Rationale: data about the role of prolactin (PRL) in breast cancer patients are controversial. This hormone might potentially play an important role in breast cancer initiation and development in rodents, as well as, at least partly, in humans. The aim of this study was to investigate the possible relationship between circulating levels of PRL and parameters of primary tumor in breast cancer patients. The main experimental group consisted of 46 female patients with histologically confirmed diagnosis of breast cancer. There were two control groups: apparently clinically healthy women (40), and female patients with other types and locations of cancer (33). Baseline levels of PRL were determined both in the main and in control groups. Parameters of primary tumor (histological diagnosis, degree of differentiation, location, and size) have been determined. Results were processed by means of nonparametric tests. The circulating levels of PRL before treatment were significantly higher in breast cancer patients in comparison to controls. The average size of the primary tumor in breast cancer patients with hyperprolactinemia before treatment was significantly higher (U=125.5, p<0.01) than in those with normoprolactinemia. The calculated correlation coefficient between PRL and the size of primary tumor in hyperprolactinemic breast cancer patients was statistically significant (r=0.68, p<0.0001). In normoprolactinemic, and in patients with other locations of cancer such a correlation did not exist. Serum levels of PRL are, probably, directly dependable on the size of primary tumor in breast cancer patients, especially in those with hyperprolactinemia, but this is not differentiation dependent phenomenon.

AIM The Carcinoembryonic antigen (CEA) is used as a tumor marker for breast cancer (BC). In order to better define clinical usefulness of CEA in breast cancer patients (BCP) we determined its baseline pre-treatment levels and correlated them with main parameters of primary tumor and metastases. PATIENTS AND METHODS The main experimental group consisted of 47 female patients with histologically confirmed diagnosis of BC. The obtained results have been compared with those of two control groups: clinically healthy women, and patients with other types and locations of cancer. In both cancer groups the parameters of primary tumor (size, grade) and metastases (time interval to metastases, location, size) have been determined. Circulating levels of CEA were measured by the means of immunoradiometric assay. Results were processed by means of t-test, two way analysis of variance in F-test, and logistic general linear model with calculations of Pearson's correlation coefficient. RESULTS Baseline levels of CEA in BCP were significantly higher than in healthy women (p < 0.0001), and in patients with other types and locations of cancer (p < 0.007). There also was significant difference (p < 0.001) between serum CEA in other cancer patients and healthy women. Baseline CEA levels were in significant positive correlation with the size of primary tumor both in all BCP (p < 0.03) and in hyperCEA BCP (p < 0.002), while in other cancer patients such a correlation did not exist. There was no correlation between CEA and degree of differentiation of primary tumor either in BCP or in other cancer patients. The average circulating levels of CEA in metastatic BCP were significantly higher (p < 0.03) in comparison to non-metastatic patients, while in other cancer patients such a difference did not show up. There was significant correlation (p < 0.0001) between circulating CEA and the size of metastases in all BCP and in subgroup of hyperCEA BCP, while in other cancer patients it was not a case. There was no correlation between serum CEA and other two metastatic parameters either in BCP or in other cancer patients. CONCLUSIONS CEA does not have high tumor specificity for BC since its baseline levels may be elevated in other types of cancer. Circulating levels of CEA in BCP are directly dependable on the size of both primary and metastatic tumor. CEA is a tumor antigen of less differentiated cancer cells. Circulating CEA is a good prognostic marker for patients with metastatic BC.

BACKGROUND AND PURPOSE Carcinoembryonic antigen (CEA) is used as a tumour marker in breast cancer (BC). In order to assess diagnostic value of CEA in BC we examined its serum levels and frequencies of its increase in breast cancer patients (BCP), and compared them to those in controls. We also determined CEA in patients with metastatic and non-metastatic BC, and calculated sensitivity and specificity of CEA in BC. PATIENTS AND METHODS The main experimental group consisted of 47 female patients with histologically proved diagnosis of BC. There were two control groups: clinically healthy women, and female patients with other locations of cancer. Circulating levels of CEA were measured by means of immunoradiometric assay. Results were processed by means of t-test and two-way analysis of variance. RESULTS Circulating levels of CEA, before treatment in BCP, were significantly higher (p<0.0001) than in healthy women, and in patients with other cancers (p<0.007), while serum CEA in other cancer patients was significantly higher (p<0.01) than in healthy control. There was a difference between frequencies of CEA increase in BCP and healthy women, while such a difference did not exist between BCP and other cancer patients. The circulating levels of CEA in metastatic BCP were significantly higher (p<0.03) in comparison to non-metastatic patients. Sensitivity and specificity of CEA in BCP was 65.0%, and 57.1%, respectively. CONCLUSIONS CEA does not have high tumour specificity for BC, since its circulating levels as well as frequencies of its increase may be elevated in patients with other types and locations of cancer, different from breast cancer. CEA can be detected in the serum of majority of patients with metastatic BC. CEA may be used as prognostic tumour marker in advanced BC.

BACKGROUND We frequently observed allergic skin reactions in patients with documented history of alcoholic liver disease (ALD). To assess the potential association between alcohol-induced liver damage and urticaria a prospective randomized trial investigating immunologic parameters in various stages of alcoholic liver disease was designed. Fifty patients were available for analysis. METHODS By means of a multivariate discriminant analysis seven out of a number of laboratory and clinical parameters (level of serum proteins, serum globulins, gamma globulins, albumin/globulin ratio, and immunoglobulins A, E, and G) have been found important for analysis. They were compared with age, general clinical status, degree of progression of alcoholic liver disease, and frequency of appearance of type I skin reactions. Results were further processed by means of logistic general linear models, Chi-square test, and summarized in a structural equation model. RESULTS Alcoholic liver disease does not influence IgA, IgG, and A/G Index directly, but it increases levels of IgE. About 13% of variance of IgA, IgG, and A/G Index are affected by group membership only in non-alcoholic liver disease, and 27% of variance of IgE can be explained by alcoholic liver disease. There were striking differences in IgE content between alcoholic liver disease and control groups. Degree of liver disease had a negative impact on A/G Index, and on IgA, and a positive on IgG. About 16% of variance can be explained by degree of liver disease. IgE is not degree related. Alcoholic liver disease as a disease was found as the most important predictor of skin reactivity (p = 0.0046). Of all immunologic parameters investigated IgE followed by A/G Index was found as the most significant predictor of allergic skin reactions. The extent of alcoholic liver disease plays not a role in allergic skin manifestations. Alcoholic nature of liver disease itself is a significant factor causing allergic skin reactions (p = 0.0002), but alcoholism itself as an independent factor contributes to increased incidence of skin allergies. CONCLUSIONS Alcoholic liver disease plays an important role in development of type I allergic skin manifestations. This effect has a direct mechanism through alcohol itself, and an indirect through elevation of IgE. Alcohol in liver disease and not liver disease causes immunologic abnormalities and accounts significantly for increased appearance of allergic skin reactions regardless of the extent of underlying liver disease.

The objective of this study to consolidate the correlation between BMI with the values of ALT and AST of the healthy adolescents in age of 18, 19 and 20 years. To the group of 237 examinees of the healthy adolescents is determined BMI, and is measured the activity of ALT and AST. In the sample of the examinees we had 22% examinees had the increased BMI > or = 25. The examinees who had the increased BMI (> or = 25), had the significant increased values ALT, and only mildly increased values AST in relation to the upper referent values. On the basis of the simple linear regression was confirmed the positive correlation between the of body mass indexes and activities ALT i AST.

Thalidomide was first introduced to the market in Germany under the brand name of Contergan in 1956, as a non-barbiturate hypnotic, advocated to ensure a good nights sleep and to prevent morning sickness in pregnancy. It was advertised for its prompt action, lack of hangover, and apparent safety. It has been banned from the market since 1963 after it caused the worldwide teratogenic disaster: babies exposed to thalidomide in utero during the first 34-50 days of pregnancy were born with severe life-threatening birth defects. Despite its unfortunate history, thalidomide has attracted scientific interest again because of its recently discovered action against inflammatory diseases and cancer. Its broad range of biological activities stems from its ability to moderate cytokine action in cancer and inflammatory diseases. Early studies examined its anxiolytic, mild hypnotic, antiemetic, and adjuvant analgesic properties. Subsequently, thalidomide was found to be highly effective in managing the cutaneous manifestations of leprosy, being superior to Aspirin in controlling leprosy-associated fever. Recent research has shown promising results with thalidomide in patients with myeloma, myelodysplastic syndrome, a variety of infectious diseases, autoimmune diseases, cancer, and progressive body weight loss related to advanced cancer and AIDS. Here we review the history of its development, pharmacokinetics, metabolism, biologic effects, and the results of clinical trials conducted thus far. Further research in this field should be directed towards better understanding of thalidomide metabolism, its mechanism of action, and the development of less toxic and more active analogs.

We describe the development of an immunofluorescent method for the detection of resistance to agents which affect the integrity of the cellular microtubular network. Three pleiotropic resistant MCF-7 human breast carcinoma cell lines mixed with vaginal adenocarcinoma cells were selected in serially increasing drug concentrations, and demonstrated a 30-fold increase in resistance to colchicine. Transport studies indicated that there was no difference in drug accumulation between the sensitive and resistant lines. The colchicine-binding capacity of cell extracts from sensitive and resistant cells was similar (Kd for sensitive cells was 1.9 x 10(-6) M and for resistant cells 1.58 x 10(-6) M). There were, however, significant differences in cytoskeletal morphology between sensitive and resistant cells. Drug-sensitive cells were mostly large (about 70 microns 2) and flattened. Their cytoplasm was filled with a microtubular network in which, in most of the cases, single fibers could be differentiated. Cells usually had a microtubule-organizing center and paracortical bundles of microtubules. In contrast, drug-resistant cells were mostly rounded and grew in clumps. In only 40% of these cells could single microtubular fibers be differentiated. Resistant cells lacked a microtubule-organizing center and had no clear paracortical bundles of microtubules. The tubulin-binding agents tested caused a sequence of morphological changes in sensitive cells. These changes included precipitation of tubulin and disappearance of cytoskeletal structure. Changes occurred initially within 3 h of incubation, but were expressed in all cells after 6 h. If, after 3 h of drug exposure, cells were subcultured in drug-free media, the cytoskeletal structure reformed within 10 h. Maximal recovery of cytoskeletal structure occurred 22 h after drug removal and was sustained up to 36 h. In contrast to changes observed in sensitive cells, drug exposure did not induce changes in the morphology of cytoskeleton in resistant cells. Cells from all three resistant lines reverted to sensitivity after 7 months of culture in drug-free media. This was first detected by immunofluorescence and then confirmed by cloning assay. Since the cytoskeletal disintegration of sensitive cells is readily detectable within a few hours of in vitro drug treatment, immunofluorescent imaging may have its clinical application in predicting the sensitivity/resistance to microtubule-binding agents.