related p27 levels to clinico‐pathological characteristics, tumour cell proliferation, and the expression of other G1–S transition regulatory proteins. Low levels of p27 were common in CRCs; 11 per cent of the tumours expressed very low levels and 44 per cent had p27 labelling indices (LIs) below 50 per cent. Except for depth of tumour invasion, no significant correlation was found between p27 expression and Dukes' stage, differentiation, growth pattern, tumour type or lymphocytic infiltration. Interestingly, tumours expressing low or very low p27 LIs were predominantly found in the right colon ( p =0·026). Expression of p27 was a strong predictor of survival, both in univariate and in multivariate survival analyses; patients with tumours of p27 LI less than 50 per cent had an impaired prognosis ( p =0·0069). p27 expression did not correlate with tumour cell proliferation, or with expression of cyclin D1 or the retinoblastoma protein (pRb). These findings support the view that p27 not merely controls cell cycle progression, but might be associated with other mechanisms responsible for aggressive tumour behaviour in colorectal cancer. Copyright © 1999 John Wiley & Sons, Ltd.