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Pancreatic Neoplasms: HELP
Articles by S. Becker
Based on 4 articles published since 2010
(Why 4 articles?)
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Between 2010 and 2020, S. Becker wrote the following 4 articles about Pancreatic Neoplasms.
 
+ Citations + Abstracts
1 Article Anti-proliferative and pro-apoptotic effects of lichen-derived compound protolichesterinic acid are not mediated by its lipoxygenase-inhibitory activity. 2015

Bessadóttir, M / Eiríksson, F F / Becker, S / Ögmundsdóttir, M H / Ómarsdóttir, S / Thorsteinsdóttir, M / Ögmundsdóttir, H M. ·Faculty of Medicine, University of Iceland, 101 Reykjavik, Iceland; Faculty of Pharmaceutical Sciences, University of Iceland, 101 Reykjavik, Iceland. · Faculty of Medicine, University of Iceland, 101 Reykjavik, Iceland. · Faculty of Pharmaceutical Sciences, University of Iceland, 101 Reykjavik, Iceland. · Faculty of Medicine, University of Iceland, 101 Reykjavik, Iceland. Electronic address: helgaogm@hi.is. ·Prostaglandins Leukot Essent Fatty Acids · Pubmed #25964147.

ABSTRACT: Lipoxygenases (LOXs) and their products are involved in several biological functions and have been associated with carcinogenesis. Protolichesterinic acid (PA), a lichen metabolite, inhibits 5- and 12-LOX and has anti-proliferative effects on various cancer cell lines. Here, PA was shown to inhibit proliferation of multiple myeloma cells, RPMI 8226 and U266, and pancreatic cancer cells AsPC-1. Apoptosis was induced only in multiple myeloma cells. Cell-cycle associated changes in expression and sub-cellular localization of 5- and 12-LOX were not affected by PA but increased cytoplasmic localisation was found to accompany morphological changes at later stages. Assessment by mass spectrometry showed that PA entered the pancreatic cancer cells. However, effects on LOX metabolites were only evident after treatment with concentrations exceeding those having anti-proliferative effects and no effects were measurable in the myeloma cells. We conclude that the anti-proliferative and pro-apoptotic effects of PA are not mediated directly through inhibition of LOX activity.

2 Article Inflammation marker and risk of pancreatic cancer: a nested case-control study within the EPIC cohort. 2012

Grote, V A / Kaaks, R / Nieters, A / Tjønneland, A / Halkjær, J / Overvad, K / Skjelbo Nielsen, M R / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Becker, S / Pischon, T / Boeing, H / Trichopoulou, A / Cassapa, C / Stratigakou, V / Palli, D / Krogh, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Sánchez, M-J / Dorronsoro, M / Navarro, C / Gurrea, A B / Siersema, P D / Peeters, P H M / Ye, W / Sund, M / Lindkvist, B / Johansen, D / Khaw, K-T / Wareham, N / Allen, N E / Travis, R C / Fedirko, V / Jenab, M / Michaud, D S / Chuang, S-C / Romaguera, D / Bueno-de-Mesquita, H B / Rohrmann, S. ·Division of Cancer Epidemiology (c020), German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, Heidelberg 69120, Germany. ·Br J Cancer · Pubmed #22617158.

ABSTRACT: BACKGROUND: Established risk factors for pancreatic cancer include smoking, long-standing diabetes, high body fatness, and chronic pancreatitis, all of which can be characterised by aspects of inflammatory processes. However, prospective studies investigating the relation between inflammatory markers and pancreatic cancer risk are scarce. METHODS: We conducted a nested case-control study within the European Prospective Investigation into Cancer and Nutrition, measuring prediagnostic blood levels of C-reactive protein (CRP), interleukin-6 (IL-6), and soluble receptors of tumour necrosis factor-α (sTNF-R1, R2) in 455 pancreatic cancer cases and 455 matched controls. Odds ratios (ORs) were estimated using conditional logistic regression models. RESULTS: None of the inflammatory markers were significantly associated with risk of pancreatic cancer overall, although a borderline significant association was observed for higher circulating sTNF-R2 (crude OR=1.52 (95% confidence interval (CI) 0.97-2.39), highest vs lowest quartile). In women, however, higher sTNF-R1 levels were significantly associated with risk of pancreatic cancer (crude OR=1.97 (95% CI 1.02-3.79)). For sTNF-R2, risk associations seemed to be stronger for diabetic individuals and those with a higher BMI. CONCLUSION: Prospectively, CRP and IL-6 do not seem to have a role in our study with respect to risk of pancreatic cancer, whereas sTNF-R1 seemed to be a risk factor in women and sTNF-R2 might be a mediator in the risk relationship between overweight and diabetes with pancreatic cancer. Further large prospective studies are needed to clarify the role of proinflammatory proteins and cytokines in the pathogenesis of exocrine pancreatic cancer.

3 Article Concentrations of IGF-I and IGFBP-3 and pancreatic cancer risk in the European Prospective Investigation into Cancer and Nutrition. 2012

Rohrmann, S / Grote, V A / Becker, S / Rinaldi, S / Tjønneland, A / Roswall, N / Grønbæk, H / Overvad, K / Boutron-Ruault, M C / Clavel-Chapelon, F / Racine, A / Teucher, B / Boeing, H / Drogan, D / Dilis, V / Lagiou, P / Trichopoulou, A / Palli, D / Tagliabue, G / Tumino, R / Vineis, P / Mattiello, A / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J-M / Ardanaz, E / Jeurnink, S / Peeters, P H M / Lindkvist, B / Johansen, D / Sund, M / Ye, W / Khaw, K-T / Wareham, N J / Allen, N E / Crowe, F L / Fedirko, V / Jenab, M / Michaud, D S / Norat, T / Riboli, E / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology and Prevention, Institute of Social and Preventive Medicine, University of Zurich, Hirschengraben 84, Zürich 8001, Switzerland. sabine.rohrmann@ifspm.uzh.ch ·Br J Cancer · Pubmed #22315049.

ABSTRACT: BACKGROUND: Insulin-like growth factors (IGFs) and their binding proteins (BPs) regulate cell differentiation, proliferation and apoptosis, and may have a role in the aetiology of various cancers. Information on their role in pancreatic cancer is limited and was examined here in a case-control study nested within the European Prospective Investigation into Cancer and Nutrition. METHODS: Serum concentrations of IGF-I and IGFBP-3 were measured using enzyme-linked immunosorbent assays in 422 cases and 422 controls matched on age, sex, study centre, recruitment date, and time since last meal. Conditional logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) adjusted for confounding variables. RESULTS: Neither circulating levels of IGF-I (OR=1.21, 95% CI 0.75-1.93 for top vs bottom quartile, P-trend 0.301), IGFBP-3 (OR=1.00, 95% CI 0.66-1.51, P-trend 0.79), nor the molar IGF-I/IGFBP-3 ratio, an indicator of free IGF-I level (OR=1.22, 95% CI 0.75-1.97, P-trend 0.27), were statistically significantly associated with the risk of pancreatic cancer. In a cross-classification, however, a high concentration of IGF-I with concurrently low levels of IGFBP-3 was related to an increased risk of pancreatic cancer (OR=1.72, 95% CI 1.05-2.83; P-interaction=0.154). CONCLUSION: On the basis of these results, circulating levels of components of the IGF axis do not appear to be the risk factors for pancreatic cancer. However, on the basis of the results of a subanalysis, it cannot be excluded that a relatively large amount of IGF-1 together with very low levels of IGFBP-3 might still be associated with an increase in pancreatic cancer risk.

4 Article Diabetes mellitus, glycated haemoglobin and C-peptide levels in relation to pancreatic cancer risk: a study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. 2011

Grote, V A / Rohrmann, S / Nieters, A / Dossus, L / Tjønneland, A / Halkjær, J / Overvad, K / Fagherazzi, G / Boutron-Ruault, M C / Morois, S / Teucher, B / Becker, S / Sluik, D / Boeing, H / Trichopoulou, A / Lagiou, P / Trichopoulos, D / Palli, D / Pala, V / Tumino, R / Vineis, P / Panico, S / Rodríguez, L / Duell, E J / Molina-Montes, E / Dorronsoro, M / Huerta, J M / Ardanaz, E / Jeurnink, S M / Beulens, J W J / Peeters, P H M / Sund, M / Ye, W / Lindkvist, B / Johansen, D / Khaw, K T / Wareham, N / Allen, N / Crowe, F / Jenab, M / Romieu, I / Michaud, D S / Riboli, E / Romaguera, D / Bueno-de-Mesquita, H B / Kaaks, R. ·Division of Cancer Epidemiology c020, German Cancer Research Center (DKFZ), Im Neuenheimer Feld 581, 69120 Heidelberg, Germany. ·Diabetologia · Pubmed #21953276.

ABSTRACT: AIMS/HYPOTHESIS: There has been long-standing debate about whether diabetes is a causal risk factor for pancreatic cancer or a consequence of tumour development. Prospective epidemiological studies have shown variable relationships between pancreatic cancer risk and blood markers of glucose and insulin metabolism, overall and as a function of lag times between marker measurements (blood donation) and date of tumour diagnosis. METHODS: Pre-diagnostic levels of HbA(1c) and C-peptide were measured for 466 participants with pancreatic cancer and 466 individually matched controls within the European Prospective Investigation into Cancer and Nutrition. Conditional logistic regression models were used to estimate ORs for pancreatic cancer. RESULTS: Pancreatic cancer risk gradually increased with increasing pre-diagnostic HbA(1c) levels up to an OR of 2.42 (95% CI 1.33, 4.39 highest [≥ 6.5%, 48 mmol/mol] vs lowest [≤ 5.4%, 36 mmol/mol] category), even for individuals with HbA(1c) levels within the non-diabetic range. C-peptide levels showed no significant relationship with pancreatic cancer risk, irrespective of fasting status. Analyses showed no clear trends towards increasing hyperglycaemia (as marked by HbA(1c) levels) or reduced pancreatic beta cell responsiveness (as marked by C-peptide levels) with decreasing time intervals from blood donation to cancer diagnosis. CONCLUSIONS/INTERPRETATION: Our data on HbA(1c) show that individuals who develop exocrine pancreatic cancer tend to have moderate increases in HbA(1c) levels, relatively independently of obesity and insulin resistance-the classic and major risk factors for type 2 diabetes. While there is no strong difference by lag time, more data are needed on this in order to reach a firm conclusion.