title: The p53-positive phenotype of breast cancers.
abstract: One hundred and eighty-one breast cancer specimens were analyzed for nuclear p53 staining by immunochemical methods. There were 123 fine-needle cytological specimens and 58 frozen tissue sections of surgical biopsies. The microscopic evaluation of the staining fitted with a 4 group classification. Ninety-one samples (50.6%) were devoid of any staining (-), while 42 (23.3%) showed only few stained nuclei (+/-), typically around 1%. Thirty-two (17.8%) samples presented with strong nuclear staining (++) which in practically all cases concerned more than 50% of the nuclei, but a few cases showed staining heterogeneity. A further 17 cases (9.4%) presented with nuclear staining which concerned 10-20% of the cancer cells (+). This four class system was used to compare p53 expression with other prognostic parameters. A strong inverse correlation was observed with steroid hormone receptor content and p53 positivity was highly significantly associated with higher S-phase. All but one of the highly positive cases were aneuploid. Twenty-five percent (29/120) of the aneuploid tumors were strongly stained and a further 10% were considered positive (+). On the other hand, only 5 out of 59 DNA-diploid tumors were considered as + and one ++. The DNA index distribution according to p53 positivity showed peaks of positivity for hypodiploid, triploid and hypertetraploid values. Negative tumors were in all regards similar to those with only few stained nuclei, in particular mean S-phases of 2.8 and 3.3% respectively. Altogether, the typical strong p53 phenotype concerned a DNA-aneuploid tumor with above median S-phase fraction (mean of 7.1%), negative steroid hormone receptors and cytoprognostic index III. The p53 positive cases (+), were frequently steroid hormone receptor positive and had on the average intermediate S-phase fractions (4.3%). The proportion of immunochemical positivity (27% in our series), is compatible with the published frequency of p53 mutations detected in breast cancers, but the differences in the phenotype according to the level of positivity should be further investigated.
authors.affiliation: INST CURIE,UMR 147 CNRS,F-75231 PARIS,FRANCE. LAB ANAT & CYTOL PATHOL,F-03200 VICHY,FRANCE. CTR CYTOPATHOL CLIN,F-75014 PARIS,FRANCE. CABINET CYTOPATHOL,F-75015 PARIS,FRANCE. CTR MED ITALIE 2,CABINET CYTOPATHOL,F-75013 PARIS,FRANCE. APPLICAT BIOL CANCEROL,F-95450 AVERNES,FRANCE.
authors.forename: G
authors.initials: G
authors.lastname: Lesec
authors.forename: E
authors.initials: E
authors.lastname: Richardcoulet
authors.forename: J
authors.initials: J
authors.lastname: Collet
authors.forename: M
authors.initials: M
authors.lastname: Demaublanc
authors.forename: S
authors.initials: S
authors.lastname: Merle
authors.forename: R
authors.initials: R
authors.lastname: Salmon
authors.forename: Y
authors.initials: Y
authors.lastname: Remvikos