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      Impact of Insulin Therapies on Cancer Incidence in Type 1 and Type 2 Diabetes: A Population-Based Cohort Study in Reggio Emilia, Italy

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          Abstract

          Objective: To assess the effect of insulin on cancer incidence in type 1 (T1DM) and type 2 diabetes (T2DM). Methods: The cohort included all 401,172 resident population aged 20–84 in December 2009 and still alive on December 2011, classified for DM status. Drug exposure was assessed for 2009–2011 and follow up was conducted from 2012 to 2016 through the cancer registry. Incidence rate ratios (IRRs) were computed for all sites and for the most frequent cancer sites. Results: among residents, 21,190 people had diabetes, 2282 of whom were taking insulin; 1689 cancers occurred, 180 among insulin users. The risk for all site was slightly higher in people with T2DM compared to people without DM (IRR 1.21, 95% CI 1.14–1.27), with no excess for T1DM (IRR 0.73, 95% CI 0.45–1.19). The excess in T2DM remained when comparing with diet-only treatment. In T2DM, excess incidence was observed for liver and pancreas and for NETs: 1.76 (95% CI 1.44–2.17) and 1.37 (95% CI 0.99–1.73), respectively. For bladder, there was an excess both in T1DM (IRR 3.00, 95% CI 1.12, 8.02) and in T2DM (IRR1.27, 95% CI 1.07–1.50). Conclusions: Insulin was associated with a 20% increase in cancer incidence. The risk was higher for liver, pancreatic, bladder and neuroendocrine tumours.

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          Diabetes mellitus as a predictor of cancer mortality in a large cohort of US adults.

          Several studies have suggested that diabetes mellitus may alter the risk of developing a variety of cancers, and the associations are biologically plausible. To learn more about the relation between diabetes and cancer mortality, the authors examined associations with selected cancers in a large, prospective US cohort of 467,922 men and 588,321 women who had no reported history of cancer at enrollment in 1982. After 16 years of mortality follow-up, diabetes was significantly associated with fatal colon cancer in men (multivariate relative risk (RR) = 1.20, 95% confidence interval (CI): 1.06, 1.37) and women (RR = 1.24, 95% CI: 1.07, 1.43) and with pancreatic cancer in men (RR = 1.48, 95% CI: 1.27, 1.73) and women (RR = 1.44, 95% CI: 1.21, 1.72). For men, diabetes was significantly associated with liver cancer (RR = 2.19, 95% CI: 1.76, 2.72) and bladder cancer (RR = 1.43, 95% CI: 1.14, 1.80). In addition, diabetes was significantly associated with breast cancer in women (RR = 1.27, 95% CI: 1.11, 1.45). These associations were not explained by high body mass. Our findings suggest that diabetes is an independent predictor of mortality from cancer of the colon, pancreas, female breast, and, in men, of the liver and bladder.
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            Diabetes and cancer: a consensus report.

            Epidemiologic evidence suggests that cancer incidence is associated with diabetes as well as certain diabetes risk factors and treatments. This consensus statement of experts assembled jointly by the American Diabetes Association and the American Cancer Society reviews the state of science concerning 1) the association between diabetes and cancer incidence or prognosis; 2) risk factors common to both diabetes and cancer; 3) possible biologic links between diabetes and cancer risk; and 4) whether diabetes treatments influence the risk of cancer or cancer prognosis. In addition, key unanswered questions for future research are posed. (c) 2010 American Cancer Society, Inc.
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              Marked Expansion of Exocrine and Endocrine Pancreas With Incretin Therapy in Humans With Increased Exocrine Pancreas Dysplasia and the Potential for Glucagon-Producing Neuroendocrine Tumors

              Controversy exists regarding the potential regenerative influences of incretin therapy on pancreatic β-cells versus possible adverse pancreatic proliferative effects. Examination of pancreata from age-matched organ donors with type 2 diabetes mellitus (DM) treated by incretin therapy (n = 8) or other therapy (n = 12) and nondiabetic control subjects (n = 14) reveals an ∼40% increased pancreatic mass in DM treated with incretin therapy, with both increased exocrine cell proliferation (P < 0.0001) and dysplasia (increased pancreatic intraepithelial neoplasia, P < 0.01). Pancreata in DM treated with incretin therapy were notable for α-cell hyperplasia and glucagon-expressing microadenomas (3 of 8) and a neuroendocrine tumor. β-Cell mass was reduced by ∼60% in those with DM, yet a sixfold increase was observed in incretin-treated subjects, although DM persisted. Endocrine cells costaining for insulin and glucagon were increased in DM compared with non-DM control subjects (P < 0.05) and markedly further increased by incretin therapy (P < 0.05). In conclusion, incretin therapy in humans resulted in a marked expansion of the exocrine and endocrine pancreatic compartments, the former being accompanied by increased proliferation and dysplasia and the latter by α-cell hyperplasia with the potential for evolution into neuroendocrine tumors.
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                Author and article information

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                Journal
                CANCCT
                Cancers
                Cancers
                MDPI AG
                2072-6694
                June 2022
                May 31 2022
                : 14
                : 11
                : 2719
                Article
                10.3390/cancers14112719
                35681699
                4f00e4e6-e449-4cfe-b192-ac9aa03948b9
                © 2022

                https://creativecommons.org/licenses/by/4.0/

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