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There are 2 main groups of breast cysts characterized by their intracystic sodium-to-potassium ratios. Women who have intracystic Na/K3 may have a higher risk of developing breast cancer than those who have intracystic Na/K3. The cell adhesion molecule, ICAM-I, has been shown to be inducible by interleukin-I (IL-I). Furthermore, ICAM-I may be involved in the progression of metastasis in certain malignancies. The aim of this study was to measure intracystic soluble ICAM-I (sICAM-I) and IL-I alpha/beta levels and to assess the relationships between these substances. Wide-ranging concentrations of sICAM-I, IL-I alpha and IL-I beta were found in breast-cyst fluid. The high-electrolyte-ratio group had intracystic levels of sICAM-I and IL-I beta which were significantly higher than those of the low-electrolyte-ratio group. No significant difference was found between IL-I alpha concentrations in the 2 groups of breast cysts. Strong positive correlations were found between sICAM-I and IL-I alpha, sICAM-I and IL-I beta, and IL-I alpha and IL-I beta. The significance of the higher concentrations of sICAM-I in the high-electrolyte-ratio group remains to be determined, but the results of this study suggest that sICAM-I levels in the high-electrolyte-ratio group may be regulated in part by IL-I alpha and IL-I beta.

Prostate-specific antigen (PSA) has been characterized as a specific prostate marker, although recent studies have suggested the existence of PSA of nonprostatic sources. We have assessed the presence of PSA by an ultrasensitive assay in 276 serum and nonserum samples from women. Our data show the presence of PSA in 90% of nonserum samples, including milk secretions, breast cysts, amniotic fluids and broncho-alveolar washings. We have also detected its presence in 58% of the sera tested, although it only exceeded 0.1 μg/l in 6 of the cases. We conclude that PSA can no longer be considered a specific prostate tissue marker; since the concentrations detected in women's serum are ultralow, this finding appears to interfere minimally with its value as a tumoral marker. © 1996 Wiley-Liss, Inc.

Prostate-specific antigen (PSA) is a 33 kDa serine protease which is produced by many different tissues in the body and has been shown to be present in low concentrations in breast milk and in about 30% of breast cancers. The presence of PSA in breast cancers is associated with the presence of steroid-hormone receptors and may be a favourable prognostic indicator. In this study, PSA immunoreactivity was measured in breast cyst fluid obtained from women with palpable breast cysts which is the most common benign breast disease. PSA was found to be present in very low concentrations in breast cyst fluid. In an attempt to understand the possible role of PSA in the breast, the effect of PSA on growth of the hormone-dependent MCF-7 and hormone-independent MDA-MB-231 human breast cancer cell lines was studied. In addition, the effect of PSA on oestrone sulphatase activity and oestrogen 17-oxidoreductase activity in these cell lines was investigated. PSA, in low concentrations, was found to inhibit MCF-7 cell growth and to stimulate the conversion of oestradiol to the less potent oestrogen oestrone in this cell line. PSA had no effect on the MDA-MB-231 cell line. Our findings suggest that PSA may act as a negative growth regulator in hormone-dependent breast cancers.

Women with palpable breast cysts which are lined with apocrine epithelium may be at higher risk of developing breast cancer than women with breast cysts which are lined with flattened epithelium, the former group being characterized by intracystic sodium to potassium ratios below 3, while the latter group has intracystic sodium to potassium ratios above 3. In this study the distribution of intracystic concentrations of the mitogenic peptides, epidermal growth factor, endothelin and gastrin-releasing peptide in the 2 groups of breast cysts were compared to see whether differences in concentrations between the 2 cyst groups might provide an explanation for the higher risk of breast cancer observed in women with "apocrine" breast cysts. The concentrations of epidermal growth factor and gastrin-releasing peptide were significantly higher in the low electrolyte ratio group (p less than 0.001). There was no difference in endothelin concentrations between the 2 groups. Negative correlations were found between epidermal growth factor concentrations and Na+/K+ and between gastrin-releasing peptide concentrations and Na+/K+ (p less than 0.001). A positive correlation was found between gastrin-releasing peptide and epidermal growth factor concentrations in breast cyst fluid (p less than 0.001). The significantly higher intracystic concentrations of both epidermal growth factor and gastrin-releasing peptide in the low-electrolyte-ratio group may provide an explanation for the higher risk of breast cancer which has been observed in women with "apocrine" breast cysts.

Women with breast cysts lined by apocrine epithelium (intracystic Na/K

Epidermal growth factor (EGF), dehydroepiandrosterone (DHA)-sulphate and [Na+] and [K+] were assayed in 78 cyst fluids from patients with a palpable breast cyst. Epidermal growth factor was detected in all but 2 cysts, the mean value +/- SEM being 506.2 +/- 39.3 ng/ml, with a range of 0-1,599 ng/ml. When the cyst fluids were sub-divided according to their [Na+]:[K+] ratio, group A cyst fluids ( [Na+]:[K+] less than 3) had a significantly higher (p less than 0.001) level of EGF than group B cyst fluids ([Na+]:[K+] greater than 3). Furthermore, the relationship between EGF and [Na+] and [K+] and between EGF and DHA-sulphate seemed to differ between the 2 cyst types and each cyst type was therefore analyzed separately.

The PIP gene is expressed in exocrine glands and, in pathologic conditions, in breast cysts and breast cancers exhibiting apocrine features. It is localized on the long arm of chromosome 7, a region frequently alterated in mammary tumors. We previously described an abnormal restriction pattern of the PIP gene in 33% of prostate carcinomas analyzed. Here, we analyze the structure of the PIP gene in primary breast carcinomas. We report that part of the 3' end, including exon 3, intron C, two-thirds of exon 4 and a small portion of intron B, is amplified and involved in the formation of extrachromosomal spcDNA molecules in 3/14 (21.4%) breast cancers analyzed. The involvement of a well-defined intragenic region of a gene in the formation of spcDNA appears to be unprecedented. Since spcDNA has been suggested to serve as an enhancer of genetic instability, the PIP gene may be the target of genomic variability processes in breast cancer.