Molekularni a bunecne mechanismy rezistence nadorovych bunek na cytostatika.

We have identified some specific clinical situations where we recommended a consideration of the in vitro tumor resistance. These situations are: the choice of a regimen where there is the highest portion of in vitro susceptible anticancer drugs to those tumors where 2 or more treatment regimens with the same level of efficacy are available; in the case where the patient has failed the standard anticancer treatment; in the patients with rare tumors where the empirical knowledge of the treatment is insufficient and in the patients with tumors of unknown origin. We particularly advocate an examination of the in vitro chemoresistance in patients who failed the standard therapy and, based on these in vitro results, the receipt of an appropriate tailored regimen by these patients. Drugs known as chemosensitizers are being introduced into the clinic although their effect is still questionable.To use them successfully demands a good knowledge of the tumor population in every individual patient which requires an excellent laboratory background.Available from STL Prague, CZ / NTK - National Technical LibrarySIGLECZCzech Republi

THE HOMO- AND COPOLYMERIZATION OF ACETYLENE WITH ETHYLENE IN THE PRESENCE OF CATALYSTS CYGLER-NATT

For the first time, the possibility of polymerization of acetylene in the medium of the simple ethers has been detected. Obtained have been the prooves of formation of tetrabutoxid of the titanium-triethylaluminium of the paramagnetic complex of the one-valent titanium in the catalytic system. The copolymers of ethylene with acetylene have been received and studied. For the first time, the possibility of the acetylene polymerization in the medium of simple ethers has been justified. It has been shown, that in the course of copolymerization, the high reactionally-able block-copolymers formAvailable from VNTIC / VNTIC - Scientific & Technical Information Centre of RussiaSIGLERURussian Federatio

Estradiol attenuates EGF-induced rapid uPAR mobilization and cell migration via the G-protein-coupled receptor 30 in ovarian cancer cells

Epidermal growth factor (EGF) stimulates proliferation and migration in ovarian cancer cells, and high tumor expression of the EGF system correlates with poor prognosis. Epidermal growth factor upregulates urokinase plasminogen activator receptor (uPAR) on the cell surface via 3 distinct mechanisms: rapid mobilization of uPAR from detergent-resistant domains, increased mRNA, and decreased degradation. G-protein-coupled receptor 30 (GPR30) is a newly identified membrane estrogen receptor (ER).The objective of this study was to explore the effects of 17beta-estradiol (E(2)) on uPAR expression and cell migration in ovarian cancer cells and further to identify the ER involved.We used 7 ovarian cancer cell lines, cell migration assay, cellular binding of (125)I-uPA, cellular degradation of (125)I-uPA/PAI-1 complex, enzyme-linked immunosorbent assay for uPAR, solid-phase enzyme immunoassay for ERalpha, and quantitative polymerase chain reaction. Estradiol attenuates the stimulatory effect of EGF on cell migration and uPAR expression. Specifically, E(2) reduces the very rapid increase of detergent extractable uPAR, which occurs within minutes of EGF stimulation and probably represents mobilization of uPAR from detergent-resistant domains such as lipid rafts. Estradiol influenced neither the amount of uPAR mRNA nor the rate of uPAR degradation or solubilization. The nuclear ER antagonists ICI 182780 and tamoxifen, which are GPR30 agonists, as well as the specifically constructed GPR30 agonist G1, mimicked the effect of E(2) on uPAR expression and cell migration. OVCAR-3 cells express mRNA for GPR30.Estradiol attenuates EGF-induced mobilization of ligated uPAR from detergent-resistant domains and subsequent migration in ovarian cancer cells. The response to various ER ligands indicates that this effect is mediated via the membrane ER GPR30