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Mechanisms of drug-induced mitotic catastrophe in cancer cells.
TLDR
The elucidation of the mechanisms of treatment-induced mitotic catastrophe should contribute to an improvement of the antitumor therapy, because most of the solid tumors bear an inactive p53 protein. Expand
Sp1 transcription factor: A long-standing target in cancer chemotherapy.
TLDR
The acknowledgment that several of those compounds are safe enough might accelerate their introduction into clinical usage in patients with tumors that over-express Sp1, as well as promoting the degradation of Sp protein factors. Expand
Mitotic Catastrophe Results in Cell Death by Caspase-Dependentand Caspase-Independent Mechanisms
Exposure of MDA-MB-231 and MCF-7/VP human breast carcinoma cells to theanthracyclines doxorubicin and WP631 induced polyploidy, formation of multinucleated cellsand cell death by mitotic catastropheExpand
Mitotic catastrophe as a consequence of chemotherapy.
TLDR
Elucidation of the factors that regulate different aspects of treatment-induced mitotic catastrophe should assist in improving the efficacy of anti-cancer therapy, providing opportunities for the development of new drugs. Expand
Cell death pathways in response to antitumor therapy.
TLDR
It is critically reviewed here how antitumor therapy may elicit the response of human cancers through different cell pathways leading to cell death. Expand
Daunorubicin-induced variations in gene transcription: commitment to proliferation arrest, senescence and apoptosis.
TLDR
Gene expression profiles, cell-cycle distribution, the presence of DNA damage and the time-dependent response of Jurkat T cells to cell death were correlated clearly, and the general behaviour of the genes suggests that cell- cycle arrest and cell death follow distinct pathways depending on drug concentration. Expand
Sp1 transcription factor as a target for anthracyclines: effects on gene transcription.
TLDR
The analysis of gene expression profiles using arrays, which include several genes containing Sp1-putative binding sites, suggests that changes in the transcriptome induce cell cycle arrest and drive a time-dependent response of cells to death stimuli through distinct pathways, which rely on the anthracycline used and its concentration. Expand
Induction of G(2)/M arrest and inhibition of c-myc and p53 transcription by WP631 in Jurkat T lymphocytes.
TLDR
A weak interdependence was found between the potent antiproliferative activity and the apoptotic response; treatment with WP631 for 24-36hr produced arrest in G(2)/M and allowed for partial DNA repair. Expand
A nuclear budding mechanism in transiently arrested cells generates drug-sensitive and drug-resistant cells.
TLDR
Nuclear budding was accompanied by changes in protein levels in the giant cells, including inhibition of p53 and enhanced expression of p21(WAF1 and the meiosis-related Mos. Expand
A comparative analysis of the time-dependent antiproliferative effects of daunorubicin and WP631.
TLDR
The results indicate that the major effect of WP631 was a G2/M arrest followed, after about 72 h of treatment, by polyploidy and mitotic (reproductive) death, in contrast, daunorubicin induced a rapid response with classic features of apoptosis. Expand
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