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Claire L. Dubois

Researcher at University of California, San Diego

Publications -  10
Citations -  1642

Claire L. Dubois is an academic researcher from University of California, San Diego. The author has contributed to research in topics: Progenitor cell & Ductal cells. The author has an hindex of 10, co-authored 10 publications receiving 1433 citations. Previous affiliations of Claire L. Dubois include University of California, Irvine.

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Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma

TL;DR: It is suggested that ductal and stem-like centroacinar cells are surprisingly refractory to oncogenic transformation, whereas acinar cells readily form PDA precursor lesions with ductal features, and formation of acinar-derived premalignant lesions depends on ectopic induction of the ductal gene Sox9.
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Sox9+ ductal cells are multipotent progenitors throughout development but do not produce new endocrine cells in the normal or injured adult pancreas

TL;DR: Although endocrine cells arise from the Sox9+ ductal domain throughout embryogenesis and the early postnatal period, Sox9 + ductal cells of the adult pancreas no longer give rise to endocrine cell neogenesis under both normal conditions and in response to PDL.
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A Notch-dependent molecular circuitry initiates pancreatic endocrine and ductal cell differentiation

TL;DR: These findings establish a novel role for Notch in initiating both ductal and endocrine development and reveal that Notch does not function in an on-off mode, but that a gradient of Notch activity produces distinct cellular states during pancreas development.
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A Dosage-Dependent Requirement for Sox9 in Pancreatic Endocrine Cell Formation

TL;DR: The results show that not only is SOX9 required for the maintenance of early pancreatic progenitors, but also governs their adoption of an endocrine fate, suggesting that defective endocrine specification might underlie the pancreatic phenotype of individuals with CD.
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Cell of origin affects tumour development and phenotype in pancreatic ductal adenocarcinoma

TL;DR: It is indicated that ductal cells are primed to form carcinoma in situ that become invasive PDAC in the presence of oncogenic Kras and Trp53 deletion, while acinar cells with the same mutations appear to require a prolonged period of transition or reprogramming to initiate PDAC.