Hypercoagulable state and neoangiogenesis are common phenomena associated with malignancy. Cancer patients have increased levels of circulating endothelium-derived microparticles (EMPs), which have been hypothesized to be involved in numerous pathophysiological processes. Hemostasis and angiogenesis are also activated in colorectal cancer (CRC) patients. The study aimed to investigate potential influence of chemotherapy on EMPs, thrombin anti-thrombin complex (TAT) and vascular endothelial growth factor (VEGF) levels in CRC patients undergoing chemotherapy. The study group consisted of 18 CRC patients: 8 stage III colon cancer (CC) and 10 stage IV rectal cancer (RC) patients. EMPs, TAT and VEGF levels were assessed before chemotherapy and after the third course. Results were compared with 10 healthy subjects. EMP concentration was measured by flow cytometry, while TAT and VEGF concentrations were assayed employing ELISA. Compared to the control group, CC and RC patients had significantly higher levels of tissue factor (TF)-bearing and non-TF-bearing EMPs before and after three courses of chemotherapy. VEGF concentrations in CRC patients were higher than in the control groups and increased following chemotherapy. TAT levels were elevated in CRC patients before chemotherapy compared to healthy subjects and significantly increased after the third course of chemotherapy. No significant correlation was found either between EMP and TAT levels, or between EMP concentrations and VEGF levels in the study group. CRC patients have increased EMPs, and TAT as well as VEGF levels tend to increase during chemotherapy.

Background/Aim: Endothelial microparticles (EMP) are small vesicles which are released from the endothelium and contribute to blood coagulation activation in various clinical settings. The aim of this study was to examine whether EMP influence blood coagulation activation in cancer patients during radiotherapy/ radiochemotherapy (RT/RCT). Materials and Methods: Sixteen head and neck cancer (HNC) patients undergoing RT/RCT and 10 controls were examined. EMP and thrombin-antithrombin complex (TAT) were measured by flow cytometry and enzyme-linked immunosorbent assay (ELISA), respectively. Tissue factor-positive EMP (TF + EMP) were defined as CD31 + /CD142 + /CD42b -. Results: TF + EMP were significantly elevated in HNC patients before RT/RCT (T 0 ) (1299±1154/μl), one day after RT/RCT (T 1d ) (1257±603/μl) and 3 months after RT/RCT (T 3m ) (1289±372/μl) compared to controls (688±647/μl). TF + EMP levels at T 0 /T 1d and T 0 , as well as at T 1d and T 3m were not significantly different. TAT levels at T 0 and T 1d did not differ significantly but at T 3m were significantly lower compared to T 0 and T 1d . TF + EMP and TAT concentrations were not significantly correlated at T 0 (r=0. 058; p=0.828), T 1d (r=0.373, p=0.154) and T 3m (r=-0.302, p=0.204).

Background: Endothelial microparticles (EMPs) released from activated or apoptotic endothelial cells may play a role in coagulation and thrombus formation. However, there is insufficient evidence regarding the impact of EMPs on angiogenesis in patients with cancer. Materials and Methods: Sixteen patients with head and neck cancer (HNC) undergoing radiotherapy/radiochemotherapy (RT/RCT) and 10 healthy controls were studied. Serum EMPs were counted by flow cytometry, and vascular endothelial growth factor (VEGF) was measured by enzymelinked immunosorbent assay (ELISA). Results: The mean EMP level was significantly higher in patients with HNC before RT/RCT (1,601±1,479 EMP/μl) compared to the control group (782±698 EMP/μl). The number of EMPs was not notably increased after RT/RCT (1,629±769 EMP/μl). There was no significant correlation between the plasma EMP number and concentration of VEGF before (r=0.131; p=0.625), 1 day after (r=−0.042, p=0.874), nor 3 months after RT/RCT (r=0.454, p=0.076). Conclusion: Released EMPs may not influence promotion of neovascularization in patients with HNC. Endothelial microparticles (EMPs) are vesicular structures with a diameter from 1 to 2 μm which are shed from activated or apoptotic endothelial cells (ECs) (1). The density of EMPs in the blood of healthy individuals ranges from 1-70×10 3 /ml (1). Knowledge about EMP formation has been obtained from experiments conducted on isolated or cultured ECs, whereas in vivo mechanisms involved in EMP generation still remain unclear. Inflammatory cytokines [e.g. tumor necrosis factor-α, (TNF-α)] bacterial lipopolysaccharides, reactive oxygen species, thrombin, camptothecin and chemotherapy were reported to induce EMP generation (1, 2). EMPs express a large variety of molecules representative of their parent cells (3). Their composition differs depending on the cells they originate from and the type of stimulus leading to their formation (4). On their surface, EMPs bear phospholipids, membrane receptors such as endothelial protein C receptor, thrombomodulin, tissue factor, adhesion molecules such as intercellular cell adhesion molecule-1, platelet-EC adhesion molecule, endothelial selectin and P-selectin (3). In addition, EMPs harbor enzymes such as matrix metalloproteinase, nicotinamide adenine dinucleotide phosphate oxidase, urokinase plasminogen activator and its receptor, and growth factor receptors (3). The density of EMPs is elevated in various clinical settings. Activated or apoptotic EC-derived EMPs are a marker of endothelial damage and their level was found to be increased in the blood of obese women, patients with terminal stage renal failure or multiple sclerosis (5-7). Moreover, it has been documented that EMPs contribute to initiation of blood coagulation and support thrombus formation (3, 8, 9). Furthermore, a higher level of EMPs was found in patients with hematological disorders e.g. lupus anticoagulant, sickle cell disease, anti-phospholipid syndrome and venous thromboembolism, than in healthy individuals (3, 9, 10). In ...