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Pancreatic Neoplasms: HELP
Articles by David R. Croucher
Based on 3 articles published since 2010
(Why 3 articles?)
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Between 2010 and 2020, David R. Croucher wrote the following 3 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article CAF hierarchy driven by pancreatic cancer cell p53-status creates a pro-metastatic and chemoresistant environment via perlecan. 2019

Vennin, Claire / Mélénec, Pauline / Rouet, Romain / Nobis, Max / Cazet, Aurélie S / Murphy, Kendelle J / Herrmann, David / Reed, Daniel A / Lucas, Morghan C / Warren, Sean C / Elgundi, Zehra / Pinese, Mark / Kalna, Gabriella / Roden, Daniel / Samuel, Monisha / Zaratzian, Anaiis / Grey, Shane T / Da Silva, Andrew / Leung, Wilfred / Anonymous561018 / Mathivanan, Suresh / Wang, Yingxiao / Braithwaite, Anthony W / Christ, Daniel / Benda, Ales / Parkin, Ashleigh / Phillips, Phoebe A / Whitelock, John M / Gill, Anthony J / Sansom, Owen J / Croucher, David R / Parker, Benjamin L / Pajic, Marina / Morton, Jennifer P / Cox, Thomas R / Timpson, Paul. ·The Garvan Institute of Medical Research & The Kinghorn Cancer Centre, Sydney, NSW, 2010, Australia. · St Vincent's Clinical School, Faculty of Medicine, University of New South Wales Sydney, Sydney, NSW, 2010, Australia. · Molecular Pathology department, the Netherlands Cancer Institute, Amsterdam, 1066CX, the Netherlands. · Graduate school of Biomedical Engineering, University of New South Wales Sydney, Sydney, NSW, 2052, Australia. · Cancer Research UK Beatson Institute, Glasgow Scotland, G61 BD, UK. · Department of Physiology, Anatomy and Microbiology, School of Life Sciences, La Trobe University, Bundoora, VIC, 3086, Australia. · Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY, 14853, USA. · Department of Bioengineering, Institute of Engineering in Medicine, University of California, San Diego, CA, 92121, USA. · Children's Medical Research Institute, University of Sydney, Sydney, NSW, 2006, Australia. · Department of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, 9054, New Zealand. · Maurice Wilkins Centre, University of Otago, Dunedin, 9054, New Zealand. · Biomedical imaging facility, Lowy Cancer Research Centre, University of New South Wales, Sydney, NSW, Australia. · Pancreatic Cancer Translational Research Group, Lowy Cancer Research Centre, School of Medical Sciences, University of New South Wales, Sydney, NSW, 2052, Australia. · Australian Centre for Nanomedicine, University of New South Wales, Sydney, NSW, 2052, Australia. · Sydney Medical School, University of Sydney, Sydney, NSW, 2006, Australia. · NSW Health Pathology, Department of Anatomical Pathology, Royal North Shore Hospital, St Leonards, Sydney, NSW, 2065, Australia. · Cancer Diagnosis and Pathology Research Group, Kolling Institute of Medical Research, St Leonards, NSW, 2065, Australia. · Schools of Life and Environmental Sciences, the Charles Perkin Centre, the University of Sydney, Sydney, NSW, 2006, Australia. · The Garvan Institute of Medical Research & The Kinghorn Cancer Centre, Sydney, NSW, 2010, Australia. t.cox@garvan.org.au. · St Vincent's Clinical School, Faculty of Medicine, University of New South Wales Sydney, Sydney, NSW, 2010, Australia. t.cox@garvan.org.au. · The Garvan Institute of Medical Research & The Kinghorn Cancer Centre, Sydney, NSW, 2010, Australia. p.timpson@garvan.org.au. · St Vincent's Clinical School, Faculty of Medicine, University of New South Wales Sydney, Sydney, NSW, 2010, Australia. p.timpson@garvan.org.au. ·Nat Commun · Pubmed #31406163.

ABSTRACT: Heterogeneous subtypes of cancer-associated fibroblasts (CAFs) coexist within pancreatic cancer tissues and can both promote and restrain disease progression. Here, we interrogate how cancer cells harboring distinct alterations in p53 manipulate CAFs. We reveal the existence of a p53-driven hierarchy, where cancer cells with a gain-of-function (GOF) mutant p53 educate a dominant population of CAFs that establish a pro-metastatic environment for GOF and null p53 cancer cells alike. We also demonstrate that CAFs educated by null p53 cancer cells may be reprogrammed by either GOF mutant p53 cells or their CAFs. We identify perlecan as a key component of this pro-metastatic environment. Using intravital imaging, we observe that these dominant CAFs delay cancer cell response to chemotherapy. Lastly, we reveal that depleting perlecan in the stroma combined with chemotherapy prolongs mouse survival, supporting it as a potential target for anti-stromal therapies in pancreatic cancer.

2 Article Intravital Imaging to Monitor Therapeutic Response in Moving Hypoxic Regions Resistant to PI3K Pathway Targeting in Pancreatic Cancer. 2018

Conway, James R W / Warren, Sean C / Herrmann, David / Murphy, Kendelle J / Cazet, Aurélie S / Vennin, Claire / Shearer, Robert F / Killen, Monica J / Magenau, Astrid / Mélénec, Pauline / Pinese, Mark / Nobis, Max / Zaratzian, Anaiis / Boulghourjian, Alice / Da Silva, Andrew M / Del Monte-Nieto, Gonzalo / Adam, Arne S A / Harvey, Richard P / Haigh, Jody J / Wang, Yingxiao / Croucher, David R / Sansom, Owen J / Pajic, Marina / Caldon, C Elizabeth / Morton, Jennifer P / Timpson, Paul. ·Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, Sydney, NSW 2010, Australia. · Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, Sydney, NSW 2010, Australia; St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia. · St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia; Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Sydney, NSW 2010, Australia. · Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Sydney, NSW 2010, Australia. · St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia; Developmental and Stem Cell Biology Division, Victor Chang Cardiac Research Institute, Sydney, NSW 2010, Australia; School of Biotechnology and Biomolecular Science, University of New South Wales, Sydney, NSW 2033, Australia. · Australian Centre for Blood Diseases, Monash University, Melbourne, VIC 3004, Australia. · Department of Bioengineering, University of Illinois, Urbana-Champaign, Urbana, IL 61801, USA. · Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, Sydney, NSW 2010, Australia; St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia; School of Medicine and Medical Science, University College Dublin, Belfield, Dublin 4, Ireland. · Cancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1QH, UK. · Cancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1QH, UK. Electronic address: j.morton@beatson.gla.ac.uk. · Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, Sydney, NSW 2010, Australia; St Vincent's Clinical School, Faculty of Medicine, University of NSW, Sydney, NSW 2010, Australia. Electronic address: p.timpson@garvan.org.au. ·Cell Rep · Pubmed #29898401.

ABSTRACT: Application of advanced intravital imaging facilitates dynamic monitoring of pathway activity upon therapeutic inhibition. Here, we assess resistance to therapeutic inhibition of the PI3K pathway within the hypoxic microenvironment of pancreatic ductal adenocarcinoma (PDAC) and identify a phenomenon whereby pronounced hypoxia-induced resistance is observed for three clinically relevant inhibitors. To address this clinical problem, we have mapped tumor hypoxia by both immunofluorescence and phosphorescence lifetime imaging of oxygen-sensitive nanoparticles and demonstrate that these hypoxic regions move transiently around the tumor. To overlay this microenvironmental information with drug response, we applied a FRET biosensor for Akt activity, which is a key effector of the PI3K pathway. Performing dual intravital imaging of drug response in different tumor compartments, we demonstrate an improved drug response to a combination therapy using the dual mTORC1/2 inhibitor AZD2014 with the hypoxia-activated pro-drug TH-302.

3 Article Intravital FRAP Imaging using an E-cadherin-GFP Mouse Reveals Disease- and Drug-Dependent Dynamic Regulation of Cell-Cell Junctions in Live Tissue. 2016

Erami, Zahra / Herrmann, David / Warren, Sean C / Nobis, Max / McGhee, Ewan J / Lucas, Morghan C / Leung, Wilfred / Reischmann, Nadine / Mrowinska, Agata / Schwarz, Juliane P / Kadir, Shereen / Conway, James R W / Vennin, Claire / Karim, Saadia A / Campbell, Andrew D / Gallego-Ortega, David / Magenau, Astrid / Murphy, Kendelle J / Ridgway, Rachel A / Law, Andrew M / Walters, Stacey N / Grey, Shane T / Croucher, David R / Zhang, Lei / Herzog, Herbert / Hardeman, Edna C / Gunning, Peter W / Ormandy, Christopher J / Evans, T R Jeffry / Strathdee, Douglas / Sansom, Owen J / Morton, Jennifer P / Anderson, Kurt I / Timpson, Paul. ·Cancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK. · The Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW 2010, Australia. · Neuromuscular and Regenerative Medicine Unit, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia. · Oncology Research Unit, School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia. · Cancer Research UK Beatson Institute, Switchback Road, Bearsden, Glasgow G61 1BD, UK. Electronic address: k.anderson@beatson.gla.ac.uk. · The Garvan Institute of Medical Research and The Kinghorn Cancer Centre, Cancer Division, St Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, NSW 2010, Australia. Electronic address: p.timpson@garvan.org.au. ·Cell Rep · Pubmed #26725115.

ABSTRACT: E-cadherin-mediated cell-cell junctions play a prominent role in maintaining the epithelial architecture. The disruption or deregulation of these adhesions in cancer can lead to the collapse of tumor epithelia that precedes invasion and subsequent metastasis. Here we generated an E-cadherin-GFP mouse that enables intravital photobleaching and quantification of E-cadherin mobility in live tissue without affecting normal biology. We demonstrate the broad applications of this mouse by examining E-cadherin regulation in multiple tissues, including mammary, brain, liver, and kidney tissue, while specifically monitoring E-cadherin mobility during disease progression in the pancreas. We assess E-cadherin stability in native pancreatic tissue upon genetic manipulation involving Kras and p53 or in response to anti-invasive drug treatment and gain insights into the dynamic remodeling of E-cadherin during in situ cancer progression. FRAP in the E-cadherin-GFP mouse, therefore, promises to be a valuable tool to fundamentally expand our understanding of E-cadherin-mediated events in native microenvironments.