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Expression of proliferating cell nuclear antigen, Ki‐67 antigen, estrogen receptor protein, and tumor suppressor p53 gene in cytologic samples of breast cancer: An immunochemical study with clinical, pathobiological, and histologic correlations
Author(s) -
Pelosi Giuseppe,
Bresaola Enrica,
Rodella Stefania,
Manfrin Erminia,
Piubello Quirino,
Schiavon Ivana,
Lannucci Antonio
Publication year - 1994
Publication title -
diagnostic cytopathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.417
H-Index - 65
eISSN - 1097-0339
pISSN - 8755-1039
DOI - 10.1002/dc.2840110206
Subject(s) - proliferating cell nuclear antigen , ki 67 , immunostaining , pathology , breast cancer , immunohistochemistry , antigen , oncogene , medicine , cancer , estrogen receptor , cancer research , biology , cell cycle , immunology
Sixty‐six unselected breast cancers were analyzed in cytologic smears and histologic sections for the expression of Ki‐67, proliferating cell nuclear antigen (PCNA). estrogen receptor protein (ERP), and p53 protein using a standard immunochemical method. The results, expressed as both positive cases and labelling index (LI), were compared with clinical and pathobiological variables. Ki‐67 and PCNA immunostaining was seen in all cases, whereas ERP was detectable in 46/63 cases and p53 protein in 20/66 cases. The expression of these markers was generally lower in cytology than in histology, though the differences were not statistically significant. PCNA‐LI and Ki‐67‐LI were closely correlated (P < 0.001), the mean PCNA:Ki‐67 ratio being 0.92 ± 0.57. Occasional discrepancies, however, were found. PCNA and Ki‐67 expression was associated with an increase in histologic grade and a decrease in ERP content of tumors, whereas p53 was statistically associated with no clinical or pathobiological variables. The data suggest that proliferative activity and oncogene overexpression may be reliably evaluated in breast cancer by FNA cytology, though PCNA is not a suitable indicator for cell proliferation. The results do not resolve the issue as to whether immunostaining for p53 protein constitutes a dedifferentiation product of the tumor, or is a fundamental aspect of the malignant progression. Survival studies in a larger series of tumors are thus needed to elucidate this point. Diagn Cytopathol 1994; 11:131–140. © 1994 Wiley‐Liss, Inc.