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

Citation
G. Pelosi et al., 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, Diagnostic cytopathology, 11(2), 1994, pp. 131-140
Citations number
NO
Categorie Soggetti
Medical Laboratory Technology",Pathology
Journal title
ISSN journal
87551039
Volume
11
Issue
2
Year of publication
1994
Pages
131 - 140
Database
ISI
SICI code
8755-1039(1994)11:2<131:EOPCNA>2.0.ZU;2-P
Abstract
Sixty-six unselected breast cancers were analyzed in cytologic smears and histologic sections for the expression of Ki-67, proliferating cel l nuclear antigen (PCNA), estrogen receptor protein (ERP), and p53 pro tein using a standard immunochemical method. The results, expressed as both positive cases and labelling index (LI), were compared with clin ical and pathobiological variables. Ki-67 and PCNA immunostaining was seen in all cases, whereas ERP was detectable in 46163 cases and p53 p rotein in 20166 cases. The expression of these markers was generally l ower in cytology than in histology, though the differences were not st atistically 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 d iscrepancies, however, were found PCNA and Ki-67 expression was associ ated with an increase in histologic grade and a decrease in ERP conten t of tumors, whereas p53 was statistically associated with no clinical or pathobiological variables. The data suggest that proliferative act ivity and oncogene overexpression may be reliably evaluated in breast cancer by FNA cytology, though PCNA is not a suitable indicator for ce ll proliferation. The results do not resolve the issue as to whether i mmunostaining 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 eluc idate this point. (C) 1994 Wiley-Liss, Inc.