Background: Arrest of the cell cycle in G2 phase following DNA damage helps protect cell
viability by allowing time for DNA repair before entry into mitosis (M phase). Abrogation of …

We have previously reported that UCN‐01 (7‐hydroxystaurosporine), a protein kinase
inhibitor that is under clinical trials as an anti‐cancer agent in the USA and Japan, enhanced …

We here report the influence of the cell cycle abrogator UCN-01 on RKO human colon
carcinoma cells differing in p53 status following exposure to two DNA damaging agents, the …

The possibility that appropriately designed chemotherapy could act selectively against p53-
defective tumor cells was explored in MCF-7 human breast cancer cells. These cells were …

Owing to its central role in multiple cellular functions, p53 is an attractive candidate for gene
replacement therapy. We studied the role of adenovirus-mediated p53 gene (p53Ad) …

We have previously shown that loss of p53 function in A2780 human ovarian
adenocarcinoma cells confers increased clonogenic resistance to several DNA-damaging …

Anticancer nucleoside analogs (eg, ara-C, gemcitabine, fludarabine) induce apoptosis by
incorporation into DNA. Removal of incorporated analogs from DNA by 3'-5'exonucleases is …

The ability of DNA damage to stabilize p53 in all cell cycle stages has not been examined in
actively growing cells. The chemotherapeutic drug camptothecin is a topoisomerase I …

Wild-type p53 is induced by DNA damage. In different cell types, this induction is suggested
either to facilitate DNA repair by inducing a cell cycle pause or to potentiate cell death via …

Recently, natural product DNA topoisomerase I inhibitors 10-hydroxycamptothecin (HCPT)
and camptothecin (CPT) have been shown to have therapeutic effects in both in vitro and in …