JNCI Journal of the National Cancer Institute最新文献

{"title":"Spectrum of cancer risk in Asian American and Pacific Islander solid organ transplant recipients.","authors":"Jun Tao, Jaimie Z Shing, Kelly J Yu, Aimée R Kreimer, Mei-Chin Hsieh, Karen S Pawlish, Jie Li, Baozhen Qiao, Judy R Rees, Kekoa Taparra, Jacqueline B Vo, Eric A Engels","doi":"10.1093/jnci/djaf069","DOIUrl":"10.1093/jnci/djaf069","url":null,"abstract":"<p><strong>Background: </strong>Solid organ transplant recipients (SOTRs) have increased cancer risk, which may differ across racial groups. Cancer risk among Asian American and Pacific Islander SOTRs is ill-defined.</p><p><strong>Methods: </strong>We evaluated Asian, Pacific Islander, and White SOTRs from a linkage of the United States SOTR registry with 34 cancer registries (1990-2019). We calculated age- and sex-adjusted incidence rate ratios (aIRRs) to compare cancer risk between races and standardized incidence ratios (SIRs) to measure risk relative to race-matched general populations.</p><p><strong>Results: </strong>Compared with Asian SOTRs, Pacific Islander SOTRs had notably higher incidence of pancreatic cancer (aIRR = 3.7, 95% confidence interval [CI] = 1.6 to 8.6) and melanoma (aIRR = 6.7, 95% CI = 1.2 to 36). Compared with White SOTRs, Asian and Pacific Islander SOTRs had lower melanoma incidence but higher nasopharyngeal carcinoma incidence. Compared with the general population, Asian SOTRs had increased risk of cancers of the anus (SIR = 7.9, 95% CI = 3.6 to 15), penis (SIR = 8.9, 95% CI = 2.9 to 21), non-epithelial skin (SIR = 9.8, 95% CI = 5.4 to 17), kidney (SIR = 5.3, 95% CI = 4.3 to 6.5), and renal pelvis (SIR = 7.4, 95% CI = 3.7 to 13); non-Hodgkin lymphoma including chronic lymphocytic leukemia (NHL/CLL) (SIR = 6.4, 95% CI = 5.6 to 7.3); Hodgkin lymphoma (SIR = 6.1, 95% CI = 2.8 to 12); and Kaposi sarcoma (SIR = 15, 95% CI = 6.6 to 30). Compared with the general population, Pacific Islander SOTRs had increased risk of cancers of the anus (SIR = 12, 95% CI = 1.5 to 45), pancreas (SIR = 3.3, 95% CI = 1.3 to 6.8), non-epithelial skin (SIR = 9.3, 95% CI = 1.1 to 34), and thyroid (SIR = 3.4, 95% CI = 1.2 to 7.4); NHL/CLL (SIR = 4.5, 95% CI = 2.3 to 7.9); and Kaposi sarcoma (SIR = 71, 95% CI = 8.6 to 258).</p><p><strong>Conclusions: </strong>Asian, Pacific Islander, and White SOTRs all experienced elevated cancer risk compared with their race-matched general population. Different cancer risks in these racial groups might be explained by differences in risk factors in the general population or unique features of SOTRs in these groups.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1456-1464"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229455/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ending nuclear weapons, before they end us†.","authors":"Kamran Abbasi, Parveen Ali, Virginia Barbour, Marion Birch, Inga Blum, Peter Doherty, Andy Haines, Ira Helfand, Richard Horton, Kati Juva, Jose F Lapena, Robert Mash, Olga Mironova, Arun Mitra, Carlos Monteiro, Elena N Naumova, David Onazi, Tilman Ruff, Peush Sahni, James Tumwine, Carlos Umaña, Paul Yonga, Chris Zielinski","doi":"10.1093/jnci/djaf102","DOIUrl":"10.1093/jnci/djaf102","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1296-1298"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229452/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144093701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Trends in young-onset cancer incidence: a modeling perspective.","authors":"Lukas Owens, Allison Fung, Jonathan Shuhendler, Joseph Glick, Marc D Ryser, Roman Gulati, Ruth Etzioni","doi":"10.1093/jnci/djaf050","DOIUrl":"10.1093/jnci/djaf050","url":null,"abstract":"<p><strong>Background: </strong>Recent increases in the diagnosis of certain cancers among younger individuals are generating intense concern. Many studies attribute the increase in the so-called \"young-onset\" cancer to an etiologic cause but questions have also arisen about the role of earlier diagnosis.</p><p><strong>Methods: </strong>We simulated incidence trends from a natural history model that includes healthy, preclinical, and clinical disease states, where the transition from the healthy to the preclinical state represents disease onset and the transition from the preclinical to the clinical state represents diagnosis. We superimposed birth-cohort effects on the rate of disease onset and period effects on the rate of disease diagnosis to identify those that match patterns of relative incidence by age group and 5-year calendar interval from 2000 to 2019 for 6 \"young-onset\" cancers (colon, rectum, female breast, stomach, pancreas, and kidney).</p><p><strong>Results: </strong>Two types of effects are broadly consistent with the observed increasing incidence trends in younger individuals: (1) a birth-cohort effect on disease onset that begins around 1970 and becomes more pronounced in later birth years or (2) a period effect consistent with progressive reduction over time in the duration of preclinical disease. An earlier, protective birth-cohort effect is consistent with recent declining trends in incidence in older individuals for colon, rectal, and stomach cancers.</p><p><strong>Conclusions: </strong>A disease model provides clues about the possible drivers of cancer incidence trends, suggests constraints on the patterns of exposures that might be implicated etiologically, and indicates that the role of diagnostic changes warrants consideration alongside potential etiologic explanations.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1350-1359"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The nucleosome remodeling and deacetylase-SWItch/sucrose non-fermentable antagonism regulates the coordinated activation of epithelial-to-mesenchymal transition and inflammation in oral cancer.","authors":"Roberto Stabile, Francesco A Tucci, Mathijs P Verhagen, Carmen Embregts, Thierry P P van den Bosch, Rosalie Joosten, Maria J De Herdt, Berdine van der Steen, Alex L Nigg, Senada Koljenović, Jose A Hardillo, Cornelis Peter Verrijzer, Adrian Biddle, Robert J Baatenburg de Jong, Pieter J M Leenen, Riccardo Fodde","doi":"10.1093/jnci/djaf065","DOIUrl":"10.1093/jnci/djaf065","url":null,"abstract":"<p><strong>Background: </strong>Phenotypic plasticity and inflammation, 2 well-established hallmarks of cancer, play key roles in local invasion and distant metastasis by enabling the rapid adaptation of tumor cells to dynamic micro-environmental changes.</p><p><strong>Results: </strong>Here, we show that in oral squamous carcinoma cell carcinoma (OSCC), the competition between the Nucleosome Remodeling and Deacetylase (NuRD) and SWItch/Sucrose Non-Fermentable (SWI/SNF) chromatin remodeling complexes plays a pivotal role in regulating both epithelial-mesenchymal plasticity (EMP) and inflammation. By perturbing these complexes, we demonstrated their opposing downstream effects on the inflammatory pathways and EMP regulation. In particular, downregulation of the BRG1-specific SWI/SNF complex deregulates key inflammatory genes, such as TNF-α and IL6, in opposite ways when compared with the loss of CDK2AP1, a key member of the NuRD complex. We showed that CDK2AP1 genetic ablation triggers a pro-inflammatory secretome encompassing several chemokines and cytokines, thus promoting the recruitment of monocytes into the tumor microenvironment (TME). Furthermore, CDK2AP1 deletion stimulates their differentiation into M2-like macrophages, as validated on tumor microarrays from OSCC patient-derived tumor samples. Further analysis of the inverse correlation between CDK2AP1 expression and TME immune infiltration revealed specific downstream effects on the abundance and localization of CD68+ macrophages.</p><p><strong>Conclusions: </strong>Our study sheds light on the role of chromatin remodeling complexes in OSCC locoregional invasion and highlights the potential of CDK2AP1 and other members of NuRD and SWI/SNF chromatin remodeling complexes as prognostic markers and therapeutic targets.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1438-1455"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229464/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143669911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dynamic ctDNA informs whole-course postoperative precise management of NSCLC (LUNGCA study).","authors":"Liang Xia, Qiang Pu, Ran Kang, Jiandong Mei, Lu Li, Ying Yang, Senyi Deng, Gang Feng, Yulan Deng, Fanyi Gan, Yidan Lin, Lin Ma, Feng Lin, Yong Yuan, Yang Hu, Chenglin Guo, Hu Liao, Chengwu Liu, Yunke Zhu, Wenping Wang, Zheng Liu, Yuyang Xu, Kaidi Li, Chuan Li, Weizhi Chen, Qingyun Li, Bo Du, Xiaolong Zhang, Yingli Kou, Yun Wang, Zhu Wu, Guowei Che, Yaohui Chen, Shensi Shen, Longqi Chen, Dan Xie, Lunxu Liu","doi":"10.1093/jnci/djaf061","DOIUrl":"10.1093/jnci/djaf061","url":null,"abstract":"<p><strong>Background: </strong>Circulating tumor DNA (ctDNA) is valuable for detecting minimal residual disease (MRD). However, studies involving long-term blood sampling are required to comprehensively interpret the clinical use of ctDNA analyses.</p><p><strong>Methods: </strong>We conducted a prospective multicenter cohort study (LUNGCA) for dynamic ctDNA monitoring in lung cancer patients receiving curative-intent surgery. ctDNA analysis was conducted on preoperative plasma samples, at postoperative 3 days and 1 month, and then every 3-6 months for up to 3 years.</p><p><strong>Results: </strong>In total, 233 non-small cell lung cancer (NSCLC) patients and 2336 longitudinal plasma samples were included; the median follow-up was 51.4 months. Post-comprehensive treatment (after radical surgery + necessary adjuvant therapy) MRD status was better at predicting relapse than postoperative MRD status (positive predictive value: 100% vs 90.0%; negative predictive value: 90.3% vs 90.1%). Patients with positive pre-adjuvant ctDNA and targetable mutations in tumor tissues had improved recurrence-free survival (RFS) with corresponding adjuvant tyrosine kinase inhibitor (TKI) treatment (hazard ratio [HR] = 0.01, P = .005), but adjuvant chemotherapy failed to improve RFS (HR = 0.6, P = .491). Of patients receiving adjuvant therapies, patients with a negative- or positive-negative ctDNA change pattern had favorable and similar RFS (P = .419), whereas patients with a positive- or negative-positive pattern had worse RFS (P < .001). TKI therapy was more effective than chemotherapy in clearing ctDNA. Post-relapse ctDNA negativity was associated with favorable OS (HR = 0.4; P = .029).</p><p><strong>Conclusions: </strong>Comprehensive interpretation of dynamic ctDNA monitoring data can inform precise whole-course postsurgical management of NSCLC patients.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1474-1484"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143709857","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":"Colon, colorectal, and all cancer incidence increase in the young due to appendix reclassification.","authors":"Archie Bleyer, Lynn A G Ries, Danielle B Cameron, Sara A Mansfield, Stuart E Siegel, Ronald D Barr","doi":"10.1093/jnci/djaf038","DOIUrl":"10.1093/jnci/djaf038","url":null,"abstract":"<p><strong>Background: </strong>Increases in colon and colorectal cancer incidence among adolescents and young adults have been reported progressively. Most of the increase may be because of an artifact caused by reclassifying appendiceal carcinoids and neuroendocrine tumor (NET) as malignant.</p><p><strong>Methods: </strong>Age-adjusted incidence and survival data were obtained from the Surveillance, Epidemiology, and End Results SEER22 database.</p><p><strong>Results: </strong>In adolescents and young adults during 2000-2020, appendix cancer had an average annual percent change in incidence increase that in males was 3.7 times greater than the next most increasing cancer (average annual percent change = 12.8, 95% confidence interval CI] = 10.9% to 14.6% vs average annual percent change = 3.4 [kidney], 95% CI = 2.7% to 3.5%) and correspondingly in females 2.9-fold greater (average annual percent change = 14.6,95% CI = 11.9% to 17.3% vs average annual percent change = 4.2 [pancreas], 95% CI = 3.6% to 4.8%). From 2000-2009 to 2015-2020, appendix cancer incidence increased 17-, 6.5-, and 2.5-fold in children aged 0-14 years, adolescents and young adults aged 15-39 years, and adults aged 40-49 years, respectively. NET accounted for 95%, 90%, and 80% of appendix cancer increase in the 3 age groups, respectively. In 3446 adolescents and young adults diagnosed during 2010-2020 with malignant appendix NET, the 6-year cancer-specific survival was 99.4% (95% CI = 99.0% to 99.6%). From 2000-2009 to 2015-2020, colon carcinoma incidence in adolescents and young adults increased 61% with the appendix included and only 11% with the appendix excluded.</p><p><strong>Conclusions: </strong>Reclassification of appendix NET/carcinoids as malignant has artifactually increased the incidence of colon, colorectum, and all cancer in children and adolescents and young adults. Appendix NET/carcinoids are rarely fatal in those aged younger than 40 years and should not be considered as cancer and included in colorectal cancer analyses. To the extent that the appendix artifact occurs in adults aged 40-49 years, recommendations for starting colorectal cancer screening earlier may be affected.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1340-1349"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229466/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143468204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Response to Önder and Çatlı.","authors":"Jessica Pearce, Alexandra Gilbert","doi":"10.1093/jnci/djaf078","DOIUrl":"10.1093/jnci/djaf078","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1514-1515"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12229451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143966312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RE: Endocrine therapy and risk of cardiovascular disease and mortality in postmenopausal breast cancer survivors.","authors":"Jing Zhang, Li Zhang, Zhike Liu, Yingjie Jia, Fanming Kong","doi":"10.1093/jnci/djaf093","DOIUrl":"10.1093/jnci/djaf093","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1520-1521"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016000","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":"Rising incidence of early-onset colorectal cancer: impact of anatomy and histology.","authors":"Sara K Char, Jennifer A Chan, Kimmie Ng","doi":"10.1093/jnci/djaf094","DOIUrl":"10.1093/jnci/djaf094","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1302-1304"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144173818","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: FGL2 as a Multimodality Regulator of Tumor-Mediated Immune Suppression and Therapeutic Target in Gliomas.","authors":"","doi":"10.1093/jnci/djaf125","DOIUrl":"10.1093/jnci/djaf125","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1526-1528"},"PeriodicalIF":9.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144187042","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}