{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,7]],"date-time":"2026-11-07T01:36:33Z","timestamp":1794015393422,"version":"4.8.0"},"reference-count":64,"publisher":"American Medical Association (AMA)","issue":"11","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Oncol"],"published-print":{"date-parts":[[2025,11,1]]},"abstract":"<jats:sec id=\"ab-coi250054-4\">\n                    <jats:title>Importance<\/jats:title>\n                    <jats:p>The oral microbiota may be involved in the development of pancreatic cancer, yet current evidence is largely limited to bacterial 16S amplicon sequencing and small retrospective case-control studies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-5\">\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To test whether the oral bacterial and fungal microbiome is associated with the subsequent development of pancreatic cancer.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-6\">\n                    <jats:title>Design, Setting, and Participants<\/jats:title>\n                    <jats:p>This cohort study used data from 2 epidemiological cohorts: the American Cancer Society Cancer Prevention Study-II Nutrition Cohort and the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Among cohort participants who provided oral samples, those who prospectively developed pancreatic cancer were identified during follow-up. Control participants who remained free of cancer were selected by 1:1 frequency matching on cohort, 5-year age band, sex, race and ethnicity, and time since oral sample collection. Data were collected from August 2023 to September 2024, and data were analyzed from August 2023 to January 2025.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-7\">\n                    <jats:title>Exposures<\/jats:title>\n                    <jats:p>\n                      The oral bacterial and fungal microbiome were characterized via whole-genome shotgun sequencing and internal transcribed spacer (ITS) sequencing, respectively. The association of periodontal pathogens of the red complex (\n                      <jats:italic>Treponema denticola<\/jats:italic>\n                      ,\n                      <jats:italic>Porphyromonas gingivalis<\/jats:italic>\n                      , and\n                      <jats:italic>Tannerella forsythia<\/jats:italic>\n                      ) and orange complex (\n                      <jats:italic>Fusobacterium nucleatum<\/jats:italic>\n                      ,\n                      <jats:italic>F periodonticum<\/jats:italic>\n                      ,\n                      <jats:italic>Prevotella intermedia<\/jats:italic>\n                      ,\n                      <jats:italic>P nigrescens<\/jats:italic>\n                      ,\n                      <jats:italic>Parvimonas micra<\/jats:italic>\n                      ,\n                      <jats:italic>Eubacterium nodatum<\/jats:italic>\n                      ,\n                      <jats:italic>Campylobacter shower<\/jats:italic>\n                      , and\n                      <jats:italic>C gracilis<\/jats:italic>\n                      ) with pancreatic cancer was tested via logistic regression. The association of the microbiome-wide bacterial and fungal taxa with pancreatic cancer was assessed by Analysis of Compositions of Microbiomes With Bias Correction 2 (ANCOM-BC2). Microbial risk scores (MRS) for pancreatic cancer were calculated from the risk-associated bacterial and fungal species.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-8\">\n                    <jats:title>Main Outcomes and Measures<\/jats:title>\n                    <jats:p>Pancreatic cancer incidence.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-9\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Of 122\u202f000 cohort participants who provided samples, 445 developed pancreatic cancer over a median (IQR) follow-up of 8.8 (4.9-13.4) years and were matched with 445 controls. Of these 890 participants, 474 (53.3%) were male, and the mean (SD) age was 67.2 (7.5) years. Three oral bacterial periodontal pathogens\u2014\n                      <jats:italic>P gingivalis<\/jats:italic>\n                      ,\n                      <jats:italic>E nodatum<\/jats:italic>\n                      , and\n                      <jats:italic>P micra<\/jats:italic>\n                      \u2014were associated with increased risk of pancreatic cancer. A bacteriome-wide scan revealed 8 oral bacteria associated with decreased and 13 oral bacteria associated with increased risk of pancreatic cancer (false discovery rate\u2013adjusted Q statistic less than .05). Of the fungi, genus\n                      <jats:italic>Candida<\/jats:italic>\n                      was associated with increased risk of pancreatic cancer. The MRS, based on 27 oral species, was associated with an increase in pancreatic cancer risk (multivariate odds ratio per 1-SD increase in MRS, 3.44; 95% CI, 2.63-4.51).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"ab-coi250054-10\">\n                    <jats:title>Conclusions and Relevance<\/jats:title>\n                    <jats:p>In this cohort study, oral bacteria and fungi were significant risk factors for pancreatic cancer development. Oral microbiota hold promise as biomarkers to identify individuals at high risk of pancreatic cancer, potentially contributing to personalized prevention.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1001\/jamaoncol.2025.3377","type":"journal-article","created":{"date-parts":[[2025,9,18]],"date-time":"2025-09-18T15:01:20Z","timestamp":1758207680000},"page":"1331","source":"Crossref","is-referenced-by-count":41,"title":["Oral Bacterial and Fungal Microbiome and Subsequent Risk for Pancreatic Cancer"],"prefix":"10.1001","volume":"11","author":[{"given":"Yixuan","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Population Health, NYU Grossman School of Medicine, New York, New York"},{"name":"NYU Laura and Isaac Perlmutter Cancer Center, New York, New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Feng","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Population Health, NYU Grossman School of Medicine, New 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