zm-252868 and Adenocarcinoma

zm-252868 has been researched along with Adenocarcinoma* in 2 studies

Other Studies

2 other study(ies) available for zm-252868 and Adenocarcinoma

ArticleYear
Tyrphostins and retinoids cooperate during inhibition of in vitro growth of ovarian cancer cells.
    Cancer letters, 2003, Jan-28, Volume: 189, Issue:2

    Chemoresistance of ovarian cancer can be overcome by co-administration of retinoids, albeit clinical proof of this hypothesis is pending. Moreover, growth factor/c-erbB signaling is crucial for ovarian tumor growth/chemosensitivity. Retinoids and c-erbB modulators therefore represent promising drugs for ovarian cancer. We demonstrate that c-erbB-1 (RG-14620, AG1517) and c-erbB-2 selective tyrphostins (AG825, AG879), and all-trans and 9-cis retinoic acid inhibit ovarian cancer cell proliferation (HOC-7, OVCAR-3). Unlike retinoids, AG1517 and AG879 induce apoptosis. The antiproliferative activity of AG1517 is enhanced by all-trans retinoic acid suggesting that c-erbB and retinoid pathways interact. Thus, these agents cooperate during ovarian cancer cell growth inhibition.

    Topics: Adenocarcinoma; Apoptosis; Benzothiazoles; Cell Division; Drug Resistance, Neoplasm; Drug Synergism; ErbB Receptors; Female; Humans; Neoplasm Proteins; Ovarian Neoplasms; Quinazolines; Receptor, ErbB-2; Tretinoin; Tumor Cells, Cultured; Tyrphostins

2003
Multiple responses to EGF receptor activation and their abrogation by a specific EGF receptor tyrosine kinase inhibitor.
    The Prostate, 2002, Jun-01, Volume: 52, Issue:1

    Epidermal growth factor receptor (EGF-R) autophosphorylation is essential for its intracellular mitogenic signaling via the MAPK pathway and for interaction in other cellular processes. Inhibition of this activity in tumor cells that predominantly utilise EGF-R therefore offers an alternative approach to therapy.. The ability of a specific inhibitor of EGF-R tyrosine kinase, ZM 252868, (TKI) to alter various parameters related to growth in DU145 and PC3 cell lines was investigated, by immunocytochemistry, Northern blotting, Western blotting and invasion assays.. In DU145 cultures, the total cell population and number of cells in cell cycle decreased in the presence of TKI whilst the apoptotic rate was significantly increased. Reduction in autophosphorylation of the EGF-R, membrane expression of EGF-R, activation of the MAPK, p38, and JNK enzymes and the invasive capacity of DU145 cells was observed in the TKI treated cells. Under the same conditions, PC3 cell growth and EGF-R expression and MAPK activation were not affected. The use of inhibitors of intracellular signaling indicated that the DU145 cells, in contrast to PC3 cells, predominantly utilize EGF-R activation of the MAPK signaling pathway for growth.. In prostatic cancer patients, in whom androgen resistance has developed and whose tumors have upregulated EGF-R for growth, specific TKI's may offer an important therapy option.

    Topics: Adenocarcinoma; Apoptosis; Blotting, Northern; Blotting, Western; Cell Count; Cell Cycle; Cell Division; Enzyme Activation; Enzyme Inhibitors; Epidermal Growth Factor; ErbB Receptors; Humans; Immunohistochemistry; Male; Mitogen-Activated Protein Kinases; Neoplasm Invasiveness; Phosphorylation; Prostatic Neoplasms; Quinazolines; RNA, Messenger; Signal Transduction; Transforming Growth Factor alpha; Tumor Cells, Cultured

2002
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