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Pancreatic Neoplasms: HELP
Articles by Nick Reed
Based on 5 articles published since 2008
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Between 2008 and 2019, N. Reed wrote the following 5 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Guideline ENETS Consensus Guidelines Update for the Management of Patients with Functional Pancreatic Neuroendocrine Tumors and Non-Functional Pancreatic Neuroendocrine Tumors. 2016

Falconi, M / Eriksson, B / Kaltsas, G / Bartsch, D K / Capdevila, J / Caplin, M / Kos-Kudla, B / Kwekkeboom, D / Rindi, G / Klöppel, G / Reed, N / Kianmanesh, R / Jensen, R T / Anonymous1590854. · ·Neuroendocrinology · Pubmed #26742109.

ABSTRACT: -- No abstract --

2 Guideline Guidelines for the management of gastroenteropancreatic neuroendocrine (including carcinoid) tumours (NETs). 2012

Ramage, John K / Ahmed, A / Ardill, J / Bax, N / Breen, D J / Caplin, M E / Corrie, P / Davar, J / Davies, A H / Lewington, V / Meyer, T / Newell-Price, J / Poston, G / Reed, N / Rockall, A / Steward, W / Thakker, R V / Toubanakis, C / Valle, J / Verbeke, C / Grossman, A B / Anonymous3000709. ·Basingstoke and North Hampshire Hospital, Aldermaston Road, Basingstoke RG24 9NA, UK. john.ramage@bnhft.nhs.uk ·Gut · Pubmed #22052063.

ABSTRACT: These guidelines update previous guidance published in 2005. They have been revised by a group who are members of the UK and Ireland Neuroendocrine Tumour Society with endorsement from the clinical committees of the British Society of Gastroenterology, the Society for Endocrinology, the Association of Surgeons of Great Britain and Ireland (and its Surgical Specialty Associations), the British Society of Gastrointestinal and Abdominal Radiology and others. The authorship represents leaders of the various groups in the UK and Ireland Neuroendocrine Tumour Society, but a large amount of work has been carried out by other specialists, many of whom attended a guidelines conference in May 2009. We have attempted to represent this work in the acknowledgements section. Over the past few years, there have been advances in the management of neuroendocrine tumours, which have included clearer characterisation, more specific and therapeutically relevant diagnosis, and improved treatments. However, there remain few randomised trials in the field and the disease is uncommon, hence all evidence must be considered weak in comparison with other more common cancers.

3 Article Combining clinicopathological predictors and molecular biomarkers in the oncogenic K-RAS/Ki67/HIF-1α pathway to predict survival in resectable pancreatic cancer. 2015

Qin, R / Smyrk, T C / Reed, N R / Schmidt, R L / Schnelldorfer, T / Chari, S T / Petersen, G M / Tang, A H. ·Department of Health Sciences Research, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA. · Division of Anatomic Pathology, Department of Laboratory Medicine and Pathology, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA. · Department of Surgery, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA. · 1] Department of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA [2] Upper Iowa University, Fayette, IA 52142, USA. · 1] Department of Medicine, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA [2] Department of Oncology, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA. · 1] Department of Surgery, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA [2] Department of Biochemistry and Molecular Biology, Mayo Clinic Cancer Center, Mayo Clinic, Rochester, MN 55905, USA [3] Department of Microbiology and Molecular Cell Biology, Leroy T. Canoles Jr. Cancer Research Center, Eastern Virginia Medical School, Norfolk, VA 23507, USA. ·Br J Cancer · Pubmed #25584484.

ABSTRACT: BACKGROUND: The dismal prognosis of patients diagnosed with pancreatic cancer points to our limited arsenal of effective anticancer therapies. Oncogenic K-RAS hyperactivation is virtually universal in pancreatic cancer, that confers drug resistance, drives aggressive tumorigenesis and rapid metastasis. Pancreatic tumours are often marked by hypovascularity, increased hypoxia and ineffective drug delivery. Thus, biomarker discovery and developing innovative means of countervailing oncogenic K-RAS activation are urgently needed. METHODS: Tumour specimens from 147 pancreatic cancer patients were analysed by immunohistochemical (IHC) staining and tissue microarray (TMA). Statistical correlations between selected biomarkers and clinicopathological predictors were examined to predict survival. RESULTS: We find that heightened hypoxia response predicts poor clinical outcome in resectable pancreatic cancer. SIAH is a tumour-specific biomarker. The combination of five biomarkers (EGFR, phospho-ERK, SIAH, Ki67 and HIF-1α) and four clinicopathological predictors (tumour size, pathological grade, margin and lymph node status) predict patient survival post surgery in pancreatic cancer. CONCLUSIONS: Combining five biomarkers in the K-RAS/Ki67/HIF-1α pathways with four clinicopathological predictors may assist to better predict survival in resectable pancreatic cancer.

4 Article Capecitabine and streptozocin ± cisplatin in advanced gastroenteropancreatic neuroendocrine tumours. 2014

Meyer, Tim / Qian, Wendi / Caplin, Martyn E / Armstrong, Graham / Lao-Sirieix, Si-Houy / Hardy, Richard / Valle, Juan W / Talbot, Denis C / Cunningham, David / Reed, Nick / Shaw, Ashley / Navalkissoor, Shaunak / Luong, Tu-Vinh / Corrie, Pippa G. ·Neuroendocrine Tumour Unit, The Royal Free Hospital, Pond Street, London, UK; UCL Cancer Institute, London, UK. · Cambridge Cancer Trials Centre, Cambridge Clinical Trials Unit - Cancer Theme, Addenbrooke's Hospital, Cambridge, UK; Medical Research Council Biostatistics Unit Hub for Trials Methodology, Cambridge, UK. · Neuroendocrine Tumour Unit, The Royal Free Hospital, Pond Street, London, UK. · Cambridge Cancer Trials Centre, Cambridge Clinical Trials Unit - Cancer Theme, Addenbrooke's Hospital, Cambridge, UK. · Department of Medical Oncology, The Christie, Manchester, UK. · Oxford Neuroendocrine Tumour Centre, Churchill Hospital, Oxford, UK. · Gastrointestinal Unit, The Royal Marsden, London, UK. · Beatson Oncology Centre, Glasgow, UK. · Oncology Centre, Addenbrooke's Hospital, Cambridge, UK. · Cambridge Cancer Trials Centre, Cambridge Clinical Trials Unit - Cancer Theme, Addenbrooke's Hospital, Cambridge, UK; Oncology Centre, Addenbrooke's Hospital, Cambridge, UK. Electronic address: pippa.corrie@addenbrookes.nhs.uk. ·Eur J Cancer · Pubmed #24445147.

ABSTRACT: BACKGROUND: Cytotoxic chemotherapy is widely used for advanced, unresectable pancreatic and other gastrointestinal foregut neuroendocrine tumours (NETs) and the most commonly used regimen combines 5-fluorouracil with streptozocin. The NET01 trial was designed to investigate whether capecitabine combined with streptozocin was an acceptable regimen with or without adding cisplatin. METHODS: Patients with advanced, unresectable NETs of pancreatic, gastrointestinal foregut or unknown primary site were randomised to receive three-weekly capecitabine (Cap) 625 mg/m(2) twice daily orally, streptozocin (Strep) 1.0 g/m(2) intravenously on day 1, with or without cisplatin (Cis) 70 mg/m(2) intravenously on day 1. The primary outcome measure was objective response. Secondary outcome measures included progression-free and overall survival, quality of life, toxicity and biochemical response. RESULTS: 86 (44 CapStrep, 42 CapStrepCis) patients were randomised. Best objective response rate was 12% (95% confidence interval (CI)=2-22%) with CapStrep and 16% (95% CI=4-27.4%) with CapStrepCis. Disease-control rate was 80% with CapStrep and 74% with CapStrepCis. The estimated median progression-free and overall survival were 10.2 and 26.7 months for CapStrep and 9.7 and 27.5 months for CapStrepCis. 44% of CapStrep and 68% of CapStrepCis patients experienced grade ≥3 adverse events. INTERPRETATION: The efficacies of the novel CapStrep±Cis regimens were very similar. CapStrep was better tolerated than CapStrepCis. The trial was registered as EudraCT: 2004-005202-71 and ISRCTN: 35124268.

5 Article Increased incidence of visceral metastases in scottish patients with BRCA1/2-defective ovarian cancer: an extension of the ovarian BRCAness phenotype. 2010

Gourley, Charlie / Michie, Caroline O / Roxburgh, Patricia / Yap, Timothy A / Harden, Sharon / Paul, Jim / Ragupathy, Kalpana / Todd, Radha / Petty, Russell / Reed, Nick / Hayward, Richard L / Mitchell, Paul / Rye, Tzyvia / Schellens, Jan H M / Lubinski, Jan / Carmichael, James / Kaye, Stan B / Mackean, Melanie / Ferguson, Michelle. ·University of Edinburgh Cancer Research Centre, Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, UK. charlie.gourley@ed.ac.uk ·J Clin Oncol · Pubmed #20406939.

ABSTRACT: PURPOSE: To compare the frequency of visceral relapse of BRCA1/2-deficient ovarian cancer to that of nonhereditary controls. PATIENTS AND METHODS: All patients diagnosed in Scotland with epithelial ovarian cancer (EOC) or primary peritoneal cancer (PPC) and a germline BRCA1/2 mutation were identified. Those with previous malignancy were excluded. Each remaining patient who experienced relapse was matched with two nonhereditary controls. RESULTS: Seventy-nine patients with EOC/PPC and germline BRCA1/2 mutations were identified. Fifteen had inadequate clinical data, two had carcinosarcoma, 27 had previous breast cancer, and 16 were in remission. Of the remaining 19 patients who were BRCA1/2 deficient, 14 patients (74%) developed visceral metastases compared with six (16%) of 38 patients in the control group. The percentages of liver, lung, and splenic metastases were 53%, 32%, and 32%, respectively, in the patients compared with 5%, 3%, and 5%, respectively, in the controls. When events occurring outside the matched follow-up period were omitted, the percentages of visceral, liver, lung, and splenic metastases were 58%, 42%, 16%, and 32% in the patients compared with 5%, 0%, 0%, and 3% in controls (P < .001, P < .001, P = .066, and P = .011, respectively). In an independent validation set, the corresponding percentages of visceral, liver, lung, and splenic metastases were 63%, 46%, 13%, and 17% in the patients compared with 11%, 4%, 2%, and 2% in controls (P < .001, P < .001, P = .153, and P = .052, respectively). CONCLUSION: Although sporadic EOC commonly remains confined to the peritoneum, BRCA1/2-deficient ovarian cancer frequently metastasizes to viscera. These data extend the ovarian BRCAness phenotype, imply BRCA1/2-deficient ovarian cancer is biologically distinct, and suggest that patients with visceral metastases should be considered for BRCA1/2 sequencing.