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Pancreatic Neoplasms: HELP
Articles by Pedro A. Pérez-Mancera
Based on 6 articles published since 2009
(Why 6 articles?)
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Between 2009 and 2019, Pedro A. Perez-Mancera wrote the following 6 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Designing a bio-inspired biomimetic in vitro system for the optimization of ex vivo studies of pancreatic cancer. 2017

Totti, Stella / Vernardis, Spyros I / Meira, Lisiane / Pérez-Mancera, Pedro A / Costello, Eithne / Greenhalf, William / Palmer, Daniel / Neoptolemos, John / Mantalaris, Athanasios / Velliou, Eirini G. ·Bioprocess and Biochemical Engineering Group (BioProChem), Department of Chemical and Process Engineering, University of Surrey, Guildford GU2 7XH, UK. · Biological Systems Engineering Laboratory (BSEL), Department of Chemical Engineering, Imperial College London, SW7 2AZ London, UK. · Department of Clinical and Experimental Medicine, University of Surrey, Guildford GU2 7XH, UK. · Department of Molecular and Clinical Cancer Medicine, University of Liverpool,Daulby Street, Liverpool L69 3GA, UK. · Department of Molecular and Clinical Cancer Medicine, University of Liverpool,Daulby Street, Liverpool L69 3GA, UK; NIHR Liverpool Pancreas Biomedical Research Unit, University of Liverpool,Daulby Street, Liverpool L69 3GA, UK. · NIHR Liverpool Pancreas Biomedical Research Unit, University of Liverpool,Daulby Street, Liverpool L69 3GA, UK. · Bioprocess and Biochemical Engineering Group (BioProChem), Department of Chemical and Process Engineering, University of Surrey, Guildford GU2 7XH, UK. Electronic address: e.velliou@surrey.ac.uk. ·Drug Discov Today · Pubmed #28153670.

ABSTRACT: Pancreatic cancer is one of the most aggressive and lethal human malignancies. Drug therapies and radiotherapy are used for treatment as adjuvants to surgery, but outcomes remain disappointing. Advances in tissue engineering suggest that 3D cultures can reflect the in vivo tumor microenvironment and can guarantee a physiological distribution of oxygen, nutrients, and drugs, making them promising low-cost tools for therapy development. Here, we review crucial structural and environmental elements that should be considered for an accurate design of an ex vivo platform for studies of pancreatic cancer. Furthermore, we propose environmental stress response biomarkers as platform readouts for the efficient control and further prediction of the pancreatic cancer response to the environmental and treatment input.

2 Review What we have learned about pancreatic cancer from mouse models. 2012

Pérez-Mancera, Pedro A / Guerra, Carmen / Barbacid, Mariano / Tuveson, David A. ·Li Ka Shing Centre, Cambridge Research Institute, and Department of Oncology, Cancer Research UK, Cambridge, England. ·Gastroenterology · Pubmed #22406637.

ABSTRACT: -- No abstract --

3 Article Chemoresistance in Pancreatic Cancer Is Driven by Stroma-Derived Insulin-Like Growth Factors. 2016

Ireland, Lucy / Santos, Almudena / Ahmed, Muhammad S / Rainer, Carolyn / Nielsen, Sebastian R / Quaranta, Valeria / Weyer-Czernilofsky, Ulrike / Engle, Danielle D / Perez-Mancera, Pedro A / Coupland, Sarah E / Taktak, Azzam / Bogenrieder, Thomas / Tuveson, David A / Campbell, Fiona / Schmid, Michael C / Mielgo, Ainhoa. ·Department of Molecular and Clinical Cancer Medicine, University of Liverpool, Liverpool, United Kingdom. · Pharmacology and Translational Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria. · Cold Spring Harbor Laboratory, Cold Spring Harbor, New York. · Lustgarten Pancreatic Cancer Research Laboratory, Cold Spring Harbor, New York. · Department of Medical Physics and Clinical Engineering, Royal Liverpool University Hospital, Liverpool, United Kingdom. · Medicine and Translational Research, Boehringer Ingelheim RCV GmbH & Co KG, Vienna, Austria. · Department of Urology, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany. · Rubenstein Center for Pancreatic Cancer Research, Memorial Sloan Kettering Cancer Center, New York, New York. ·Cancer Res · Pubmed #27742686.

ABSTRACT: Tumor-associated macrophages (TAM) and myofibroblasts are key drivers in cancer that are associated with drug resistance in many cancers, including pancreatic ductal adenocarcinoma (PDAC). However, our understanding of the molecular mechanisms by which TAM and fibroblasts contribute to chemoresistance is unclear. In this study, we found that TAM and myofibroblasts directly support chemoresistance of pancreatic cancer cells by secreting insulin-like growth factors (IGF) 1 and 2, which activate insulin/IGF receptors on pancreatic cancer cells. Immunohistochemical analysis of biopsies from patients with pancreatic cancer revealed that 72% of the patients expressed activated insulin/IGF receptors on tumor cells, and this positively correlates with increased CD163

4 Article Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes. 2012

Biankin, Andrew V / Waddell, Nicola / Kassahn, Karin S / Gingras, Marie-Claude / Muthuswamy, Lakshmi B / Johns, Amber L / Miller, David K / Wilson, Peter J / Patch, Ann-Marie / Wu, Jianmin / Chang, David K / Cowley, Mark J / Gardiner, Brooke B / Song, Sarah / Harliwong, Ivon / Idrisoglu, Senel / Nourse, Craig / Nourbakhsh, Ehsan / Manning, Suzanne / Wani, Shivangi / Gongora, Milena / Pajic, Marina / Scarlett, Christopher J / Gill, Anthony J / Pinho, Andreia V / Rooman, Ilse / Anderson, Matthew / Holmes, Oliver / Leonard, Conrad / Taylor, Darrin / Wood, Scott / Xu, Qinying / Nones, Katia / Fink, J Lynn / Christ, Angelika / Bruxner, Tim / Cloonan, Nicole / Kolle, Gabriel / Newell, Felicity / Pinese, Mark / Mead, R Scott / Humphris, Jeremy L / Kaplan, Warren / Jones, Marc D / Colvin, Emily K / Nagrial, Adnan M / Humphrey, Emily S / Chou, Angela / Chin, Venessa T / Chantrill, Lorraine A / Mawson, Amanda / Samra, Jaswinder S / Kench, James G / Lovell, Jessica A / Daly, Roger J / Merrett, Neil D / Toon, Christopher / Epari, Krishna / Nguyen, Nam Q / Barbour, Andrew / Zeps, Nikolajs / Anonymous1421514 / Kakkar, Nipun / Zhao, Fengmei / Wu, Yuan Qing / Wang, Min / Muzny, Donna M / Fisher, William E / Brunicardi, F Charles / Hodges, Sally E / Reid, Jeffrey G / Drummond, Jennifer / Chang, Kyle / Han, Yi / Lewis, Lora R / Dinh, Huyen / Buhay, Christian J / Beck, Timothy / Timms, Lee / Sam, Michelle / Begley, Kimberly / Brown, Andrew / Pai, Deepa / Panchal, Ami / Buchner, Nicholas / De Borja, Richard / Denroche, Robert E / Yung, Christina K / Serra, Stefano / Onetto, Nicole / Mukhopadhyay, Debabrata / Tsao, Ming-Sound / Shaw, Patricia A / Petersen, Gloria M / Gallinger, Steven / Hruban, Ralph H / Maitra, Anirban / Iacobuzio-Donahue, Christine A / Schulick, Richard D / Wolfgang, Christopher L / Morgan, Richard A / Lawlor, Rita T / Capelli, Paola / Corbo, Vincenzo / Scardoni, Maria / Tortora, Giampaolo / Tempero, Margaret A / Mann, Karen M / Jenkins, Nancy A / Perez-Mancera, Pedro A / Adams, David J / Largaespada, David A / Wessels, Lodewyk F A / Rust, Alistair G / Stein, Lincoln D / Tuveson, David A / Copeland, Neal G / Musgrove, Elizabeth A / Scarpa, Aldo / Eshleman, James R / Hudson, Thomas J / Sutherland, Robert L / Wheeler, David A / Pearson, John V / McPherson, John D / Gibbs, Richard A / Grimmond, Sean M. ·The Kinghorn Cancer Centre, 370 Victoria Street, Darlinghurst, Sydney, New South Wales 2010, Australia. ·Nature · Pubmed #23103869.

ABSTRACT: Pancreatic cancer is a highly lethal malignancy with few effective therapies. We performed exome sequencing and copy number analysis to define genomic aberrations in a prospectively accrued clinical cohort (n = 142) of early (stage I and II) sporadic pancreatic ductal adenocarcinoma. Detailed analysis of 99 informative tumours identified substantial heterogeneity with 2,016 non-silent mutations and 1,628 copy-number variations. We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6). Integrative analysis with in vitro functional data and animal models provided supportive evidence for potential roles for these genetic aberrations in carcinogenesis. Pathway-based analysis of recurrently mutated genes recapitulated clustering in core signalling pathways in pancreatic ductal adenocarcinoma, and identified new mutated genes in each pathway. We also identified frequent and diverse somatic aberrations in genes described traditionally as embryonic regulators of axon guidance, particularly SLIT/ROBO signalling, which was also evident in murine Sleeping Beauty transposon-mediated somatic mutagenesis models of pancreatic cancer, providing further supportive evidence for the potential involvement of axon guidance genes in pancreatic carcinogenesis.

5 Article The deubiquitinase USP9X suppresses pancreatic ductal adenocarcinoma. 2012

Pérez-Mancera, Pedro A / Rust, Alistair G / van der Weyden, Louise / Kristiansen, Glen / Li, Allen / Sarver, Aaron L / Silverstein, Kevin A T / Grützmann, Robert / Aust, Daniela / Rümmele, Petra / Knösel, Thomas / Herd, Colin / Stemple, Derek L / Kettleborough, Ross / Brosnan, Jacqueline A / Li, Ang / Morgan, Richard / Knight, Spencer / Yu, Jun / Stegeman, Shane / Collier, Lara S / ten Hoeve, Jelle J / de Ridder, Jeroen / Klein, Alison P / Goggins, Michael / Hruban, Ralph H / Chang, David K / Biankin, Andrew V / Grimmond, Sean M / Anonymous291514 / Wessels, Lodewyk F A / Wood, Stephen A / Iacobuzio-Donahue, Christine A / Pilarsky, Christian / Largaespada, David A / Adams, David J / Tuveson, David A. ·Li Ka Shing Centre, Cambridge Research Institute, Cancer Research UK, Cambridge CB2 0RE, UK. ·Nature · Pubmed #22699621.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDA) remains a lethal malignancy despite much progress concerning its molecular characterization. PDA tumours harbour four signature somatic mutations in addition to numerous lower frequency genetic events of uncertain significance. Here we use Sleeping Beauty (SB) transposon-mediated insertional mutagenesis in a mouse model of pancreatic ductal preneoplasia to identify genes that cooperate with oncogenic Kras(G12D) to accelerate tumorigenesis and promote progression. Our screen revealed new candidate genes for PDA and confirmed the importance of many genes and pathways previously implicated in human PDA. The most commonly mutated gene was the X-linked deubiquitinase Usp9x, which was inactivated in over 50% of the tumours. Although previous work had attributed a pro-survival role to USP9X in human neoplasia, we found instead that loss of Usp9x enhances transformation and protects pancreatic cancer cells from anoikis. Clinically, low USP9X protein and messenger RNA expression in PDA correlates with poor survival after surgery, and USP9X levels are inversely associated with metastatic burden in advanced disease. Furthermore, chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X expression in human PDA cell lines, indicating a clinical approach for certain patients. The conditional deletion of Usp9x cooperated with Kras(G12D) to accelerate pancreatic tumorigenesis in mice, validating their genetic interaction. We propose that USP9X is a major tumour suppressor gene with prognostic and therapeutic relevance in PDA.

6 Article Exome sequencing identifies frequent mutation of the SWI/SNF complex gene PBRM1 in renal carcinoma. 2011

Varela, Ignacio / Tarpey, Patrick / Raine, Keiran / Huang, Dachuan / Ong, Choon Kiat / Stephens, Philip / Davies, Helen / Jones, David / Lin, Meng-Lay / Teague, Jon / Bignell, Graham / Butler, Adam / Cho, Juok / Dalgliesh, Gillian L / Galappaththige, Danushka / Greenman, Chris / Hardy, Claire / Jia, Mingming / Latimer, Calli / Lau, King Wai / Marshall, John / McLaren, Stuart / Menzies, Andrew / Mudie, Laura / Stebbings, Lucy / Largaespada, David A / Wessels, L F A / Richard, Stephane / Kahnoski, Richard J / Anema, John / Tuveson, David A / Perez-Mancera, Pedro A / Mustonen, Ville / Fischer, Andrej / Adams, David J / Rust, Alistair / Chan-on, Waraporn / Subimerb, Chutima / Dykema, Karl / Furge, Kyle / Campbell, Peter J / Teh, Bin Tean / Stratton, Michael R / Futreal, P Andrew. ·Cancer Genome Project, Wellcome Trust Sanger Institute, Hinxton CB10 1SA, UK. ·Nature · Pubmed #21248752.

ABSTRACT: The genetics of renal cancer is dominated by inactivation of the VHL tumour suppressor gene in clear cell carcinoma (ccRCC), the commonest histological subtype. A recent large-scale screen of ∼3,500 genes by PCR-based exon re-sequencing identified several new cancer genes in ccRCC including UTX (also known as KDM6A), JARID1C (also known as KDM5C) and SETD2 (ref. 2). These genes encode enzymes that demethylate (UTX, JARID1C) or methylate (SETD2) key lysine residues of histone H3. Modification of the methylation state of these lysine residues of histone H3 regulates chromatin structure and is implicated in transcriptional control. However, together these mutations are present in fewer than 15% of ccRCC, suggesting the existence of additional, currently unidentified cancer genes. Here, we have sequenced the protein coding exome in a series of primary ccRCC and report the identification of the SWI/SNF chromatin remodelling complex gene PBRM1 (ref. 4) as a second major ccRCC cancer gene, with truncating mutations in 41% (92/227) of cases. These data further elucidate the somatic genetic architecture of ccRCC and emphasize the marked contribution of aberrant chromatin biology.