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Pancreatic Neoplasms: HELP
Articles by Jonathan Fawcett
Based on 9 articles published since 2010
(Why 9 articles?)
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Between 2010 and 2020, Jonathan Fawcett wrote the following 9 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Review Ampullary cancer of intestinal origin and duodenal cancer - A logical clinical and therapeutic subgroup in periampullary cancer. 2017

Chandrasegaram, Manju D / Gill, Anthony J / Samra, Jas / Price, Tim / Chen, John / Fawcett, Jonathan / Merrett, Neil D. ·the Prince Charles Hospital, Brisbane, Queensland 4032, Australia. · Sydney Medical School, University of Sydney, New South Wales 2006, Australia. · Queen Elizabeth Hospital, Adelaide, South Australia 5011, Australia. · Flinders Medical Centre, Adelaide, South Australia 5042, Australia. · School of Medicine, University of Queensland, Queensland 4006, Australia. · Department of Upper GI Surgery, Bankstown Hospital, Sydney, New South Wales 2200, Australia. ·World J Gastrointest Oncol · Pubmed #29085567.

ABSTRACT: Periampullary cancers include pancreatic, ampullary, biliary and duodenal cancers. At presentation, the majority of periampullary tumours have grown to involve the pancreas, bile duct, ampulla and duodenum. This can result in difficulty in defining the primary site of origin in all but the smallest tumors due to anatomical proximity and architectural distortion. This has led to variation in the reported proportions of resected periampullary cancers. Pancreatic cancer is the most common cancer resected with a pancreaticoduodenectomy followed by ampullary (16%-50%), bile duct (5%-39%), and duodenal cancer (3%-17%). Patients with resected duodenal and ampullary cancers have a better reported median survival (29-47 mo and 22-54 mo) compared to pancreatic cancer (13-19 mo). The poorer survival with pancreatic cancer relates to differences in tumour characteristics such as a higher incidence of nodal, neural and vascular invasion. While small ampullary cancers can present early with biliary obstruction, pancreatic cancers need to reach a certain size before biliary obstruction ensues. This larger size at presentation contributes to a higher incidence of resection margin involvement in pancreatic cancer. Ampullary cancers can be subdivided into intestinal or pancreatobiliary subtype cancers with histomolecular staining. This avoids relying on histomorphology alone, as even some poorly differentiated cancers preserve the histomolecular profile of their mucosa of origin. Histomolecular profiling is superior to anatomic location in prognosticating survival. Ampullary cancers of intestinal subtype and duodenal cancers are similar in their intestinal origin and form a logical clinical and therapeutic subgroup of periampullary cancers. They respond to 5-FU based chemotherapeutic regimens such as capecitabine-oxaliplatin. Unlike pancreatic cancers,

2 Article Nonsteroidal anti-inflammatory drugs, statins, and pancreatic cancer risk: a population-based case-control study. 2016

Kho, Pik Fang / Fawcett, Jonathan / Fritschi, Lin / Risch, Harvey / Webb, Penelope M / Whiteman, David C / Neale, Rachel E. ·Population Health Department, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane, QLD, 4006, Australia. · School of Medicine, University of Queensland, Brisbane, Australia. · School of Public Health, Curtin University, Perth, Australia. · School of Public Health, Yale University, New Haven, CT, USA. · School of Public Health, University of Queensland, Brisbane, Australia. · Population Health Department, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane, QLD, 4006, Australia. Rachel.Neale@qimrberghofer.edu.au. · School of Public Health, University of Queensland, Brisbane, Australia. Rachel.Neale@qimrberghofer.edu.au. ·Cancer Causes Control · Pubmed #27817122.

ABSTRACT: PURPOSE: Studies suggest that aspirin, other nonsteroidal anti-inflammatory drugs (NSAIDs), and statins may reduce risk of some cancers. However, findings have been conflicting as to whether these agents reduce the risk of pancreatic cancer. METHODS: We used data from the Queensland Pancreatic Cancer Study, a population-based case-control study. In total, 704 cases and 711 age- and sex-matched controls were recruited. Participants completed an interview in which they were asked about history of NSAID and statin use. We included 522 cases and 653 controls who had completed the medication section of the interview in this analysis. Unconditional multivariable logistic regression was used to estimate associations between medication use and pancreatic cancer. RESULTS: We found no consistent evidence of an association between use of NSAIDs or statins and risk of pancreatic cancer. There was some suggestion of a protective effect in infrequent users of selective COX-2 inhibitors, but no association in more frequent users. We did not find evidence of protective effects in analyses stratified by sex, smoking status, time between diagnosis and interview, or presence/absence of metastases. CONCLUSIONS: Overall, our results do support the hypothesis that use of NSAIDs or statins may reduce the odds of developing pancreatic cancer.

3 Article Association between family cancer history and risk of pancreatic cancer. 2016

Schulte, Annaka / Pandeya, Nirmala / Fawcett, Jonathan / Fritschi, Lin / Klein, Kerenaftali / Risch, Harvey A / Webb, Penelope M / Whiteman, David C / Neale, Rachel E. ·Department of Population Health, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland 4006, Australia; School of Medicine, University of Queensland, 288 Herston Road, Herston, Queensland 4006, Australia. Electronic address: Annaka.Schulte@qimrberghofer.edu.au. · Department of Population Health, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland 4006, Australia; School of Population Health, Level 2, Population Health Building, 887 Mayne Road, University of Queensland, Herston, Queensland 4006, Australia. · Department of Population Health, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Queensland 4006, Australia. · School of Public Health, Curtin University, Kent Street, Bentley, Perth, Western Australia 6102, Australia. · Yale School of Public Health, 60 College St, New Haven, CT 06510, United States. ·Cancer Epidemiol · Pubmed #27810486.

ABSTRACT: PURPOSE: Family history of pancreatic adenocarcinoma is an established risk factor for the disease. However, associations of pancreatic cancer with other familial cancers are less clear. We analyzed data from the Queensland Pancreatic Cancer Study (QPCS), an Australian population-based case-control study, to investigate associations between family history of various cancer types and risk of pancreatic cancer. MATERIALS AND METHODS: Our study included 591 pancreatic cancer patients and 646 controls, all of whom self-reported the histories of cancer in their first-degree relatives. We used logistic regression to estimate adjusted odds ratios (ORs) and their 95% confidence intervals (CIs). Based on our results, we conducted a systematic literature review using the Medline (OVID) database to identify articles pertaining to the association between family history of melanoma and risk of pancreatic cancer. A meta-analysis including associations in five published studies, unpublished results from a study co-author and the QPCS results was then performed using the DerSimonian and Laird random-effects model. RESULTS: Cases were more likely than controls to report a family history of pancreatic cancer (OR 2.20, 95% CI 1.16-4.19) and melanoma (OR 1.74, 95% CI 1.03-2.95), but not of breast, ovarian, respiratory, other gastrointestinal or prostate cancer. Meta-analysis of melanoma family history and pancreatic cancer risk yielded an OR of 1.22 (95% CI 1.00-1.51). CONCLUSIONS: Our results yield further evidence of increased risk of pancreatic cancer in those with family histories of the disease. We also provide suggestive evidence of an association between family history of melanoma and risk of pancreatic cancer.

4 Article Association between Helicobacter pylori and pancreatic cancer risk: a meta-analysis. 2015

Schulte, Annaka / Pandeya, Nirmala / Fawcett, Jonathan / Fritschi, Lin / Risch, Harvey A / Webb, Penelope M / Whiteman, David C / Neale, Rachel E. ·Department of Population Health, Royal Brisbane Hospital, QIMR Berghofer Medical Research Institute, Locked Bag 2000, Brisbane, QLD, Australia, Annaka.Schulte@qimrberghofer.edu.au. ·Cancer Causes Control · Pubmed #25951801.

ABSTRACT: PURPOSE: Gastric colonization with Helicobacter pylori (H. pylori) has been implicated in the pathogenesis of pancreatic cancer, but results of epidemiological studies have been inconclusive. We analyzed data from the Queensland Pancreatic Cancer Study, an Australian population-based case-control study, and incorporated our findings into an updated meta-analysis. METHODS: Blood samples were obtained from 580 patients and 626 controls, and enzyme-linked immunosorbent assay kits were used to determine seropositivity to H. pylori and its virulence protein, cytotoxin-associated gene A (CagA). Odds ratios (ORs) and 95 % confidence intervals (CIs) were calculated using logistic regression. Results were incorporated into a meta-analysis along with results of studies identified through systematic literature review. Adjusted ORs and 95 % CIs were calculated using the DerSimonian and Laird random-effects model. RESULTS: No overall association was observed between H. pylori seropositivity and risk of pancreatic cancer (OR 1.00; 95 % CI 0.74-1.35). Nonsignificantly decreased pancreatic cancer risk was observed with CagA seropositivity (OR 0.74; 95 % CI 0.48-1.15) and increased risk with CagA-negative H. pylori seropositivity (OR 1.23; 95 % CI 0.83-1.82). Ten studies were included in the meta-analysis. There was no significant overall association between H. pylori seropositivity and pancreatic cancer risk (OR 1.13; 95 % CI 0.86-1.50), but evidence of CagA strain-specific associations (OR 0.78; 95 % CI 0.67-0.91 and OR 1.30; 95 % CI 1.02-1.65 for CagA-positive and CagA-negative strains, respectively). CONCLUSIONS: Our results provide further evidence for the existence of strain-specific associations between H. pylori and pancreatic cancer.

5 Article Occupational exposure to N-nitrosamines and pesticides and risk of pancreatic cancer. 2015

Fritschi, Lin / Benke, Geza / Risch, Harvey A / Schulte, Annaka / Webb, Penelope M / Whiteman, David C / Fawcett, Jonathan / Neale, Rachel E. ·School of Public Health, Curtin University, Perth, Western Australia, Australia. · Department of Epidemiology and Preventive Medicine, Monash University, The Alfred Centre, Melbourne, Victoria, Australia. · Department of Chronic Disease Epidemiology, Yale School of Public Health, New Haven, Connecticut, USA. · Department of Population Health, QIMR Berghofer Medical Research Institute, Royal Brisbane Hospital, Herston, Queensland, Australia. · Princess Alexandra Hospital, Brisbane, Queensland, Australia. ·Occup Environ Med · Pubmed #25780030.

ABSTRACT: OBJECTIVES: Animal evidence shows that N-nitrosamines and similar xenobiotic compounds are pancreatic carcinogens. We aimed to determine whether occupational exposure to N-nitrosamines or to pesticides increases risk of pancreatic cancer development. METHODS: Participants (504 cases, 643 controls) in a population-based case-control study (The Queensland Pancreatic Cancer Study) provided data on demographic, medical and lifestyle factors and lifetime job histories. Specific questions were asked regarding work in rubber and leather industries, metalworking jobs and occupational or direct use of pesticides on animals or crops. An occupational hygienist reviewed this information (blind to case status) to assess likelihood of exposure to N-nitrosamines and pesticides, and estimated level and frequency of such exposures. RESULTS: No associations were found for risk of pancreatic cancer and occupational exposure to N-nitrosamines (OR=0.85, 95% CI 0.51 to 1.42) and no associations were seen with level or frequency of exposure. No associations were observed for ever exposure to pesticides in general (OR=0.90, 95% CI 0.61 to 1.33) or to any of the pesticide subgroups. Stratification by history of cigarette smoking did not change these results. CONCLUSIONS: This comprehensive analysis of a large case-control study does not support an association between occupational exposure to N-nitrosamines or pesticide use and risk of pancreatic cancer.

6 Article Association between hypermethylation of DNA repetitive elements in white blood cell DNA and pancreatic cancer. 2014

Neale, Rachel E / Clark, Paul J / Fawcett, Jonathan / Fritschi, Lin / Nagler, Belinda N / Risch, Harvey A / Walters, Rhiannon J / Crawford, William J / Webb, Penelope M / Whiteman, David C / Buchanan, Daniel D. ·QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. Electronic address: Rachel.neale@qimrberghofer.edu.au. · QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. · University of Queensland, Brisbane, Queensland, Australia. · Curtin University, Perth, Western Australia, Australia. · Yale School of Public Health, New Haven, CT, United States. · Department of Pathology, The University of Melbourne, Carlton, 3010 Victoria, Australia; Centre for Epidemiology and Biostatistics, Melbourne School of Population and Global Health, The University of Melbourne, Carlton, Victoria 3010, Australia. ·Cancer Epidemiol · Pubmed #25201440.

ABSTRACT: Pancreatic cancer is a leading cause of cancer-related deaths worldwide. Methylation of DNA may influence risk or be a marker of early disease. The aim of this study was to measure the association between methylation of three DNA repetitive elements in white blood cell (WBC) DNA and pancreatic cancer. DNA from WBCs of pancreatic cancer cases (n=559) and healthy unrelated controls (n=603) were tested for methylation of the LINE-1, Alu and Sat2 DNA repetitive elements using MethyLight quantitative PCR assays. Odds ratios (ORs) and 95% confidence intervals (95%CI) between both continuous measures of percent of methylated sample compared to a reference (PMR) or quintiles of PMR and pancreatic cancer, adjusted for age, sex, smoking, BMI, alcohol and higher education, were estimated. The PMR for each of the three markers was higher in cases than in controls, although only LINE-1 was significantly associated with pancreatic cancer (OR per log unit=1.37, 95%CI=1.16-1.63). The marker methylation score for all three markers combined was significantly associated with pancreatic cancer (p-trend=0.0006). There were no associations between measures of PMR and either presence of metastases, or timing of blood collection in relation to diagnosis, surgery, chemotherapy or death (all p>0.1). We observed an association between methylation of LINE-1 in WBC DNA and risk of pancreatic cancer. Further studies are needed to confirm this association.

7 Article Cigarette smoking and pancreatic cancer risk: more to the story than just pack-years. 2014

Schulte, Annaka / Pandeya, Nirmala / Tran, Bich / Fawcett, Jonathan / Fritschi, Lin / Risch, Harvey A / Webb, Penelope M / Whiteman, David C / Neale, Rachel E / Anonymous4970782. ·Department of Population Health, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia; School of Medicine, University of Queensland, Brisbane, Queensland, Australia. Electronic address: Annaka.Schulte@qimrberghofer.edu.au. · Department of Population Health, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia; School of Population Health, University of Queensland, Brisbane, Australia. · Department of Population Health, QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia. · Western Australian Institute for Medical Research, University of Western Australia, Nedlands, Western Australia, Australia. ·Eur J Cancer · Pubmed #24461200.

ABSTRACT: PURPOSE: Cigarette smoking is an established risk factor for pancreatic adenocarcinoma. However, few studies have thoroughly investigated the effects of independent smoking dimensions (duration, intensity, cumulative dose and time since quitting) on risk estimates. We analysed data from the Queensland Pancreatic Cancer Study (QPCS), an Australian population-based case-control study, with the aim of determining which smoking component is primarily important to pancreatic cancer risk. METHODS: Our study included 705 pancreatic cancer patients and 711 controls. Logistic regression and generalised additive logistic regression (for non-linear dose effects) were used to determine odds ratios (ORs) and 95% confidence intervals (CIs). RESULTS: Compared to never-smokers, current smokers had an increased risk of pancreatic cancer (OR=3.4; 95% CI 2.4-5.0) after adjustment for age, sex, education, alcohol intake and birth country. Of the various smoking dimensions, smoking duration and time since quitting had a greater effect on OR estimates (OR 1.3; 95% CI 1.1-1.4 and OR 0.8; 95% CI 0.7-0.8) than smoking intensity (OR 1.1; 95% CI 0.9-1.2), once ever-smoking was accounted for. CONCLUSIONS: This study confirms the association between cigarette smoking and pancreatic adenocarcinoma, and provides evidence to suggest that smoking pattern, in addition to dose effect, may affect disease risk.

8 Article Association between ultraviolet radiation, skin sun sensitivity and risk of pancreatic cancer. 2013

Tran, Bich / Whiteman, David C / Webb, Penelope M / Fritschi, Lin / Fawcett, Jonathan / Risch, Harvey A / Lucas, Robyn / Pandeya, Nirmala / Schulte, Annaka / Neale, Rachel E / Anonymous6580770. ·Population Health Division, QIMR Berghofer Medical Research Institute, Australia; Centre for Research Excellence in Sun and Health, Australia. Electronic address: b.tran@uws.edu.au. ·Cancer Epidemiol · Pubmed #24075798.

ABSTRACT: BACKGROUND: Ecological studies showing an inverse association between pancreatic cancer incidence and mortality and levels of ultraviolet radiation (UVR), suggest that higher levels of sun exposure may reduce risks of pancreatic cancer but there has been only one individual-level study that examined this issue. We aimed to examine the association between pancreatic cancer and markers of exposure to solar UVR, namely skin type, treatment of skin lesions, ambient UVR and time outdoors on work days. METHODS: We used data from an Australian case-control study. Location at birth, residential location during adulthood, outdoors work, history of skin lesion treatment and sensitivity of the skin to the sun were obtained by questionnaire. We limited the analyses to Caucasians who answered the questionnaire about UVR (controls=589/711 recruited; cases=496/705 recruited). We used NASA's Total Ozone Mapping Spectrometer to estimate ambient UVR. RESULTS: Being born in or living in areas of higher ambient UVR (compared to lower ambient UVR) was associated with about 30-40% lower risk of pancreatic cancer. People with fair skin colour had 47% lower risk of pancreatic cancer than those with dark skin colour (95% CI 0.37-0.75). There was some suggestion of increased risk with increased average number of hours spent outside at work. CONCLUSIONS: This study suggests that people with light skin colour or those born or living in areas of high ambient UVR have lower risk of pancreatic cancer. Our analysis supports an association between UVR and pancreatic cancer, possibly mediated through production of vitamin D.

9 Article Surgical management in patients with pancreatic cancer: a Queensland perspective. 2013

Wylie, Neil / Adib, Reza / Barbour, Andrew P / Fawcett, Jonathan / Hill, Alexander / Lynch, Stephen / Martin, Ian / O'Rourke, Thomas R / Puhalla, Harald / Rutherford, Leigh / Slater, Kellee / Whiteman, David C / Neale, Rachel E / Anonymous3170740. ·Queensland Institute of Medical Research, Brisbane, Queensland, Australia. ·ANZ J Surg · Pubmed #23095039.

ABSTRACT: BACKGROUND: Little has been published regarding presenting symptoms, investigations and outcomes for patients with pancreatic cancer in Australia. Data from a series of patients undergoing attempted resection in Queensland, Australia, are presented with the aim of assisting development of consistent strategies in disease management. METHODS: We reviewed the medical records of 121 patients who underwent attempted surgical resection and who took part in a case-control study between 2007 and 2009. Information relating to symptoms, investigations, surgical procedures and outcomes was captured. RESULTS: The mean age was 63 years and 60% were men. The most common presenting symptoms were jaundice (64%) and pain (63%). Over 80% of patients had multiple imaging investigations or laparoscopy prior to surgery. Seventy-eight patients (64%) had a completed resection and 23% of these had involved margins. The presence of metastases and/or involvement of vessels or adjacent structures precluded resection in the remaining patients. The 1-year survival for patients whose resections were completed was 77% compared with 51% for those whose tumours were not resectable (Pā€‰=ā€‰0.004). There was no 30-day mortality and 68% of patients were alive 1 year after diagnosis. Resections were performed in 11 different hospitals but over 90% of patients underwent their surgery in one of five high-volume centres. CONCLUSION: The Queensland experience is consistent with that reported internationally. A significant proportion of attempted resections was not completed because preoperative staging underestimated disease extent. Most patients with potentially resectable disease are being treated in high-volume centres.