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p27/kip1 expression in normal epithelium, benign and neoplastic breast lesions
Author(s) -
De Paola Franca,
Maria Vecci Anna,
Maria Granato Anna,
Liverani Marilena,
Monti Franco,
Maria Innoceta Anna,
Gianni Lorenzo,
Saragoni Luca,
Ricci Monica,
Falcini Fabio,
Amadori Dino,
Volpi Annalisa
Publication year - 2002
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/path.1011
Subject(s) - fibroadenoma , pathology , epithelium , malignant transformation , immunohistochemistry , biology , hyperplasia , breast cancer , lymph node , neoplastic transformation , phyllodes tumor , cancer , medicine , carcinogenesis , genetics
The development of cancer in the breast and in other sites is a complex process requiring a number of different genetic and epigenetic alterations. The accumulation of the genetic changes is thought to underlie the progression from precancerous lesions to carcinomas. The expression of p27/kip1 protein, a cyclin‐dependent kinase inhibitor, was investigated by immunohistochemistry in normal epithelial specimens, benign alterations, and malignant lesions of the breast. The number of p27/kip1‐positive cells ranged from none to more than 98% in the overall series. Wide ranges of p27/kip1‐positive cells were consistently observed within each histological category, but the median value progressively decreased in typical hyperplasia and fibroadenoma, with an even more marked reduction in malignant lesions, compared with normal epithelium. Moreover, the percentage of cells expressing p27/kip1 in tumours was about three times lower in invasive than in in situ lesions and was inversely related to tumour size, but not to lymph node involvement. In conclusion, the degree to which p27 expression is altered in typical hyperplastic lesions and fibroadenomas indicates that the deregulation of p27 may occur very early on during breast cell transformation, but the usefulness of its determination to categorize subgroups of lesions at different risk of evolution remains somewhat doubtful. Copyright © 2001 John Wiley & Sons, Ltd.