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Pancreatic Neoplasms: HELP
Articles by Colin William Steele
Based on 7 articles published since 2010
(Why 7 articles?)
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Between 2010 and 2020, C. Steele wrote the following 7 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Editorial Timing is everything: Brca2 and p53 mutations in pancreatic cancer. 2011

Morton, Jennifer P / Steele, Colin W / Sansom, Owen J. · ·Gastroenterology · Pubmed #21352873.

ABSTRACT: -- No abstract --

2 Review Targeting inflammation in pancreatic cancer: Clinical translation. 2016

Steele, Colin William / Kaur Gill, Nina Angharad / Jamieson, Nigel Balfour / Carter, Christopher Ross. ·Colin William Steele, Nigel Balfour Jamieson, Christopher Ross Carter, Department of Pancreaticobiliary Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, United Kingdom. ·World J Gastrointest Oncol · Pubmed #27096033.

ABSTRACT: Preclinical modelling studies are beginning to aid development of therapies targeted against key regulators of pancreatic cancer progression. Pancreatic cancer is an aggressive, stromally-rich tumor, from which few people survive. Within the tumor microenvironment cellular and extracellular components exist, shielding tumor cells from immune cell clearance, and chemotherapy, enhancing progression of the disease. The cellular component of this microenvironment consists mainly of stellate cells and inflammatory cells. New findings suggest that manipulation of the cellular component of the tumor microenvironment is possible to promote immune cell killing of tumor cells. Here we explore possible immunogenic therapeutic strategies. Additionally extracellular stromal elements play a key role in protecting tumor cells from chemotherapies targeted at the pancreas. We describe the experimental findings and the pitfalls associated with translation of stromally targeted therapies to clinical trial. Finally, we discuss the key inflammatory signal transducers activated subsequent to driver mutations in oncogenic Kras in pancreatic cancer. We present the preclinical findings that have led to successful early trials of STAT3 inhibitors in pancreatic adenocarcinoma.

3 Review Exploiting inflammation for therapeutic gain in pancreatic cancer. 2013

Steele, C W / Jamieson, N B / Evans, T R J / McKay, C J / Sansom, O J / Morton, J P / Carter, C R. ·The Beatson Institute for Cancer Research, Glasgow G61 1BD, UK. ·Br J Cancer · Pubmed #23385734.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy associated with <5% 5-year survival, in which standard chemotherapeutics have limited benefit. The disease is associated with significant intra- and peritumoral inflammation and failure of protective immunosurveillance. Indeed, inflammatory signals are implicated in both tumour initiation and tumour progression. The major pathways regulating PDAC-associated inflammation are now being explored. Activation of leukocytes, and upregulation of cytokine and chemokine signalling pathways, both have been shown to modulate PDAC progression. Therefore, targeting inflammatory pathways may be of benefit as part of a multi-target approach to PDAC therapy. This review explores the pathways known to modulate inflammation at different stages of tumour development, drawing conclusions on their potential as therapeutic targets in PDAC.

4 Review Clinical potential of microRNAs in pancreatic ductal adenocarcinoma. 2011

Steele, Colin W / Oien, Karin A / McKay, Colin J / Jamieson, Nigel B. ·Beatson Institute for Cancer Research, Glasgow, UK. ·Pancreas · Pubmed #22001830.

ABSTRACT: OBJECTIVES: Aggressive invasion and early metastases are characteristic features of pancreatic ductal adenocarcinoma (PDAC). More than 90% of patients have surgically nonresectable disease at presentation. Despite increasing knowledge of the genetics of this complex disease, systemic therapies, particularly gemcitabine, have modest clinical benefit and marginal survival advantage. MicroRNAs have been shown to have a role in oncogenesis, invasion, and metastases via epigenetic posttranscriptional gene regulation. Our objective was to discuss the clinical impact of microRNAs within PDAC. METHODS: This review details the understanding of microRNAs to date and explores the clinical utility of microRNAs in PDAC. RESULTS: Recent studies have focused on the impact of microRNA expression in PDAC, many of which have shown the diagnostic, predictive, and prognostic utility of microRNA profiling in PDAC identifying numerous potential targets including miR-21, miR-196a, and miR-217. CONCLUSIONS: MicroRNA stability in body fluid and tissue samples makes this area one of the most promising for earlier detection of PDAC. Indeed, microRNAs may in the future serve as a long-awaited screening tool for PDAC. Furthermore, microRNA expression profiling in PDAC may be incorporated into modern treatment algorithms to enhance therapeutic management. Equally as exciting is the potential for novel therapeutics directed against these important disease mediators.

5 Article CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma. 2016

Steele, Colin W / Karim, Saadia A / Leach, Joshua D G / Bailey, Peter / Upstill-Goddard, Rosanna / Rishi, Loveena / Foth, Mona / Bryson, Sheila / McDaid, Karen / Wilson, Zena / Eberlein, Catherine / Candido, Juliana B / Clarke, Mairi / Nixon, Colin / Connelly, John / Jamieson, Nigel / Carter, C Ross / Balkwill, Frances / Chang, David K / Evans, T R Jeffry / Strathdee, Douglas / Biankin, Andrew V / Nibbs, Robert J B / Barry, Simon T / Sansom, Owen J / Morton, Jennifer P. ·Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK. · Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK. · Oncology iMED, AstraZeneca, Alderley Park, Macclesfield SK10 4TG, UK. · Centre for Cancer and Inflammation, Barts Cancer Institute, London EC1M 6BQ, UK. · Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8QQ UK. · Department of Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, UK. · Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK. · Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK. Electronic address: o.sansom@beatson.gla.ac.uk. ·Cancer Cell · Pubmed #27265504.

ABSTRACT: CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.

6 Article Targeting the LOX/hypoxia axis reverses many of the features that make pancreatic cancer deadly: inhibition of LOX abrogates metastasis and enhances drug efficacy. 2015

Miller, Bryan W / Morton, Jennifer P / Pinese, Mark / Saturno, Grazia / Jamieson, Nigel B / McGhee, Ewan / Timpson, Paul / Leach, Joshua / McGarry, Lynn / Shanks, Emma / Bailey, Peter / Chang, David / Oien, Karin / Karim, Saadia / Au, Amy / Steele, Colin / Carter, Christopher Ross / McKay, Colin / Anderson, Kurt / Evans, Thomas R Jeffry / Marais, Richard / Springer, Caroline / Biankin, Andrew / Erler, Janine T / Sansom, Owen J. ·Cancer Research UK Beatson Institute Garscube Estate, Glasgow, UK. · The Garvan Institute of Medical Research, Sydney, NSW, Australia. · Cancer Research UK Manchester Institute, Withington Manchester, UK. · West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, Glasgow, UK. · Institute of Cancer Sciences University of Glasgow Garscube Estate, Glasgow, UK. · Cancer Research UK Beatson Institute Garscube Estate, Glasgow, UK Institute of Cancer Sciences University of Glasgow Garscube Estate, Glasgow, UK. · Institute of Cancer Research, London, UK. · Biotech Research & Innovation Centre (BRIC), University of Copenhagen, Copenhagen (UCPH), Denmark janine.erler@bric.ku.dk o.sansom@beatson.gla.ac.uk. · Cancer Research UK Beatson Institute Garscube Estate, Glasgow, UK janine.erler@bric.ku.dk o.sansom@beatson.gla.ac.uk. ·EMBO Mol Med · Pubmed #26077591.

ABSTRACT: Pancreatic ductal adenocarcinoma (PDAC) is one of the leading causes of cancer-related mortality. Despite significant advances made in the treatment of other cancers, current chemotherapies offer little survival benefit in this disease. Pancreaticoduodenectomy offers patients the possibility of a cure, but most will die of recurrent or metastatic disease. Hence, preventing metastatic disease in these patients would be of significant benefit. Using principal component analysis (PCA), we identified a LOX/hypoxia signature associated with poor patient survival in resectable patients. We found that LOX expression is upregulated in metastatic tumors from Pdx1-Cre Kras(G12D/+) Trp53(R172H/+) (KPC) mice and that inhibition of LOX in these mice suppressed metastasis. Mechanistically, LOX inhibition suppressed both migration and invasion of KPC cells. LOX inhibition also synergized with gemcitabine to kill tumors and significantly prolonged tumor-free survival in KPC mice with early-stage tumors. This was associated with stromal alterations, including increased vasculature and decreased fibrillar collagen, and increased infiltration of macrophages and neutrophils into tumors. Therefore, LOX inhibition is able to reverse many of the features that make PDAC inherently refractory to conventional therapies and targeting LOX could improve outcome in surgically resectable disease.

7 Minor RE: nab-Paclitaxel Plus Gemcitabine for Metastatic Pancreatic Cancer: Long-Term Survival From a Phase III Trial. 2015

Palani Velu, Lavanniya K / Steele, Colin W / Dickson, Euan J / Carter, C Ross / McKay, Colin J / Horgan, Paul G / McMillan, Donald C / Jamieson, Nigel B. ·Academic Unit of Surgery, School of Medicine, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow Royal Infirmary, Glasgow, Scotland (LKPV, PGH, DCM, NBJ) · West of Scotland Pancreatic Unit, Glasgow Royal Infirmary, Glasgow, Scotland (LKPV, CWS, EJD, CRC, CJM, PGH, DCM, NBJ). ·J Natl Cancer Inst · Pubmed #26251329.

ABSTRACT: -- No abstract --