{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T20:15:28Z","timestamp":1792700128193,"version":"4.5.0"},"reference-count":43,"publisher":"Oxford University Press (OUP)","issue":"3","funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000016","name":"Department of Health and Human Services","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000016","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000054","name":"National Cancer Institute","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100000054","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["75N910D00024"],"award-info":[{"award-number":["75N910D00024"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>The associations between different types of diabetes, characterized by distinct pathophysiology and genetic architecture, and pancreatic ductal adenocarcinoma (PDAC) risk are not understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We investigated associations of genetic susceptibility to type 2 diabetes (T2D), 8 T2D mechanistic clusters, type 1 diabetes (T1D), and maturity-onset diabetes of the young (MODY) with PDAC risk. We used genome-wide association study (GWAS) summary-level statistics for T2D (242\u00a0283 cases, 1\u00a0569\u00a0734 controls), T1D (18\u00a0942 cases, 501\u00a0638 controls), and PDAC (10\u00a0244 cases and 360\u00a0535 controls) in individuals of European ancestry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Two-sample Mendelian randomization (MR) using the Robust Adjusted Profile Score (MR-RAPS) method indicated that genetically predicted T2D was associated with PDAC risk (OR\u2009=\u20091.10; 95% CI = 1.05 to 1.15), particularly the T2D obesity (OR\u2009=\u20091.28; 95% CI = 1.15 to 1.42) and lipodystrophy (OR\u2009=\u20091.25; 95% CI = 1.03 to 1.51) clusters. No association was observed for T1D with PDAC risk (OR\u2009=\u20091.01; 95% CI = 0.99 to 1.02). Pathway\/gene-set analysis using the summary-based Adaptive Rank Truncated Product (sARTP) method revealed a significant association between the MODY gene-sets and PDAC risk (P\u2009=\u20091.5\u2009\u00d7\u200910\u22128), which remained after excluding 20 known PDAC GWAS loci (P\u2009=\u20097.6\u2009\u00d7\u200910\u22124). HNF1A, FOXA3, and HNF4A were the top contributing genes after excluding the previously identified GWAS loci regions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our results from this genetic association study support that T2D, particularly the obesity and lipodystrophy mechanistic clusters, and MODY genomic susceptibility regions play a role in the etiology of PDAC.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/jnci\/djaf308","type":"journal-article","created":{"date-parts":[[2025,11,8]],"date-time":"2025-11-08T12:54:56Z","timestamp":1762606496000},"page":"437-447","source":"Crossref","is-referenced-by-count":4,"title":["Different diabetes types and pancreatic ductal adenocarcinoma: a Mendelian randomization and pathway\/gene-set analysis"],"prefix":"10.1093","volume":"118","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9862-9434","authenticated-orcid":false,"given":"Ting","family":"Zhang","sequence":"first","affiliation":[{"name":"Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Rockville, MD,","place":["United States"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xing","family":"Hua","sequence":"additional","affiliation":[{"name":"Division of Cancer Epidemiology and Genetics, National Cancer Institute, National Institutes of Health , Rockville, MD,","place":["United States"]},{"name":"Cancer Genomics Research Laboratory, Frederick National Laboratory for Cancer Research, Leidos Biomedical Research Inc , Rockville, MD,","place":["United 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