R
Rachel A. Ridgway
Researcher at Edinburgh Cancer Research Centre
Publications - 70
Citations - 9185
Rachel A. Ridgway is an academic researcher from Edinburgh Cancer Research Centre. The author has contributed to research in topics: Wnt signaling pathway & Stem cell. The author has an hindex of 36, co-authored 63 publications receiving 7637 citations. Previous affiliations of Rachel A. Ridgway include University of Glasgow & University of Edinburgh.
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Journal ArticleDOI
Crypt stem cells as the cells-of-origin of intestinal cancer
Nick Barker,Rachel A. Ridgway,Johan H. van Es,Marc van de Wetering,Harry Begthel,Maaike van den Born,Esther Danenberg,Alan Richard Clarke,Owen J. Sansom,Hans Clevers +9 more
TL;DR: It is concluded that stem-cell-specific loss of Apc results in progressively growing neoplasia in long-lived intestinal stem cells.
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Macrophage-derived Wnt opposes Notch signaling to specify hepatic progenitor cell fate in chronic liver disease.
Luke Boulter,Olivier Govaere,Thomas G. Bird,Sorina Radulescu,Prakash Ramachandran,Antonella Pellicoro,Rachel A. Ridgway,Sang Soo Seo,Bart Spee,Nico Van Rooijen,Nico Van Rooijen,Owen J. Sansom,John P. Iredale,Sally Lowell,Tania Roskams,Stuart J. Forbes +15 more
TL;DR: It is found that during biliary regeneration, expression of Jagged 1 by myofibroblasts promoted Notch signaling in HPCs and thus their biliary specification to cholangiocytes and thus the promotion of their specification to hepatocytes.
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p53 status determines the role of autophagy in pancreatic tumour development
Mathias T. Rosenfeldt,Jim O'Prey,Jennifer P. Morton,Colin Nixon,Gillian M. Mackay,Agata Mrowinska,Amy Au,Taranjit Singh Rai,Liang Zheng,Rachel A. Ridgway,Peter D. Adams,Kurt I. Anderson,Eyal Gottlieb,Owen J. Sansom,Kevin M. Ryan +14 more
TL;DR: It is shown, in a humanized genetically-modified mouse model of pancreatic ductal adenocarcinoma (PDAC), that autophagy’s role in tumour development is intrinsically connected to the status of the tumour suppressor p53, and treatment with hydroxychloroquine significantly accelerates tumour formation in mice containing oncogenic Kras but lacking p53.
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Mutant p53 drives metastasis and overcomes growth arrest/senescence in pancreatic cancer
Jennifer P. Morton,Paul Timpson,Saadia A. Karim,Rachel A. Ridgway,Dimitris Athineos,Brendan Doyle,Nigel B. Jamieson,Karin A. Oien,Andrew M. Lowy,Valerie G. Brunton,Margaret C. Frame,T.R. Jeffry Evans,Owen J. Sansom +12 more
TL;DR: By using ‘knock-in’ mutations of Trp53, two critical acquired functions of a stably expressed mutant form of p53 that drive PDAC are identified; first, an escape from KrasG12D-induced senescence/growth arrest and second, the promotion of metastasis.
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Hepatic progenitor cells of biliary origin with liver repopulation capacity
Wei-Yu Lu,Thomas G. Bird,Luke Boulter,Atsunori Tsuchiya,Alicia M. Cole,Trevor Hay,Rachel V. Guest,Davina Wojtacha,Tak Yung Man,Alison C. MacKinnon,Rachel A. Ridgway,Timothy J. Kendall,Michael Williams,Thomas Jamieson,Alex Raven,David C. Hay,John P. Iredale,Alan Richard Clarke,Owen J. Sansom,Stuart J. Forbes +19 more
TL;DR: A mouse model where the E3 ubiquitin ligase Mdm2 is inducibly deleted in more than 98% of hepatocytes, causing apoptosis, necrosis and senescence with nearly all hepatocytes expressing p21 is described, resulting in florid HPC activation, which is necessary for survival, followed by complete, functional liver reconstitution.