J A Johnson1, S L Bowker. 1. Department of Public Health Sciences, University of Alberta, Edmonton, AB, Canada. jeff.johnson@ualberta.ca
Abstract
AIMS/HYPOTHESIS: The purpose of this study was to explore the relationship between hyperglycaemia in type 2 diabetes and risk of cancer incidence or cancer mortality. We were interested to determine if data from major randomised controlled trials would support a hypothesis that improving glycaemic control may reduce the risk of cancer outcomes. METHODS: We included major randomised controlled trials conducted with an overall aim of intensified glycaemic control in type 2 diabetes. We abstracted data from published papers and supplemental material and conducted separate meta-analyses of cancer mortality and cancer incidence. RESULTS: Four trials reported cancer mortality for the intensive (222 events in 53,892 person-years) and standard control (155 events in 38,743 person-years) arms (UK Prospective Diabetes Study [UKPDS] 33, UKPDS 34, Action to Control Cardiovascular Risk in Diabetes [ACCORD] and Veterans Affairs Diabetes Trial [VADT]); the summary risk ratio for cancer mortality was 1.00 (95% CI 0.81-1.24; I² = 0%). Excluding the UKPDS metformin trial resulted in a pooled risk estimate of 1.03 (95% CI 0.83-1.29; I² = 0%). Three trials reported cancer incidence for the study arms (Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation [ADVANCE], PROspective pioglitAzone Clinical Trial In macroVascular Events [PROactive], Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes [RECORD]) with 357 events in 47,974 person-years with improved glycaemic control and 380 events in 45,009 person-years in the control arms; the pooled risk ratio for cancer incidence was 0.91 (95% CI 0.79-1.05; I² = 0%). CONCLUSIONS/ INTERPRETATION: Data from large randomised controlled trials of intensified glycaemic control suggest that cancer risk is not reduced by improving glycaemic control in type 2 diabetes. These data therefore do not support the hypothesis that hyperglycaemia is causally linked to increased cancer risk.
AIMS/HYPOTHESIS: The purpose of this study was to explore the relationship between hyperglycaemia in type 2 diabetes and risk of cancer incidence or cancer mortality. We were interested to determine if data from major randomised controlled trials would support a hypothesis that improving glycaemic control may reduce the risk of cancer outcomes. METHODS: We included major randomised controlled trials conducted with an overall aim of intensified glycaemic control in type 2 diabetes. We abstracted data from published papers and supplemental material and conducted separate meta-analyses of cancer mortality and cancer incidence. RESULTS: Four trials reported cancer mortality for the intensive (222 events in 53,892 person-years) and standard control (155 events in 38,743 person-years) arms (UK Prospective Diabetes Study [UKPDS] 33, UKPDS 34, Action to Control Cardiovascular Risk in Diabetes [ACCORD] and Veterans Affairs Diabetes Trial [VADT]); the summary risk ratio for cancer mortality was 1.00 (95% CI 0.81-1.24; I² = 0%). Excluding the UKPDS metformin trial resulted in a pooled risk estimate of 1.03 (95% CI 0.83-1.29; I² = 0%). Three trials reported cancer incidence for the study arms (Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation [ADVANCE], PROspective pioglitAzone Clinical Trial In macroVascular Events [PROactive], Rosiglitazone Evaluated for Cardiac Outcomes and Regulation of Glycaemia in Diabetes [RECORD]) with 357 events in 47,974 person-years with improved glycaemic control and 380 events in 45,009 person-years in the control arms; the pooled risk ratio for cancer incidence was 0.91 (95% CI 0.79-1.05; I² = 0%). CONCLUSIONS/ INTERPRETATION: Data from large randomised controlled trials of intensified glycaemic control suggest that cancer risk is not reduced by improving glycaemic control in type 2 diabetes. These data therefore do not support the hypothesis that hyperglycaemia is causally linked to increased cancer risk.
Authors: M Monami; D Balzi; C Lamanna; A Barchielli; G Masotti; E Buiatti; N Marchionni; E Mannucci Journal: Diabetes Metab Res Rev Date: 2007-09 Impact factor: 4.876
Authors: Pamela J Goodwin; Kathleen I Pritchard; Marguerite Ennis; Mark Clemons; Margaret Graham; I George Fantus Journal: Clin Breast Cancer Date: 2008-12 Impact factor: 3.225
Authors: Philip D Home; Stuart J Pocock; Henning Beck-Nielsen; Paula S Curtis; Ramon Gomis; Markolf Hanefeld; Nigel P Jones; Michel Komajda; John J V McMurray Journal: Lancet Date: 2009-06-06 Impact factor: 79.321
Authors: Rangaswamy Govindarajan; Luke Ratnasinghe; Debra L Simmons; Eric R Siegel; Madhu V Midathada; Lawrence Kim; Peter J Kim; Randall J Owens; Nicholas P Lang Journal: J Clin Oncol Date: 2007-04-20 Impact factor: 44.544
Authors: Lorenzo Scappaticcio; Maria Ida Maiorino; Giuseppe Bellastella; Dario Giugliano; Katherine Esposito Journal: Endocrine Date: 2016-12-31 Impact factor: 3.633
Authors: Peter Boyle; Alice Koechlin; Cécile Pizot; Mathieu Boniol; Chris Robertson; Patrick Mullie; Geremia Bolli; Julio Rosenstock; Philippe Autier Journal: Eur J Nutr Date: 2012-11-03 Impact factor: 5.614
Authors: Erwin P Klein Woolthuis; Wim J C de Grauw; Susanne M van Keeken; Reinier P Akkermans; Eloy H van de Lisdonk; Job F M Metsemakers; Chris van Weel Journal: Ann Fam Med Date: 2013 Jan-Feb Impact factor: 5.166