Faina Vikhanskaya

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Tumour-derived p53 mutants are thought to have acquired 'gain-of-function' properties that contribute to oncogenicity. We have tested the hypothesis that p53 mutants suppress p53-target gene expression, leading to enhanced cellular growth. Silencing of mutant p53 expression in several human cell lines was found to lead to the upregulation of wild-type(More)
We examined the consequences of p73␣ overexpression on gene expression and cellular response to anticancer agents in clones from the human ovarian cancer cell line A2780. Using microarray filters, the expression of 588 genes in two clones overexpressing p73␣ (A2780/p73.4 and A2780/ p73.5) in comparison with empty vector-transfected cells was evaluated.(More)
p73 is a member of the p53 family often overexpressed in human cancer. Its regulation, particularly following DNA damage, is different from that of p53. Following DNA damage, we found induction of p73 at both the protein and mRNA levels. Furthermore, by using different p73 promoter fragments, we found a role for E2F1 in mediating transcription of p73.(More)
Inhibition of clonogenic potential by the glycinamideribonucleosyl transformylase inhibitor 5,10-dideazatetrahydrofolic acid (DDATHF, Lometrexol) was evaluated in vitro in a human ovarian carcinoma cell line, SW626. Drug-induced inhibition of clonogenic potential is a function of the dose and time of exposure and is independent of the formation of DNA(More)
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