Genes and Environment最新文献

{"title":"Multi-omics insights into the mechanisms and prognosis of IPF.","authors":"Dong Chen, Qianwei Chen, Honghui Liu, Zhoutong Wang, Xinyu Liu, Juan Hu, Chao Lu","doi":"10.1186/s41021-026-00364-0","DOIUrl":"10.1186/s41021-026-00364-0","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) represents another progressive and devastating interstitial lung disease found across populations, with a prominent male predominance accounting for approximately 70% of cases. Regional variation in IPF-related genetic polymorphisms, especially in the Americas, Europe, and Asia, points to a hereditary basis. Family history is the main risk factor. Rare mutations may alter outcomes through gene interactions. Environmental factors such as smoking can worsen genetic risk by epigenetic mechanisms like DNA methylation. Unlike studies that focus narrowly on specific genetic variants or processes, this study integrates the genetic variation map, multi-omics regulatory networks, and the effects of environmental exposures in IPF. This links clinical decision-making and gene discovery. This study examines mechanisms, therapies, and prognoses to clarify the impact of epigenetics and genetics on disease development. It also proposes using a multi-gene risk score (MGRS) to predict outcomes and design targeted treatments. The research advances the translation of basic knowledge into therapies. Theoretical and clinical support can aid doctors treating IPF.Clinical trial numberNot applicable.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"48 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13621748/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149074314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aflatoxin exposure and health impacts: global burden and advances in detection technologies.","authors":"Gudisa Bereda","doi":"10.1186/s41021-026-00363-1","DOIUrl":"10.1186/s41021-026-00363-1","url":null,"abstract":"<p><strong>Background and aims: </strong>Aflatoxins are food contaminants that cause exposure and adverse health effects and are detected using modern analytical methods. This review summarizes global aflatoxin exposure levels, exposure routes, associated health effects, and detection technologies.</p><p><strong>Methods: </strong>This narrative review was guided by the Scale for the Assessment of Narrative Review Articles (SANRA) framework. Relevant literature was retrieved from PubMed, Scopus, Web of Science, and Google Scholar. Studies addressing aflatoxin exposure, health effects, and detection technologies were included and qualitatively synthesized.</p><p><strong>Results: </strong>This review showed that in Côte d'Ivoire, peanut paste had 100% AFB1 contamination, with levels of 4535 µg/kg (AFB1) and 8094 µg/kg (total aflatoxins), and 99% of samples exceeded European Union limits. Dietary intake is the main route of exposure (0.3-180 ng/kg/day), with additional exposure via prenatal transfer, breastfeeding (0.01-0.55 ng/mL AFM1), and complementary feeding. Biomarkers show high aflatoxin exposure: 97% (Malaysia) and 94% (pregnant women in Nepal; 0.45-2939.30 pg/mg). Aflatoxin exposure is responsible for 4.6-28.2% of global hepatocellular carcinoma cases, contributes to approximately 250,000 deaths annually, and is associated with a 2-4-fold higher risk of cancer in children. High-performance liquid chromatography coupled with fluorescence detection (HPLC-FLD) is widely used, while Liquid chromatography-tandem mass spectrometry (LC-MS/MS) is the gold standard (< 1 ng/mL). Electrochemical immunosensors reach 0.3 pg/mL, and lateral flow assays provide rapid but less sensitive screening.</p><p><strong>Conclusion: </strong>Aflatoxin exposure is a major global public health concern. Improved detection methods and food safety measures are essential to reduce exposure and disease burden.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"48 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13425974/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148648457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Application of chimeric mice with human hepatocytes for the evaluation of metabolically activated genotoxic substances.","authors":"Mayu Fujikawa, Ryoko Matsuyama, Chihiro Yamasaki, Chise Tateno, Hiroyuki Asano","doi":"10.1186/s41021-026-00362-2","DOIUrl":"10.1186/s41021-026-00362-2","url":null,"abstract":"<p><strong>Background: </strong>The in vivo micronucleus (MN) assay is used for evaluation of chromosomal aberration induced by chemicals, and the liver MN assay can detect genotoxic compounds which require metabolic activation to induce micronucleus formation. However, species differences in liver metabolism are known, and therefore results obtained from mouse and rat liver MN assays may not always be directly extrapolated to humans. Chimeric mouse with human hepatocytes (the PXB-mouse®) is expected to be used in genotoxicity studies as an animal model of metabolic reactions in humans. To date, the use of the liver MN assay with PXB-mice has been reported, but its application has been limited to compounds that do not require metabolic activation to induce chromosomal aberrations.</p><p><strong>Results: </strong>In this study, we used the liver MN assay in PXB-mice to evaluate diethylnitrosamine (DEN) and N-nitrosodimethylamine (NDMA), both of which require metabolic activation to induce chromosomal aberrations. After repeated administration of DEN for 14 days or NDMA for 28 days, statistically significant increases in micronucleus frequency were observed.</p><p><strong>Conclusion: </strong>From the results of this examination, it was demonstrated that the liver MN assay using PXB-mice can detect the genotoxicity of compounds that require metabolic activation to exert genotoxicity. Although some issues remain, such as the presence of residual mouse hepatocytes, the liver MN assay using PXB-mice is expected to provide supportive information for more accurate evaluation of chemical genotoxicity in humans.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13435476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148283491","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanistic investigation of flavonoid-mediated inhibition of N-methyl-N-nitrosourea-induced mutagenicity via noncovalent DNA binding.","authors":"Chisato Matsuoka, Nao Takatama, Takuya Muraoka, Keiko Inami","doi":"10.1186/s41021-026-00361-3","DOIUrl":"10.1186/s41021-026-00361-3","url":null,"abstract":"<p><strong>Background: </strong>Previous research using the Ames assay showed that licoricidin (LCD) and isoliquiritigenin (ILTG) can block mutations caused by N-methyl-N-nitrosourea (MNU) in Salmonella typhimurium (S. typhimurium) TA1535. With the aim to clarify the antimutagenic mechanism of these flavonoids, we evaluated the noncovalent interactions of test compounds (LCD, ILTG, ethidium bromide (EtBr), or Hoechst 33258) with calf thymus DNA (ctDNA) using a UV-Vis spectrophotometer and quantified the DNA adducts formed when treated with a mixture of MNU and the test compounds. Additionally, we measured the half-life of MNU and the amount of each test compound remaining in the reaction mixture.</p><p><strong>Results: </strong>The spectral and thermodynamic parameters indicated considerable binding between flavonoids (LCD and ILTG) and DNA. Intercalative EtBr and the minor-groove binder Hoechst 33258 inhibited MNU-induced mutagenicity in S. typhimurium TA1535. O⁶-Methylguanine (O⁶-MeG) and N³-methyladenine (N³-MeA) were quantified in a mixture of ctDNA and the test compounds (LCD, ILTG, EtBr, and Hoechst 33258) using LC‒MS/MS. The amount of the DNA adducts decreased with increasing concentrations of the compounds. Moreover, the half-lives of MNU were similar in the presence and absence of flavonoids (LCD and ILTG). No new products were detected, and no significant changes in the flavonoids remaining in the reaction mixture were observed, indicating that LCD and ILTG did not react directly with MNU.</p><p><strong>Conclusions: </strong>LCD and ILTG directly bind to DNA and suppress DNA adduct formation. However, interaction with DNA alone does not fully account for their antimutagenic activity, implying the involvement of other mechanisms.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13276938/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148217358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A PUFA-rich diet increases endogenous genotoxic stress and mitochondrial DNA damage in mice.","authors":"Masatomi Shimizu, Ayako Daizo, Kenichi Kawada, Masayo Ikeda, Petr Grúz","doi":"10.1186/s41021-026-00360-4","DOIUrl":"10.1186/s41021-026-00360-4","url":null,"abstract":"<p><strong>Background: </strong>Substitution of dietary saturated fat with seed oils highly enriched in n-6 polyunsaturated fatty acids (PUFAs) has been advocated as healthy strategy to offset elevated cholesterol levels. However, both n-6 as well as n-3 PUFAs, considered essential because vertebrates lack the enzymatic apparatus for their de novo synthesis, are the main source of endogenous DNA damage during the aging process due to their high oxidizability. The membrane pacemaker theory of aging is an extension to the oxidative theory of aging and postulates that higher PUFA content in membrane lipids determines the lifespan of different species.</p><p><strong>Objective: </strong>We have examined whether a saturated fat-rich diet lacking the essential fatty acids versus a PUFA-rich diet differentially affects lipid profiles and membrane fatty-acid composition, as well as markers of oxidative protein and DNA damage and mitochondrial DNA (mtDNA) integrity in vivo.</p><p><strong>Methods: </strong>Three-week-old male C57BL/6J mice were fed isocaloric, high-fat diets containing either coconut oil (SFA-rich) or soybean oil (PUFA-rich) for 12 weeks. Plasma and liver lipids were measured, and the fatty acid composition was analyzed in liver and erythrocyte membranes. Endogenous DNA damage was assessed using 1,N⁶-etheno-2'-deoxyadenosine (εdA) detection in blood and liver. mtDNA damage and lipid peroxidation derived protein adducts from liver were also examined.</p><p><strong>Results: </strong>Mice were maintained on a SFA-rich diet for 12 weeks without exhibiting any symptoms of essential fatty acid deficiency (EFAD) as described in historical literature despite the massive synthesis of compensatory n-9 PUFAs. Furthermore, EFAD mice showed reduced levels of endogenous εdA and mtDNA damage as well as protein adducts originating from the primary n-6 PUFA lipid peroxidation product, 4-hydroxy-2-nonenal. However, some other lipid peroxidation-derived protein adducts, such as malondialdehyde and, surprisingly, 4-hydroxy-2-hexenal, were elevated on a SFA-rich diet.</p><p><strong>Conclusions: </strong>A PUFA-rich diet, relative to the SFA-rich diet, is associated with increased lipid-peroxidation linked adducts and a greater degree of mtDNA damage in vivo, in parallel with membrane enrichment in n-6 PUFA. These findings provide clear evidence of the biological effects of a PUFA-rich diet on endogenous genotoxic stress.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13244832/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987369","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A report on the international conference on environmental mutagenesis in relation to human health held during the annual meeting of the Environmental Mutagen Society of India, January 29-31, 2026.","authors":"Bani Bandana Ganguly","doi":"10.1186/s41021-026-00359-x","DOIUrl":"10.1186/s41021-026-00359-x","url":null,"abstract":"<p><p>The 48th Annual Meeting and International Conference of the Environmental Mutagen Society of India (EMSI) on 'Environmental Mutagenesis & Epigenomics in Relation to Human Health' was held at Jamshedpur Co-Operative College, in association with Kolhan University, Jharkhand, India, from January 29-31, 2026. There were 141 deliberations in total, with participation from researchers, academicians, Vice-Chancellors, and state government officials from India and eight other countries. The scientific topics, including environmental impact on humans and aquaculture, transgenerational plant protection, molecular insights into cancer research, plants with antimutagenic potential, and sustainable agriculture through the use of bio-pesticides and bio-fertilizers, broadly justified the conference theme. The molecular mechanisms of pathogenesis were discussed through lectures on signalling pathways, gene expression, and DNA damage and repair, highlighting targeted drug development. Additionally, in silico docking of synthetic drugs and nanoparticles was discussed in detail. Notably, nanotoxicology, microplastics, airborne particulate matter, and prenatal arsenic exposure were shown to have a significant impact on human health. As Jharkhand and neighbouring states depend largely on agricultural yield, discussions on the use of plant-based medicines, harnessing infection and immunity, and agricultural eco-toxicology suggested ways to protect farmers' health and the food chain from the overuse of chemicals. Altogether, the deliberations supported several Sustainable Development Goals and highlighted cost-effective agricultural modalities. These messages were disseminated to the public through local media via daily briefings. Notably, this EMSI conference provided a platform for scientific exchange that attracted administrators and pollution control regulators aimed at protecting human health by mitigating environmental exposure.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"48 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13173872/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147941152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential for Computational Genotoxicity: A Report on Symposium 3 of the 53rd Annual Meeting of the Japanese Environmental Mutagen and Genome Society (JEMS), 2024.","authors":"Naoki Koyama, Ayako Furuhama, Naomi L Kruhlak, Nicolas Ken Shinada, Kazuki Izawa","doi":"10.1186/s41021-026-00358-y","DOIUrl":"10.1186/s41021-026-00358-y","url":null,"abstract":"<p><p>Symposium 3 of the 53rd Annual Meeting of the Japanese Environmental Mutagen and Genome Society (JEMS), entitled \"Potential for Computational Genotoxicity,\" was held at Shujitsu University, Okayama, Japan, on December 8, 2024. The symposium discussed the application of advanced informatics technologies, such as (quantitative) structure-activity relationship ((Q)SAR) and error-corrected next-generation sequencing (ecNGS), to the field of genotoxicity within the framework of computational genotoxicity. In this symposium, we invited three scientists who are global leaders in the field of computational genotoxicity. This report summarizes the key discussions and presentations from the symposium. The organizers hope this summary will increase awareness of computational genotoxicity.</p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":"48 1","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12980948/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147443387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A genome-wide interaction study of thyroid-stimulating hormone levels and particulate matter exposure among Koreans.","authors":"Young Jun Park, Hyun-Jin Kim, Ho-Young Son, Juhyun Kim, Jae Moon Yun, Hyuktae Kwon, Belong Cho, Jin-Ho Park, Jong-Il Kim","doi":"10.1186/s41021-026-00357-z","DOIUrl":"10.1186/s41021-026-00357-z","url":null,"abstract":"<p><p>BACKGROUND: Although the associations between air pollution exposure and thyroid function have been reported, the interactive effects of the genes involved remain unknown. Therefore, we aimed to identify candidate genetic loci involved in thyroid function by interacting with annual average exposure to particulate matter with a diameter of 10 microns or smaller (PM10) in Korean adults. A total of 1,863 and 1,458 adults were included in the discovery and replication steps, respectively. The average annual concentration of PM10 exposure was considered, and the participants were classified into two groups (low-to-moderate exposure and high-exposure groups) for binary analyses. A genome-wide single-nucleotide polymorphism analysis using a PM10 exposure interaction study was performed to determine thyroid-stimulating hormone levels in Korean adults. RESULTS: Although no SNPs surpassed the stringent genome-wide significance threshold of Pint < 5E-08, one SNP (rs11781213) near MSRA reached a suggestive level of significance of Pint < 5E-07. Two genetic susceptibility loci (FAM84B/PCAT1 and STARD13) were replicated at a nominal significance level of Pint < 1E-05 for the discovery cohort, and Pint < 0.05 for the replication cohort. A genetic variant (rs7169081 G > A) between CGNL1 and GCOM1 was of functional interest. CONCLUSIONS: This is the first study reporting genome-wide-air pollution interaction results for thyroid function. The association between long-term PM10 exposure and thyroid hormone levels may be partly explained by identifying several suggestive loci, including MSRA, PCAT1, and GCOM1. </p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13041225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147365005","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In vivo mammalian micronucleus test in mice confirms lack of genotoxic potential of a protein-rich powder derived from Xanthobacter sp. SoF1.","authors":"Bean Choi, John R Endres, Amy Clewell, Gábor Hirka, Erzsébet Béres","doi":"10.1186/s41021-026-00356-0","DOIUrl":"10.1186/s41021-026-00356-0","url":null,"abstract":"<p><p>BACKGROUND: The growing interest and demand for alternative protein sources has propelled research and production of protein-rich microbial biomass products for human consumption. The potential genotoxicity of a protein-rich biomass derived from Xanthobacter sp. SoF1 (SoF1), an autotrophic hydrogen-oxidizing bacteria, was evaluated in the bone marrow of male NMRI mice in the current work. This study was conducted as the final step of a comprehensive toxicological safety assessment that has been previously published. While a genotoxic evaluation including a bacterial reverse mutation test, an in vitro chromosomal aberration assay in human lymphocytes, and an in vitro micronucleus test in human lymphocytes was previously conducted without incidence, an in vivo mammalian micronucleus test was lacking and thus, this study was performed to provide additional relevant in vivo insights into the genotoxicity of SoF1. RESULTS: No treatment-related adverse effects were observed and no increases in the frequencies of micronucleated immature erythrocytes (MPCEs) in male mice (5/group) at any dose level (0, 500, 1000, and 2000 mg/kg bw) of the test item by oral gavage were observed when compared with the concurrent negative and historical negative control groups. CONCLUSION: The test item did not exhibit any clastogenic or aneugenic activity in the bone marrow of mice under the applied experimental conditions. </p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13001180/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ellagic acid is associated with reduced pancreatic carcinogenesis and modulation of the IL-6/STAT3 pathway.","authors":"Hiroyuki Kato, Aya Naiki-Ito, Masayuki Komura, Yuko Nagayasu, Motonori Sato, Xiaochen Kuang, Aya Nagano, Satoru Takahashi","doi":"10.1186/s41021-026-00353-3","DOIUrl":"10.1186/s41021-026-00353-3","url":null,"abstract":"<p><p>BACKGROUND: The 5-year survival of pancreatic ductal adenocarcinoma (PDAC) remains about 10% despite therapeutic advances, underscoring the need for effective preventive and early intervention strategies. Ellagic acid (EA), a naturally occurring polyphenol, has been associated with demonstrated antitumor activity in several malignancies. However, its potential role in preventing PDAC development remains unclear. In this study, we examined the chemopreventive potential and underlying mechanisms of EA in a hamster model of PDAC induced by a high-fat diet and N-nitrosobis(2-oxopropyl)amine. RESULTS: Dietary EA (0.1% w/w) was associated with significantly reduction in both the incidence and multiplicity of PDACs compared to controls. The proportion of histologically normal pancreatic ducts increased and the Ki-67 labeling index decreased in pancreatic intraepithelial neoplasia (PanIN) following EA exposure. In vitro, cell proliferation decreased in a dose-dependent manner, G1 arrest was induced, and invasion was diminished after EA treatment. Multiplex Western blotting revealed lower inhibition of the IL-6/STAT3 pathway. The proportion of pSTAT3-positive cells in hamster PanINs and PDACs was significantly lower in the EA-treated groups than in controls. Because a high-fat diet is known to elevate adipocytokines, and resistin (Res) has been implicated in STAT3 regulation, the Res/STAT3 axis was also examined. Res-associated promotion of invasion was observed but there was no proliferation in vitro, and pSTAT3 expression did not increase. Similarly, serum Res levels did not differ significantly across groups, suggesting a limited contribution of the Res/STAT3 pathway in this hamster model. CONCLUSIONS: EA treatment was associated with reduced pancreatic carcinogenesis in vivo. The IL-6/STAT3 pathway appears to be a primary molecular target under our experimental conditions, whereas the contribution of Res is likely minimal. These findings support the potential of EA as a preventive agent against pancreatic cancer. </p>","PeriodicalId":12709,"journal":{"name":"Genes and Environment","volume":" ","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964673/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147343811","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}