• MeSH
• ascitická tekutina chemie   imunologie   MeSH
• chemokin CXCL12 diagnostické užití   krev   MeSH
• chemokiny * klasifikace   krev   sekrece   MeSH
• exsudáty a transsudáty chemie   imunologie   MeSH
• interleukin-8 diagnostické užití   krev   MeSH
• lidé MeSH
• monocytární chemoatraktivní proteiny diagnostické užití   krev   MeSH
• Check Tag
• lidé MeSH

BACKGROUND: Complex networks of chemokines are part of the immune reaction targeted against tumor cells. Chemokines influence cancer growth. It is unclear whether the concentrations of chemokines at the time of NSCLC (non-small cell lung cancer) diagnosis differ from healthy controls and reflect the extent of NSCLC. AIMS: To compare chemokine concentrations (CCL2, CCL8, CXCL12) in the plasma of patients with resectable NSCLC to those without cancer. To determine whether the chemokine concentrations differ relative to the stage of disease. METHODS: Sixty-nine patients undergoing surgery for proven/suspected NSCLC were enrolled. They underwent standard diagnostic and staging procedures to determine resectability, surgery was performed. Forty-two patients were diagnosed with NSCLC, while 27patients had benign lung lesions and functioned as the control group. Chemokine concentrations in peripheral blood were assessed using ELISA. Parametric statistics were used for the analysis of results. RESULTS: There were no differences in plasma chemokine concentrations in NSCLC patients compared to controls. CXCL12 concentrations correlated positively with tumor extent expressed as clinical stage, (mean values: stage I 5.08 ng/mL, SEM 0.59; stage II and IIIA 7.82 ng/mL; SEM 1.06; P=0.022). Patients with NSCLC stages II+IIIA had significantly higher CXCL12 concentrations than controls (mean values: stage II+IIIA 7.82 ng/mL; SEM 1.06; controls 5.3 ng/mL; SEM 0.46; P=0.017). CONCLUSION: CXCL12 was related to tumor growth and could potentially be used as a biomarker of advanced disease.

• MeSH
• biologické markery MeSH
• chemokin CCL2 MeSH
• chemokin CCL8 MeSH
• chemokin CXCL12 MeSH
• chemokiny MeSH
• lidé MeSH
• nádory plic * chirurgie   patologie   MeSH
• nemalobuněčný karcinom plic * chirurgie   patologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH

Dipeptidyl peptidase-IV (DPP-IV) represents a unique proteolytic activity cleaving N-terminal X-Pro dipeptides. In addition to canonical DPP-IV/CD26, a number of other molecules have been discovered which exhibit DPP-IV-like enzymatic activity and various degree of structural similarity. These comprise enzymatically active fibroblast activation protein-alpha, DPP-II, DPP8, DPP9 and enzymatically inactive DPP6 and DPP10 that have been grouped as "DPP-IV activity and/or structure homologues" (DASH). Because the enzymatically active DASH can share similar sets of biologically active substrates and are frequently coexpressed within single cell or on tissue level, it is tempting to consider their participation on biological function(s) previously attributed to DPP-IV/CD26. It is speculated that disrupted expression and enzymatic activity of some DASH might corrupt the message carried by their substrates, with consequent promotion of abnormal cell behavior. Thus, modulation of activity of a particular enzyme using e.g. inhibitors, specific antibodies or modifying its expression may be an attractive therapeutic concept in cancer treatment. This review summarizes current knowledge of the expression and possible function of DPP-IV enzymatic activity bearing molecules in human brain tumors.

• MeSH
• biologické modely MeSH
• buněčná diferenciace MeSH
• chemokin CXCL12 metabolismus   MeSH
• chemokiny metabolismus   MeSH
• dipeptidylpeptidasa 4 metabolismus   MeSH
• financování organizované MeSH
• glioblastom metabolismus   MeSH
• gliom enzymologie   metabolismus   MeSH
• lidé MeSH
• mozek metabolismus   MeSH
• nádory mozku enzymologie   metabolismus   MeSH
• proteasy metabolismus   MeSH
• receptory CXCR4 metabolismus   MeSH
• regulace genové exprese enzymů MeSH
• regulace genové exprese u nádorů MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• přehledy MeSH

A considerable amount of scientific evidence indicates that a number of pharmaceuticals that could be detected in the environment can contribute towards the development of problems associated with human reproductive systems, as well as those of wildlife. We investigated the estrogenic and androgenic effects of select pharmaceuticals with high production volume and environmental relevance. We examined the receptor-binding activities of these pharmaceuticals in the T47D human cell line using altered secretion of cytokine CXCL12. Functional yeast-luciferase reporter gene assays were also employed to confirm the mechanism of receptor binding by estrogen and androgen. Non-steroidal anti-inflammatory drugs, namely ibuprofen, diclofenac and antiarrhythmic agent amiodarone showed strong anti-estrogenic effects in the T47D cell line. In the yeast-luciferase assay, these anti-inflammatory drugs also demonstrated anti-estrogenic potency and inhibited the E2 response in a concentration-dependent manner. Amiodarone did not exhibit any response in the yeast-luciferase assay; therefore, the endocrine disruption presumably occurred at a different level without directly involving the receptor. All the anti-inflammatory drugs considered in this study, including ketoprofen, naproxen and clofibrate, exhibited a dose-dependent antagonism towards the androgen receptor in the yeast-luciferase assays. Several other drugs, including the stimulant caffeine, did not show any response in the tests that were employed. A risk assessment analysis using 'Hazard Quotient' suggested a potential risk, especially in the cases of ibuprofen, ketoprofen, diclofenac and clofibrate. The results reveal the intrinsic endocrine disrupting nature of several pharmaceuticals and thus could contribute towards explaining a number of adverse health effects on humans and wildlife.

• MeSH
• androgenní receptory metabolismus   MeSH
• androgeny analýza   toxicita   MeSH
• antagonisté estrogenu analýza   toxicita   MeSH
• antiflogistika nesteroidní analýza   toxicita   MeSH
• biotest metody   MeSH
• chemické látky znečišťující vodu analýza   toxicita   MeSH
• chemokin CXCL12 sekrece   MeSH
• endokrinní disruptory analýza   toxicita   MeSH
• estradiol toxicita   MeSH
• léčivé přípravky analýza   MeSH
• lidé MeSH
• luciferasy genetika   MeSH
• nádorové buněčné linie MeSH
• receptory pro estrogeny antagonisté a inhibitory   MeSH
• reportérové geny MeSH
• Saccharomyces cerevisiae genetika   MeSH
• vztah mezi dávkou a účinkem léčiva MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH