No abstract

VEGF-A is the most potent angiogenic factor in tumour angiogenesis. Its effects are mediated via two receptors VEGFR-1 and VEGFR-2. Primary aim of our study was to examine the expression of VEGFR-1 in breast cancer and its correlation to VEGF expression, lymph node status, tumour size, histological grade, and hormone receptor status. To examine the VEGFR-1 and VEGF expressions in tumour and surrounding tissue of 51 breast cancer patients, and in healthy breast tissue of 30 benign breast diseases patients, we used three-step immunohistochemical staining. VEGFR-1 and VEGF expressions were significantly increased in breast cancer tumour in relation to surrounding tissue (P < 0.01), and the VEGF expression was significantly increased in lymph node positive breast cancer patients (P < 0.01). VEGFR-1 and VEGF expressions were significantly higher in breast cancer tumour compared with healthy breast tissue (P < 0.01). Significant correlation between VEGF and VEGFR-1 expressions was found (P < 0.05). No significant correlations between VEGF and VEGFR-1 expressions and tumour size, histological grade, and hormone receptor status were found. Increased expression of VEGFR-1 and VEGF in breast cancer tumour and significant correlation between these proteins suggest the possible role of VEGF/VEGFR-1 signalization in breast cancer development, although VEGFR-1 potential prognostic value was not confirmed.

131 Ab stra ctIn tro duc tion: The aim of this stu dy was to in ves ti ga te the pre sen ce and the expres sion le ve ls of the in ter leu kin 13 (IL-13) in the pri ma ry brea st cancer tu mour tis sue in re la tion to the un chan ged brea st tis sue in the sa me pa tien ts and to the brea st tis sue in the pa tien ts wi th be ni gn brea st di sea se, and to in ves ti ga te the cor re la tion be tween the IL-13 expres sion le ve ls and the pat ho his to lo gi cal fac to rs, and be tween IL-13 expres sion and es tro ge ns and pro ges te ro ne re cep tor sta tus. Ma te ria ls and met ho ds: 50 pa tien ts wi th in va si ve duc tal brea st can cer and 20 pa tien ts wi th be ni gn brea st di sea ses we re in clu ded in this prospec ti ve ca se-con trol stu dy. The three-step im mu no his toc he mi cal stai ni ng was used for tes ti ng the le ve ls of IL-13 expres sion and hor mo ne re cep tor sta tus. Re sul ts: IL-13 was pre se nt in brea st can cer tu mour tis sue, and in the sur roun di ng un chan ged tis sue in the sa me pa tien ts, and in brea st tis sue in patien ts wi th be ni gn brea st di sea se. The expres sion of IL-13 was sig ni fi can tly hig her in brea st can cer tu mour com pa red wi th sur roun di ng tis sue (P < 0.05) of the sa me, lymph no de-po si ti ve pa tien ts. In ad di tion, IL-13 expres sion was sig ni fi can tly hig her in brea st can cer tu mour com pa red wi th brea st tis sue in pa tien ts wi th be ni gn brea st di sea ses (P < 0.01). The re was sig ni fi ca nt cor re la tion be tween IL-13 expres sion and tu mour si ze in pa tien ts wi th lymph node-ne ga ti ve brea st can cer (r = 0.405, P = 0.050). The re was no sig ni fi ca nt cor re la tion be tween IL-13 expres sion and the ot her pat ho his tolo gi cal fac to rs, and no sig ni fi ca nt cor re la tion be tween IL-13 expres sion and the lymph no de sta tus. Con clu sion: Obtai ned re sul ts sug ge st pos sib le in vol ve me nt of IL-13 in brea st car ci no ge ne sis. Key wor ds: in ter leu kin 13; brea st can cer; brea st tis sue; beni gn brea st di sea se Re cei ved: No vem ber

The predictive value of cystatin C as a marker of course of the disease has been evaluated. Fifty-two pairs of serum samples of patients with B non-Hodgkin lymphoma have been collected at the time of diagnosis and before fourth cycle of chemotherapy. The levels of cystatin C, CRP, β 2M, LDH, and IL-6 in samples have been measured, and clinical parameters of course of the disease (B symptoms, clinical stage, patients' age, and IPI) have been noted. In total patient's group cystatin C levels correlated with β 2M and IPI. In aggressive lymphomas, the inhibitor levels correlated with clinical stage of disease and were significantly higher in patients with elevated LDH activity. In aggressive nodal lymphomas its levels correlated with β 2M, IPI, and clinical stage of disease. The cystatin C level was significantly increased in total group of patients over 60 years old, while in particular types of lymphoma, no statistical significance has been obtained. Our results indicate that cystatin C should be taken into consideration in disease monitoring. However, we expect that the disease-free and overall survival analysis will give the definitive answer about the reliability of cystatin C as an indicator of course of aggressive lymphomas.

Introduction: Significance of serum uric acid (UA) in cerebrovascular disease still remains controversial. UA is most abundant natural antioxidant in human plasma. Its antioxidant properties might protect against free radical damage, thereby reducing the risk of oxidative stress-related cognitive impairment and dementia. Aim: In our investigation, we determine the level of UA in 100 male patients diagnosed with the first ischemic brain stroke (blood samples were collected during the acute phase and post-acute phase), 100 male patients diagnosed with vascular dementia and 100 male healthy volunteers (control group). Methods: UA was determined using DIMENSION LxR automatic analyzer. Measurement of UA concentration was based on an enzymatic method (range 208-428 µmol/L). Results: The prevalence of hyperuricemia among ischemic stroke and vascular dementia patients was 30% and 8%, respectively. Serum UA concentration was higher 7 and 14 days after the stroke compared to the acute phase (24-48 hours after hospitalization) and these concentrations were significantly higher than those measured in the control group. UA levels measured at 24-48 hours after the first symptoms of ischemic stroke were strongly correlated with those measured after 7 days of treatment (r = 0.79, p = 0.001) or after 14 days (r = 0.839, p = 0.0049). No significant differences were found between ischemic stroke and vascular dementia groups. Conclusion: UA concentrations were higher in ischemic stroke and vascular dementia groups than in controls. UA increase may reflect vascular atherosclerosis and tissue hypoxia. UA monitoring in patients with cerebrovascular disease is essential, because UA is more harmful than protective.