ReviewLangenbeck's archives of surgery2005
Diabetes mellitus: a risk factor for pancreatic cancer?
Review in Langenbeck's archives of surgery, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Diabetes and cancer I: risk, survival, and implications for screening.Cancer causes & control : CCC · 2012Pooled it
- Gene signature for prognosis in comparison of pancreatic cancer patients with diabetes and non-diabetes.PeerJ · 2020Article
- Blood Glucose Homeostasis in the Course of Partial Pancreatectomy--Evidence for Surgically Reversible Diabetes Induced by Cholestasis.PloS one · 2015Article
- Distal gastrectomy in pancreaticoduodenectomy is associated with accelerated gastric emptying, enhanced postprandial release of GLP-1, and improved insulin sensitivity.Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract · 2014Article
- Duration of diabetes and pancreatic cancer in a case-control study in the Midwest and the Iowa Women's Health Study (IWHS) cohort.JOP : Journal of the pancreas · 2013Article
- Advances in biomarker research for pancreatic cancer.Current pharmaceutical design · 2012Review
- Advances in diagnosis, treatment and palliation of pancreatic carcinoma: 1990-2010.World journal of gastroenterology · 2011Review
- High glucose promotes cell proliferation and enhances GDNF and RET expression in pancreatic cancer cells.Molecular and cellular biochemistry · 2011Article
- Diabetic ketoacidosis in type 2 diabetics: a novel presentation of pancreatic adenocarcinoma.Journal of general internal medicine · 2010Article
- Promoting Effects of Sucrose-rich Diet on N-Nitrosobis (2-oxopropyl) amine-induced Pancreatic Carcinogenesis in Hamsters.Journal of toxicologic pathology · 2010Article
- Diabetic Ketoacidosis as the Initial Presenting Symptom of Pancreatic Adenocarcinoma: A Discussion about Screening Utilizing ENDPAC Scoring Coupled with CT Scans and Endoscopic Ultrasound.Case reports in oncologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The relationship between pancreatic cancer (PC) and diabetes is controversial. While some investigators assume that type II diabetes is a predisposition to PC, recent data argue that diabetes and altered glucose metabolism are a consequence of PC, and yet, the clinical presentation of the altered glucose metabolism in these patients varies considerably. Around 70% of patients with PC have impaired glucose tolerance (IGT) or frank diabetes. Of these, nearly 60% show an improvement of IGT or diabetes after surgery, whereas the rest show only mild or no improvement. It appears that biologically there are three types of PC: (1) PC not associated with IGT or diabetes; (2) PC associated with IGT or diabetes in which the abnormality improves postoperatively; (3) PC associated with IGT or diabetes in which the abnormality does not improve postoperatively. Based on our own studies, we suggest that the reason for impaired glucose metabolism in most patients is the alteration of islet cells either by the carcinogen directly, or by diabetogenic substances released by cancer cells. The extent of the islet alteration (i.e. focal or diffuse) may determine whether the removal of tumor alone can improve the metabolic alteration. The elucidation of the mechanism is of immense importance for providing an early tumor marker and for developing preventative or therapeutic modalities.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.