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Pierre Dubus

Researcher at University of Bordeaux

Publications -  165
Citations -  11710

Pierre Dubus is an academic researcher from University of Bordeaux. The author has contributed to research in topics: Cancer & Cell cycle. The author has an hindex of 43, co-authored 157 publications receiving 10447 citations. Previous affiliations of Pierre Dubus include Centre Hospitalier Universitaire de Bordeaux & French Institute of Health and Medical Research.

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Chronic pancreatitis is essential for induction of pancreatic ductal adenocarcinoma by K-Ras oncogenes in adult mice.

TL;DR: It is reported that selective expression of an endogenous K-Ras(G12V) oncogene in embryonic cells of acinar/centroacinar lineage results in pancreatic intraepithelial neoplasias (PanINs) and invasive PDA, suggesting that PDA originates by differentiation of acINs or their precursors into ductal-like cells.
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Cdk1 is sufficient to drive the mammalian cell cycle

TL;DR: It is shown that mouse embryos lacking all interphase Cdks undergo organogenesis and develop to midgestation and that in the absence of interphaseCdks, Cdk1 can execute all the events that are required to drive cell division.
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Cyclin-dependent kinase 2 is essential for meiosis but not for mitotic cell division in mice

TL;DR: CDK2 is essential for completion of prophase I during meiotic cell division in male and female germ cells, an unforeseen role for this cell cycle kinase.
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Mammalian Cells Cycle without the D-Type Cyclin-Dependent Kinases Cdk4 and Cdk6

TL;DR: The results indicate that D-type cyclin-dependent kinases are not essential for cell cycle entry and suggest the existence of alternative mechanisms to initiate cell proliferation upon mitogenic stimulation.
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Loss of Cdk4 expression causes insulin-deficient diabetes and Cdk4 activation results in beta-islet cell hyperplasia.

TL;DR: Results establish Cdk4 as an essential regulator of specific cell types as well as establishing its role as a regulator of insulin-deficient diabetes and pancreatic hyperplasia in mice expressing a mutant Cdk 4 that cannot bind the cell-cycle inhibitor P16INK4a.