JNCI Journal of the National Cancer Institute最新文献

{"title":"RE: Association of radiation-induced normal tissue toxicity with a high genetic risk for rheumatoid arthritis.","authors":"Qu Zheng, Bao-Qiang Dong, Yiyan Han","doi":"10.1093/jnci/djaf144","DOIUrl":"https://doi.org/10.1093/jnci/djaf144","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293685","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of non-steroidal anti-inflammatory medications and aspirin with colorectal cancer incidence in older adults.","authors":"Farzana Y Zaman, Suzanne G Orchard, Galina Polekhina, Peter Gibbs, Wendy B Bernstein, Finlay Macrae, Jeanne Tie, Jeremy Millar, Lucy Gately, Luz María Rodríguez, Gj Van Londen, Victoria Mar, Emma Hiscutt, Nikki Adler, Aaron Kent, Wee Loon Ong, Andrew Haydon, Erica Warner, Andrew T Chan, John Zalcberg","doi":"10.1093/jnci/djaf145","DOIUrl":"https://doi.org/10.1093/jnci/djaf145","url":null,"abstract":"<p><strong>Background: </strong>The relationship between aspirin, and/or other non-steroidal anti-inflammatories (NSAIDs), and colorectal cancer (CRC) risk in older adults is uncertain. This study investigated the association between non-aspirin NSAIDs (NA-NSAIDs) use, alone or combined with aspirin, on CRC incidence in older adults.</p><p><strong>Methods: </strong>This is a post-hoc analysis of ASPREE randomized controlled trial data and its observational continuation, ASPREE-XT (median follow-up, 8.4 years (IQR: 7.2-9.6)). NA-NSAID exposure was ascertained by self-report and medical record review at baseline, for all ASPREE participants, and for Australian participants, via linkage to the Pharmaceutical Benefits Scheme (PBS). CRC was an adjudicated secondary endpoint of ASPREE. We investigated the association between NA-NSAID use alone, and in combination with randomised aspirin use, on the incidence of CRC in time-to-event analyses.</p><p><strong>Results: </strong>Of 19,114 ASPREE participants, 2713 (14%) reported NA-NSAID use at baseline. NA-NSAID use was associated with a reduced incidence of CRC (HR NA-SAID use:Yes vs No = 0.74; 95%CI: 0.56-0.98). This association between NA-NSAIDs and CRC was not modified by aspirin (P-value for interaction term of 0.81). When assessing NA-NSAID use over 2 years post-randomization in Australian participants who consented to the use of PBS data (N = 13,725), a similar reduction in CRC risk was observed (HR High NA-NSAID use vs None = 0.52, 95%CI 0.32-0.83).</p><p><strong>Conclusions: </strong>NA-NSAID use in Australian and American adults over the age of 70 years was associated with a reduced CRC incidence, which increased with increasing exposure. Aspirin did not modify the effect of NA-NSAIDs on CRC incidence.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identifying and mitigating the biological effectors of the social determinants of health in cancer.","authors":"Monica Wagner, Christopher L Benson, Samilia Obeng-Gyasi, Suzanne Conzen, Lauren E Mccullough, Chanita Hughes Halbert, Stanton L Gerson","doi":"10.1093/jnci/djaf141","DOIUrl":"https://doi.org/10.1093/jnci/djaf141","url":null,"abstract":"<p><p>Recognizing the interconnectedness between social determinants of health (SDOH) and biological factors associated with cancer, the research community is working to identify and refine biological markers of SDOH that can help us better understand this complex interaction. The National Academies of Science, Engineering, and Medicine convened a workshop with the intent of exploring this interaction and how these factors affect cancer onset and cancer-related health outcomes1. Workshop presentations and discussions provided an overview of biological effectors and SDOH; emerging research in these areas, including the development and validation of biomarkers and strategies to improve the evidence base for monitoring, diagnosing, policy, research, and clinical practice opportunities to improve health and address the impact of SDOH on cancer risk, diagnosis and outcomes.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284378","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in uterine cancer incidence and mortality: insights from a natural history model.","authors":"William D Hazelton, Matthew Prest, Ling Chen, Kevin Rouse, Elena B Elkin, Jennifer S Ferris, Xiao Xu, Nina B Bickell, Chung Yin Kong, Stephanie Blank, Eric J Feuer, Goli Samimi, Brandy M Heckman-Stoddard, Tracy M Layne, Jason D Wright, Evan R Myers, Laura J Havrilesky","doi":"10.1093/jnci/djaf135","DOIUrl":"https://doi.org/10.1093/jnci/djaf135","url":null,"abstract":"<p><strong>Background: </strong>Uterine cancer incidence and mortality are increasing, with concomitant disparities in outcomes between racial groups. Natural history modeling can evaluate risk factors, predict future trends, and simulate approaches to reducing mortality and disparities.</p><p><strong>Methods: </strong>We designed a natural history model of uterine cancer using a multistage clonal expansion design. The model is informed by National Health and Nutrition Examination Surveys (NHANES), National Health Examination Surveys (NHES), age, period, birth cohort, and birth certificate data on reproductive histories (RH) and body mass index (BMI), and is fit and calibrated to Surveillance, Epidemiology, and End Results (SEER) data by race/ethnicity and histologic subgroup. We projected future incidence and estimated the degree of contribution of BMI, RH, and competing hysterectomy to excess uterine cancer incidence.</p><p><strong>Results: </strong>The model accurately replicated SEER incidence for endometrioid (EM), non-endometrioid (non-EM), and sarcoma subgroups for non-Hispanic Black (NHB) and non-Hispanic White (NHW) patients. For EM, non-EM, and Sarcomas, BMI-attributable risks are greater for NHW than NHB; RH-attributable risks are greater for NHB. Between 2018 and 2050, EM incidence is projected to rise by 64.9% in NHB and17.5% in NHW; non-EM projected rise is 41.4% in NHB and 22.5% in NHW; sarcoma incidence projected increase is 36% in NHB and 29.2% in NHW.</p><p><strong>Conclusions: </strong>Uterine cancer risk is substantially explained by RH and BMI, with differences observed between NHB and NHW and future projections indicating perpetuation of disparities. Lower rates of hysterectomy and rising obesity rates will likely contribute to continued increases in uterine cancer incidence.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to Yin and Dong.","authors":"Tanja Stocks, Josef Fritz","doi":"10.1093/jnci/djaf111","DOIUrl":"https://doi.org/10.1093/jnci/djaf111","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RE:Comparing waist circumference with body mass index on obesity-related cancer risk: a pooled Swedish study.","authors":"Shuting Yin, Jie Dong","doi":"10.1093/jnci/djaf110","DOIUrl":"https://doi.org/10.1093/jnci/djaf110","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Proteogenomic and observational evidence implicate ANGPTL4 as a potential therapeutic target for colorectal cancer prevention.","authors":"James Yarmolinsky, Matthew A Lee, Evelyn Lau, Ferran Moratalla-Navarro, Emma E Vincent, Ruifang Li-Gao, Patrick C N Rensen, Ko Willems van Dijk, Kostas K Tsilidis, Apiwat Sangphukieo, Elmira Ebrahimi, Jochen Hampe, Loïc Le Marchand, Franzel J B van Duijnhoven, Kala Visvanathan, Michael O Woods, Marcela Guevara, Sabina Sieri, Giovanna Masala, Keren Papier, Shama Virani, Tom Dudding, Abbas Dehghan, Alexander G Smith, Dennis Wang, Victor Moreno, Marc J Gunter, Ioanna Tzoulaki","doi":"10.1093/jnci/djaf137","DOIUrl":"https://doi.org/10.1093/jnci/djaf137","url":null,"abstract":"<p><strong>Background: </strong>The role of lipid-perturbing medications in cancer risk is unclear.</p><p><strong>Methods: </strong>We employed cis-Mendelian randomization and colocalisation to evaluate the role of 5 lipid-perturbing drug targets (ANGPTL3, ANGPTL4, APOC3, CETP, PCSK9) in risk of 5 cancers (breast, colorectal, head and neck, ovarian, prostate). We triangulated findings using pre-diagnostic protein measures in prospective analyses in EPIC (977 colorectal cancer cases, 4,080 sub-cohort members) and the UK Biobank (860 colorectal cancer cases, 50,177 controls). To gain mechanistic insight into the role of ANGPTL4 in carcinogenesis, we examined the impact of the ANGPTL4 p.E40K loss-of-function variant on differential gene expression in normal colon tissue in BarcUVa-Seq. Finally, we evaluated the association of colon tumour ANGPTL4 expression with cancer-specific mortality in TCGA.</p><p><strong>Results: </strong>In analysis of 78,473 cases and 107,143 controls, genetically-proxied circulating ANGPTL4 inhibition was associated with reduced colorectal cancer risk (ORSD decrease: 0.76,95%CI:0.66-0.89,P=5.52x10-4,PPcolocalisation=0.83). This association was replicated using pre-diagnostic circulating ANGPTL4 concentrations in EPIC (HRlog10 decrease:0.91,95%CI:0.84-0.98,P=0.01) and the UK Biobank (HRSD decrease:0.93,95%CI:0.86-0.99,P=0.03). In gene-set enrichment analysis of differential gene expression in 445 colon tissue samples, ANGPTL4 loss-of-function down-regulated several cancer-related biological pathways (P  FDR<0.05), including those involved in cellular proliferation, epithelial-to-mesenchymal transition, and bile acid metabolism. In analysis of 465 colon cancer patients, lower ANGPTL4 tumour expression was associated with reduced colorectal cancer-specific mortality risk (HRlog2 decrease:0.66,95%CI:0.50-0.87,P=2.92x10-3).</p><p><strong>Conclusions: </strong>Our integrative proteogenomic and observational analyses suggest a potential protective role of lower circulating ANGPTL4 concentrations in colorectal cancer risk. These findings support further evaluation of ANGPTL4 as a therapeutic target for colorectal cancer prevention.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: The association of where patients with prostate cancer live and receive care on racial treatment inequities.","authors":"","doi":"10.1093/jnci/djaf142","DOIUrl":"https://doi.org/10.1093/jnci/djaf142","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Suppression of LKB1-mutant lung adenocarcinoma by natural killer cells from females.","authors":"Yijian Fan, Rui Jin, Lenore Monterroza, Xiuju Liu, Chunzi Huang, Angelo Marra, Xiulei Mo, Haian Fu, Melissa Gilbert-Ross, Adam I Marcus, Rabindra Tirouvanziam, Yuan Liu, Frank Schneider, Wei Zhou","doi":"10.1093/jnci/djaf138","DOIUrl":"https://doi.org/10.1093/jnci/djaf138","url":null,"abstract":"<p><strong>Background: </strong>This study addressed the enigma of sex differences in smoking-related lung cancer, particularly focusing on the low LKB1 mutation frequency in female patients with lung adenocarcinoma (LUAD).</p><p><strong>Methods: </strong>Sex-bias was studied with a genetically engineered mouse model and various tail-vein injection models. Immune cells were analyzed by antibody-depletion study, flow cytometry, and immunofluorescence. The relevance of our findings to human disease was validated by evaluating various LUAD datasets. All statistical tests are 2-sided.</p><p><strong>Results: </strong>A significant percentage of females are resistant to LKB1-mutant tumor formation in our models, reflecting this sex difference in humans. NK cells were identified as a critical factor in this sex-biased response. This sex difference was observed primarily in LKB1-mutant LUADs, probably due to their low MHC-I level, making them the ideal target for NK cells through the \"missing-self\" recognition. While females resistant to LKB1-mutant LUAD formation did not have enhancement of any specific NK subpopulation, our immunofluorescence analysis revealed high numbers of NKs in female lungs even with the presence of LKB1-mutant LUAD. Our GSEA analysis of TCGA-LUAD dataset also showed that female LKB1-mutant LUAD patients have a stronger NK-mediated response after adjusting for other male-female differences using LKB1-wild type LUAD dataset.</p><p><strong>Conclusion: </strong>Females have a stronger NK-mediated response against LKB1-mutant LUAD, which was present both in our mouse model and the human LUAD dataset. This study revealed a novel role of NK cells in suppressing LKB1-mutant LUAD in females, which should be assessed in the clinical setting in the future.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144284382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mental disorders and socioeconomic outcomes in women with cervical cancer, their children and co-parents.","authors":"Jiangrong Wang, Stina Salomonsson, Demet Sönmez, Sara Nordqvist Kleppe, Adina L Feldman, Marcus Sven Andersson, Goran Bencina, Fang Fang, Karin Sundström","doi":"10.1093/jnci/djaf129","DOIUrl":"https://doi.org/10.1093/jnci/djaf129","url":null,"abstract":"<p><strong>Background: </strong>Cervical cancer often affects women who are in the middle of life and may carry substantial mental and socioeconomic impact also on families. We performed a generation-spanning study to elucidate this burden.</p><p><strong>Methods: </strong>We utilized nationwide registers during 1991-2018 in Sweden to perform two matched cohort studies based on a source population of more than 5 million women. The individual sub-study included 6060 cases of cervical cancer diagnosed during 2006-2018 and 5 population comparators individually matched to each case by age, birth year and region (n = 30300). The family sub-study included 9332 cases of cervical cancer diagnosed during 1991-2016 and 45,674 matched population comparators and all their children and co-parents.</p><p><strong>Results: </strong>We found an increased risk for mental disorders in cases compared to comparators, particularly during the first two years post-diagnosis (HR = 3.74, 95% CI = 3.45-4.06). Socioeconomic status changed negatively in cases after their diagnosis a decreased income and increased need for financial aid appeared within 2 years whereas unemployment escalated from two years after cancer diagnosis. We further found an increased risk of mental disorders in both children and co-parents of the cases, compared to the children and co-parents of the comparators.Furthermore, we observed negative socioeconomic trajectories in the co-parents and lower educational attainment in the children of the cases, especially if the case had died of her cancer.</p><p><strong>Conclusions: </strong>Women with cervical cancer, and their close family members, display increased risk of negative mental health and socioeconomic outcomes after diagnosis. The lower educational attainment in children appears particularly worrying.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":9.9,"publicationDate":"2025-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}