INTRODUCTION The aim of this study was to investigate the presence and the expression levels of the interleukin 13 (I1-13) in the primary breast cancer tumour tissue in relation to the unchanged breast tissue in the same patients and to the breast tissue in the patients with benign breast disease, and to investigate the correlation between the IL-13 expression levels and the pathohistological factors, and between IL-13 expression and estrogens and progesterone receptor status. MATERIALS AND METHODS 50 patients with invasive ductal breast cancer and 20 patients with benign breast diseases were included in this prospective case-control study. The three-step immunohistochemical staining was used for testing the levels of IL-13 expression and hormone receptor status. RESULTS IL-13 was present in breast cancer tumour tissue, and in the surrounding unchanged tissue in the same patients, and in breast tissue in patients with benign breast disease. The expression of IL-13 was significantly higher in breast cancer tumour compared with surrounding tissue (P < 0.05) of the same, lymph node-positive patients. In addition, IL-13 expression was significantly higher in breast cancer tumour compared with breast tissue in patients with benign breast diseases (P < 0.01). There was significant correlation between IL-13 expression and tumour size in patients with lymph node-negative breast cancer (r = 0.405, P = 0.050). There was no significant correlation between IL-13 expression and the other pathohistological factors, and no significant correlation between IL-13 expression and the lymph node status. CONCLUSION Obtained results suggest possible involvement of IL-13 in breast carcinogenesis.

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The study was designed to determine pre-, intra-and postoperative serum cortisol and prolactin (PRL) concentrations in patients subjected to low abdominal surgery under total intravenous anesthesia (TIVA) with propofol-fentanyl, and under general balanced anesthesia with isoflurane-fentanyl. The prospective study included 50 patients of both sexes, aged between 35 and 60 years, subjected to elective low abdominal surgery. Patients were randomly divided into two groups: an experimental group, consisting of 25 ASA I/II (American Society of Anesthesiologists I/II classification) patients treated under TIVA with propofol-fentanyl, and a control group consisting of 25 ASA I/II patients treated under balanced anesthesia with isoflurane-fentanyl. The length of the surgery and the degree of the surgical trauma did not differ significantly between the two anesthesia groups. Blood samples for cortisol and PRL measurements were drawn at exact time points: 30 minutes before the beginning of the surgery (T0), 30 minutes after the beginning of the surgery (T1), at the end of the surgery (T2), 2 hours after the surgery (T3), and 24 hours after the surgery (T4). Serum levels of cortisol and PRL were measured using commercially available kits. The results were evaluated with the nonparametric Mann-Whitney test. The serum concentration of cortisol measured at T1 time point in patients treated under TIVA was significantly lower (p=0.04) than that in patients treated under general balanced anesthesia. The average circulating levels of PRL measured at T1, T2 and T3 time points in patients treated under TIVA were significantly lower (p=0.003; p=0.002; p<0.05; respectively) than those in patients treated under balanced anesthesia. The results obtained suggest that the endocrine stress response developed in response to surgery is probably attenuated in patients treated under TIVA with propofol-fentanyl and, thus, that these patients are less stressed in comparison to patients treated under general balanced anesthesia with isoflurane-fentanyl.

Bac kgrou nd: To de ter mi ne pre-, in tra-and pos to pe ra ti ve se rum glu co se and lac ta te con cen tra tio ns in pa tien ts sub jec ted to low ab do mi nal sur ge ry un der to tal in tra ve nous anes the sia (TIVA) wi th pro po fo l-fen ta nyl, and in tho se under ge ne ral ba lan ced anes the sia wi th isofl u ra ne-fen ta nyl. Ma te ria ls and Met ho ds: This pros pec ti ve stu dy in clu ded 50 pa tien ts of both sexes, aged be tween 35 and 60 yea rs, sub jec ted to low ab do mi nal sur gery. Pa tien ts we re ran dom ly di vi ded in to two grou ps: expe ri men tal group of 25 ASA I/II (Ame ri can So cie ty of Anes the sio lo gis ts I/II clas si fi ca tion) pa tien ts trea ted un der TIVA, and con trol group of 25 ASA I/II pa tien ts trea ted un der ba lan ced anes the sia. The len gth of sur ge ry and the deg ree of sur gi cal trau ma did not diff er sig ni fi can tly be tween the two anes the sia grou ps of pa tien ts. Blood sam ples for glu co se and lac ta te mea su re men ts we re drawn at exa ct ti me poin ts: 30 mi nu tes be fo re the be gin ni ng of the sur ge ry (T0), 30 mi nu tes af ter the be gin ni ng of the sur ge ry (T1), at the end of the sur ge ry (T2), 2 hou rs af ter the sur ge ry (T3), and 24 hou rs af ter the sur ge ry (T4). Se rum le ve ls of gluco se and lac ta te we re mea su red usi ng com mer cial ly avai lab le ki ts.

AIM To correlate prolactin concentrations in the sera of patients with metastatic breast cancer with time interval to appearance of metastases, their location, and size. METHOD The prospective study included 46 female patients with histologically confirmed diagnosis of breast cancer. The patients were recruited from the Health Center outpatient clinic and University Hospital Center day-care hospital in Banja Luka, Bosnia and Herzegovina, from January to August 1988. The follow up lasted 5 years. Serum concentrations of prolactin were measured in all patients before (baseline levels) and after the therapy at regular time intervals during the observation period. Their prolactin concentrations were compared with prolactin concentrations in 40 healthy women and 33 female patients with other types of cancer, who served as control groups. Time interval to metastases development, their size, and location were determined in breast cancer patients and compared with those in patients with other types of cancer. RESULTS The baseline serum concentrations of prolactin were higher in breast cancer patients than in healthy women (610 vs 442 mU/L; p=0.04; Mann-Whitney test), and in patients with other locations of cancers (662 vs 481 mU/L, respectively; p=0.02; Mann Whitney test). Metastases developed in all hyperprolactinemic patients, whereas a third of normoprolactinemic were free of metastases. The average time interval before the occurrence of metastases in patients with very high serum concentrations of prolactin was significantly shorter than that in patients with very low prolactin concentrations (54.3 vs 6.1 months; p<0.001; Mann Whitney test). In hyperprolactinemic patients with metastatic breast cancer, there was a significant correlation between the serum concentration of prolactin before treatment and the time to metastases (r= -0,47; p=0.03) and the size of metastases (r=0,64; p=0.001). CONCLUSION Hyperprolactinemia could be an indicator of disease progression and poor prognosis in patients with metastatic breast cancer.

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.

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.

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.