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
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
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.