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Christoph Lengauer

Researcher at Johns Hopkins University

Publications -  78
Citations -  33782

Christoph Lengauer is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Chromosome instability & Cancer. The author has an hindex of 51, co-authored 75 publications receiving 32786 citations. Previous affiliations of Christoph Lengauer include Howard Hughes Medical Institute & Johns Hopkins University School of Medicine.

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DNMT1 and DNMT3b cooperate to silence genes in human cancer cells.

TL;DR: It is demonstrated that two enzymes cooperatively maintain DNA methylation and gene silencing in human cancer cells, and compelling evidence that such methylation is essential for optimal neoplastic proliferation is provided.
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14-3-3σ Is a p53-Regulated Inhibitor of G2/M Progression

TL;DR: It is discovered that 14-3-3σ is strongly induced by γ irradiation and other DNA-damaging agents, and mediated by a p53-responsive element located 1.8 kb upstream of its transcription start site.
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Tumorigenesis: RAF/RAS oncogenes and mismatch-repair status.

TL;DR: The results not only provide genetic support for the idea that mutations in BRAF and KRAS exert equivalent effects in tumorigenesis, but also emphasize the role of repair processes in establishing the mutation spectra that underpin human cancer.
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Disruption of p53 in human cancer cells alters the responses to therapeutic agents

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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14-3-3σ is required to prevent mitotic catastrophe after DNA damage

TL;DR: An improved approach to the generation of human somatic-cell knockouts is described, which is used to generate human colorectal cancer cells in which both 14-3-3σ alleles are inactivated, and results may indicate a mechanism for maintaining the G2 checkpoint and preventing mitotic death.