T
Todd Waldman
Researcher at Georgetown University
Publications - 81
Citations - 13319
Todd Waldman is an academic researcher from Georgetown University. The author has contributed to research in topics: Mutation & Cell cycle. The author has an hindex of 42, co-authored 79 publications receiving 12509 citations. Previous affiliations of Todd Waldman include Howard Hughes Medical Institute & Johns Hopkins University School of Medicine.
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Journal ArticleDOI
Requirement for p53 and p21 to Sustain G2 Arrest After DNA Damage
Fred Bunz,A. Dutriaux,Christoph Lengauer,Todd Waldman,Shibin Zhou,J. P. Brown,John M. Sedivy,Kenneth W. Kinzler,Bert Vogelstein +8 more
TL;DR: After DNA damage, many cells appear to enter a sustained arrest in the G2 phase of the cell cycle but this arrest could be sustained only when p53 was present in the cell and capable of transcriptionally activating the cyclin-dependent kinase inhibitor p21.
Journal Article
p21 is necessary for the p53-mediated G1 arrest in human cancer cells.
TL;DR: Results unambiguously establish p21 as a critical mediator of one well-documented p53 function and have important implications for understanding cell cycle checkpoints and the mechanism(s) through which p53 inhibits human neoplasia.
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Disruption of p53 in human cancer cells alters the responses to therapeutic agents
Fred Bunz,Paul M. Hwang,Chris Torrance,Chris Torrance,Todd Waldman,Yonggang Zhang,Larry E. Dillehay,Jerry R. Williams,Christoph Lengauer,Kenneth W. Kinzler,Bert Vogelstein +10 more
TL;DR: It was found that p53 had profound effects on drug responses, and these effects varied dramatically depending on the drug, having significant implications for future efforts to maximize therapeutic efficacy in patients with defined genetic alterations.
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Uncoupling of S phase and mitosis induced by anticancer agents in cells lacking p21
TL;DR: It is shown that p21WAF1/CIP1, the prototype inhibitor of cyclin-dependent kinases (CDKs)4, is required for coordination of the S and M phases of the eukaryotic cell cycle, and in the absence of p21, DNA-damaged cells arrest in a G2-like state, but then undergo additional S phases without intervening normal mitoses.
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Synthetic lethal targeting of PTEN mutant cells with PARP inhibitors
Ana M. Mendes-Pereira,Sarah A. Martin,Rachel Brough,Afshan McCarthy,Jessica R. Taylor,Jung-Sik Kim,Todd Waldman,Christopher J. Lord,Alan Ashworth +8 more
TL;DR: The data presented here now suggests that the clinical assessment of PARP inhibitors should be extended beyond those with BRCA mutations to a larger group of patients with PTEN mutant tumours.