Source Of Prostate-specific Antigen Research Articles

PROSTATE-SPECIFIC ANTIGEN AND ITS MOLECULAR FORMS IN BLOOD SERUM OF HEALTHY WOMEN AND WOMEN WITH BREAST DISEASE

The purpose of the study was to provide data on the sources of prostate-specific antigen (Psa) in women, as well as on serum Psa levels in healthy women and in women with benign and malignant breast cancer. Material and methods. We analyzed 50 publications available from PubMed, Medline, Google scholar concerning non-prostatic sources of Psa and its use as a serum tumor-associated marker for benign and malignant breast tumors. Results. In our study, we focus on the recent findings on non-prostatic sources and regulation of Psa synthesis in women as well as on changes in serum concentrations of this marker in patients with benign and malignant breast tumors. Various Psa isoforms (total Psa and free Psa) and free/total ratio for the detection of breast cancer and the assessment of treatment response and early detection of breast cancer recurrence were analyzed. Conclusion . the results obtained highlight the value of the assessment of Psa isoforms for early detection, prediction of therapy response and detection of breast cancer relapse. However, further studies are needed to identify the role of Psa isoforms in the diagnosis and monitoring of breast cancer patients.

The Dilemma of a Rising Prostate-Specific Antigen Level After Local Therapy: What Are Our Options?

Prostate cancer is the most common solid tumor diagnosed in men in the United States and Western Europe. Primary treatment with radiation or surgery is largely successful at controlling localized disease. However, a significant number (up to one third of men) may develop biochemical recurrence (BR), defined as a rise in serum prostate-specific antigen (PSA) level. A general presumption is that BR will lead to overt progression in patients over subsequent years. There are a number of factors that a physician must consider when counseling and recommending treatment to a patient with a rising PSA. These include the following (1) various PSA-based definitions of BR; (2) source of PSA (ie, local or distant disease, residual benign prostate); (3) available modalities to treat the disease with the least morbidity; and (4) timing of therapy. In this article we review the current and future factors that clinicians should consider in the diagnosis and treatment of recurrent prostate cancer.

Immunohistochemical Study of Prostate-Specific Antigen in Normal and Pathological Human Tissues: Special Reference to the Male and Female Prostate and Breast

Immunohistochemical methods were used to study the expression of prostate-specific antigen (PSA) in more than 400 samples of normal and pathological human tissues, including the female and male breast, male and female prostate (Skene's gland), and selected other tissues. In the normal female and male breast, no immunohistochemical positivity of PSA was observed in epithelial structures. In contradistinction to normal breast, normal male and female prostate tissue exhibited regular and marked PSA positivity. Variable expression of PSA was observed in membranes of adipocytes in breast tissue and axilla, apocrine sweat glands, endothelium of small vessels, gastric parietal cells, and some further rare normal extraprostatic tissue components. Unlike normal breast tissue, apocrine rnetaplasia in benign female breast disease and in male gynecomastia displayed distinct positivity for PSA. In cancerous female breast, expression of PSA decreased with the decreasing degree of differentiation. High expression was recorded in the signetring cell variant of ductal female breast carcinoma. If we disregard the absence of expression of PSA in the normal breast and its minimal and variable PSA expression of some normal extraprostatic structures, it is evident that in the female, similarly as in the male, the prostate is the principal source of PSA. In cases of discussed pathological breast tissues and other pathological tissues known to produce PSA, the total amount of PSA is the summation of normal prostatic and anomalous extraprostatic pathological tissue production in the male and female patient. (The J Histotechnol 23:105, 2000)

Prostate-specific antigen found in type I breast cyst fluids is a secretory product of the apocrine cells lining breast gross cysts.

Prostate-specific antigen (PSA), a serine protease thought to be exclusively produced by the prostate epithelial cells, has been recently found in human breast tissues and fluids. PSA in breast cancer is associated with the presence of steroid-hormones and receptors, and its presence seems to be a favourable prognostic indicator. In order to clarify whether the cells lining breast cysts may represent the source of PSA found in human breast cyst fluid, we performed an ultrastructural immunolocalization of PSA in the cells surrounding Type I breast cysts, obtained from breast cyst fluids of women affected by breast gross cystic disease, the most commonly occurring benign breast lesions associated with increased cancer risk. These apocrine cells show morphological features typical of actively synthesizing and secreting cells, and a PSA labelling distributed on free ribosomes, RER cisternae, and secretory granules, indicating that the metabolically active apocrine cells lining the Type I cysts are responsible for the production and secretion of PSA in Type I breast cyst fluids. The synthesis and intracystic accumulation of this serine protease in biosynthetically active apocrine Type I cysts can play an important role in the natural history of breast gross cystic disease as well as in the mechanism of cyst evolution.

The increased circulating prostate-specific antigen concentrations in women with hirsutism do not respond to acute changes in adrenal or ovarian function.

Serum prostate-specific antigen (PSA) is produced in several female tissues and appears to be up-regulated by androgens. We have studied serum PSA concentrations in women with different forms of hyperandrogenism, focusing on the influence of changes in ovarian and adrenal function on these concentrations. Thirty-seven hirsute women were studied in the follicular phase of the menstrual cycle. Basal and ACTH-stimulated plasma samples were obtained, and sampling was repeated 1 (gonadal stimulation) and 21 (gonadal suppression) days after receiving a single im 3.75-mg dose of triptorelin. Eleven nonhyperandrogenic women served as controls. Hirsute women had increased PSA levels compared to controls. When considering the source of the hyperandrogenism, ovarian patients (those with increased serum androgen levels that normalized during gonadal suppression) and adrenal patients (those with increased androgen levels that remained elevated during gonadal suppression) presented increased PSA values, whereas hirsute patients without hyperandrogenemia had normal PSA levels. PSA levels did not change during ovarian or adrenal stimulation or during gonadal suppression with respect to initial values. Basal PSA levels showed significant correlations with basal total testosterone (r = 0.59; P < 0.001), free androgen index (r = 0.68; P < 0.001), sex hormone-binding globulin (r = -0.58; P < 0.001), dehydroepiandrosterone sulfate (r = 0.39; P < 0.01), 17-hydroxyprogesterone (r = 0.32; P < 0.05), and age (r = -0.33; P < 0.05) when patients and controls were considered as a whole. In conclusion, basal PSA levels are increased in hirsute patients and correlate with the degree of hyperandrogenism when patients and controls are considered as a whole. The adrenal and the ovary do not appear to be the source of PSA, suggesting that hyperandrogenism induces PSA secretion in tissues other than the adrenal and the ovary.