Al A. Elbendary

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Transforming growth factor beta (TGF beta) is an important regulator of cellular proliferation. In normal ovarian epithelial cells, TGF beta acts to inhibit growth. However, in ovarian cancer cell lines, this effect is usually lost. Although the regulatory pathway of TGF beta remains unclear, TGF beta-treated cells arrest late in G1. This inhibition appears(More)
In many cell types, p53-mediated growth inhibition is dependent on induction of p21, which is an inhibitor of cyclin-dependent kinases that are required for cell cycle progression. Failure of mutant p53 proteins to transactivate p21 may lead to uncontrolled proliferation. Because many ovarian cancers have mutations in the p53 gene, we examined p21 levels in(More)
OBJECTIVE To review our current understanding of the molecular genetic events involved in the development of epithelial ovarian cancers. METHODS Molecular biologic techniques have been used to examine the role of growth-stimulatory genes (oncogenes) and -inhibitory genes (tumor suppressors) in ovarian cancer. RESULTS A number of different peptide growth(More)
The efficacy of weekly paclitaxel has not been well characterized in either cervical or endometrial cancer. Eligible women had disseminated endometrial or squamous cell cancer of the cervix, one prior chemotherapy regimen, measurable disease, and a Gynecologic Oncology Group (GOG) performance status of 0–2. At entry, all laboratory results were within(More)
Previously, we found that transforming growth factor beta (TGF-beta) inhibits proliferation of normal human ovarian epithelial cells. In addition, although only 1 of 5 immortalized ovarian cancer cell lines was inhibited, TGF-beta inhibited proliferation of 19 of 20 primary epithelial ovarian cancers. In this study, we examined whether TGF-beta induces(More)
OBJECTIVE To determine whether chemotherapy drugs elicit programmed cell death (apoptosis) in ovarian cancer cells. METHODS Monolayers of immortalized ovarian cancer cell lines and primary ovarian cancer cells obtained from ascites were grown in the presence of cisplatin, 4-hydroxyperoxy-cyclophosphamide (the active metabolite of cyclophosphamide) or(More)
OBJECTIVE To determine whether mutation in the DNA of the estrogen-receptor gene occurs in endometrial cancer. METHODS Polymerase chain reaction amplification and single-stranded conformation polymorphism analysis of the entire coding region (exons 1-8) of the human estrogen-receptor gene, as well as an untranslated region (exon I*) in the gene, were(More)
15013 Background: The antitumor activity of other regimens of paclitaxel (from Bristol-Myers Squibb Oncology, Bristol-Myers Squibb Company, Princeton, NJ, U. S. A.) has been identified in both cervical and endometrial cancer. A less toxic and better tolerated regimen for paclitaxel is a one hour infusion every 7 days. The primary aim of this study was to(More)
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