{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:09:43Z","timestamp":1790172583773,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2019,12,19]],"date-time":"2019-12-19T00:00:00Z","timestamp":1576713600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[2020,8]]},"abstract":"<jats:p>Myotonic dystrophy type I (DM1) is an autosomal dominant multisystem disorder characterized by myotonia and muscle weakness. Type 2 diabetes (T2D) and cancer have been shown to be part of the DM1 phenotype. Metformin, a well\u2010established agent for the management of T2D, is thought to have cancer\u2010preventive effects in the general population. In our study, we aimed to assess the association between T2D, metformin use and the risk of cancer in DM1 patients. We identified a cohort of 913 DM1 patients and an age\u2010, sex\u2010 and clinic\u2010matched cohort of 12,318 DM1\u2010free controls from the UK Clinical Practice Research Datalink, a large primary care records database. We used Cox regression models to assess cancer risk in T2D patients who were metformin users or nonusers compared to patients without T2D. Separate analyses were conducted for DM1 patients and controls. T2D was more prevalent in DM1 than in controls (8% <jats:italic>vs<\/jats:italic>. 3%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.0001). DM1 patients with T2D, compared to those without T2D, were more likely to develop cancer (hazard ratio [HR] = 3.60, 95% confidence interval [CI] = 1.18\u201310.97; <jats:italic>p<\/jats:italic> = 0.02), but not if they were treated with metformin (HR = 0.43, 95% CI = 0.06\u20133.35; <jats:italic>p<\/jats:italic> = 0.42). Among controls, we observed no significant associations between T2D and cancer risk in either users or nonusers of Metformin (HR = 1.28, 95% CI = 0.91\u20131.79; <jats:italic>p<\/jats:italic> = 0.16 and HR = 1.13, 95% CI = 0.72\u20131.79; <jats:italic>p<\/jats:italic> = 0.59, respectively). These results show an association between T2D and cancer risk in DM1 patients and may provide new insights into the possible benefits of Metformin use in DM1.<\/jats:p>","DOI":"10.1002\/ijc.32801","type":"journal-article","created":{"date-parts":[[2019,11,21]],"date-time":"2019-11-21T04:06:05Z","timestamp":1574309165000},"page":"785-792","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Diabetes, metformin and cancer risk in myotonic dystrophy type I"],"prefix":"10.1002","volume":"147","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-5043-8789","authenticated-orcid":false,"given":"Rotana","family":"Alsaggaf","sequence":"first","affiliation":[{"name":"Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute  Bethesda MD"},{"name":"Department of Epidemiology and Public Health University of Maryland  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7791-2698","authenticated-orcid":false,"given":"Ruth M.","family":"Pfeiffer","sequence":"additional","affiliation":[{"name":"Biostatistics Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute  Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5841-4183","authenticated-orcid":false,"given":"Youjin","family":"Wang","sequence":"additional","affiliation":[{"name":"Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute  Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Diane Marie M.","family":"St. George","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Public Health University of Maryland  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min","family":"Zhan","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Public Health University of Maryland  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathryn R.","family":"Wagner","sequence":"additional","affiliation":[{"name":"Hugo W. Moser Research Institute at Kennedy Krieger Institute  Baltimore MD"},{"name":"Departments of Neurology and Neuroscience Johns Hopkins University School of Medicine  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1193-877X","authenticated-orcid":false,"given":"Sania","family":"Amr","sequence":"additional","affiliation":[{"name":"Department of Epidemiology and Public Health University of Maryland  Baltimore MD"},{"name":"Marlene and Stuart Greenebaum Comprehensive Cancer Center University of Maryland  Baltimore MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark H.","family":"Greene","sequence":"additional","affiliation":[{"name":"Clinical Genetics Branch, Division of Cancer Epidemiology and Genetics National Cancer Institute  Bethesda MD"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shahinaz M.","family":"Gadalla","sequence":"additional","affiliation":[{"name":"Clinical Genetics 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