{"title":"RE: Effects of a high-fiber, high-fruit, and high-vegetable, low-fat dietary intervention on the rectal tissue microbiome.","authors":"Muhammad Ifham Hanif, Mentari Maratus Sholihah","doi":"10.1093/jnci/djaf225","DOIUrl":"10.1093/jnci/djaf225","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence suggests that bacteria residing in colorectal tissue are plausibly associated with colorectal cancer. Prior studies investigated the effects of dietary interventions on the fecal microbiome, but few assessed colorectal tissue microbiome endpoints. We investigated the effects of a high-fiber, high-fruit, high-vegetable, and low-fat dietary intervention on the rectal tissue microbiome in the Polyp Prevention Trial (PPT).</p><p><strong>Methods: </strong>PPT is a 4-year randomized clinical trial with intervention goals of consuming (1) at least 18 g of fiber per 1000 kcal/day; (2) at least 3.5 servings of fruits and vegetables per 1000 kcal/day; and (3) no more than 20% of kcal/day from fat. Using 16S ribosomal RNA gene sequencing, we characterized bacteria in rectal biopsies collected at baseline and the end of years 1 and 4 (n = 233 in intervention arm and n = 222 in control arm). We estimated effects of the intervention on alpha and beta diversity and relative abundance of a priori-selected bacteria using repeated-measures linear mixed-effects models.</p><p><strong>Results: </strong>The intervention did not statistically significantly modify rectal tissue alpha diversity. Compared with the control arm, relative abundance of a priori-selected Porphyromonas (absolute intervention effects [standard errors] at T1 vs T0 = -0.24 [0.07] and T4 vs T0 = -0.12 [0.07]; P = .004) and Prevotella (absolute intervention effects at T1 vs T0 = -0.40 [0.14] and at T4 vs T0 = -0.32 [0.15]; P = .01) were more strongly decreased in the intervention arm.</p><p><strong>Conclusion: </strong>The PPT intervention did not influence rectal tissue microbiome diversity or the relative abundance of most bacteria, except for 2 oral-originating bacteria that were previously associated with colorectal cancer presence.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"2142-2143"},"PeriodicalIF":7.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144882913","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}
Ming Sun, Christel Häggström, Marisa da Silva, Innocent B Mboya, Ylva Trolle Lagerros, Karl Michaëlsson, Sven Sandin, Jerzy Leppert, Sara Hägg, Sölve Elmståhl, Patrik K E Magnusson, Stefan Söderberg, Weiyao Yin, Abbas Chabok, Angela Wood, Tanja Stocks, Josef Fritz
{"title":"Comparing waist circumference with body mass index on obesity-related cancer risk: a pooled Swedish study.","authors":"Ming Sun, Christel Häggström, Marisa da Silva, Innocent B Mboya, Ylva Trolle Lagerros, Karl Michaëlsson, Sven Sandin, Jerzy Leppert, Sara Hägg, Sölve Elmståhl, Patrik K E Magnusson, Stefan Söderberg, Weiyao Yin, Abbas Chabok, Angela Wood, Tanja Stocks, Josef Fritz","doi":"10.1093/jnci/djaf075","DOIUrl":"10.1093/jnci/djaf075","url":null,"abstract":"<p><strong>Background: </strong>General adiposity, assessed by body mass index (BMI), is a well-established cancer risk factor. This study compared waist circumference (WC), a measure of abdominal adiposity, with BMI as a risk factor for obesity-related cancers, and assessed whether WC provides additional information beyond BMI.</p><p><strong>Methods: </strong>We analyzed data from 339 190 individuals in a pooled Swedish cohort with baseline BMI and WC assessments from 1981 to 2019 (61% objectively measured, mean age 51.4 years). Cancer diagnoses were obtained from the Swedish Cancer Register. Hazard ratios (HRs) for WC and BMI were calculated using multivariable-adjusted Cox regression. To account for WC's greater variability, we corrected HRs using regression dilution ratios. To assess WC's additional contribution beyond BMI, we analyzed WC residuals in multivariable, BMI-adjusted models.</p><p><strong>Results: </strong>During a median follow-up of 13.9 years (interquartile range: 8.0-22.5), 18 185 IARC-established obesity-related cancers were recorded. In men, a 1-standard deviation (SD) increase in WC was associated with a 25% higher risk of obesity-related cancers (HR1-SD = 1.25, 95% CI = 1.21 to 1.30), compared to a 19% increase for BMI (HR1-SD = 1.19, 95% CI = 1.15 to 1.23, P = 0.014 for heterogeneity). Among women, associations were weaker and similar for both WC (HR1-SD = 1.13, 95% CI = 1.11 to 1.16) and BMI (HR1-SD = 1.13, 95% CI = 1.11 to 1.15, P = 0.357 for heterogeneity). Waist circumference residuals were more strongly associated with obesity-related cancer risk in men (HR1-SD = 1.09, 95% CI = 1.06 to 1.12) than in women (HR1-SD = 1.03, 95% CI = 1.02 to 1.05). Including an additional 6893 potential obesity-related cancers yielded similar patterns of associations.</p><p><strong>Conclusion(s): </strong>Waist circumference is a stronger risk factor than BMI for obesity-related cancer in men, conveying additional risk information, whereas this is less evident in women.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":"1999-2009"},"PeriodicalIF":7.2,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12505136/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143742999","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}
Emma Hazelwood, Lucy J Goudswaard, Matthew A Lee, Marina Vabistsevits, Dimitri J Pournaras, Hermann Brenner, Daniel D Buchanan, Stephen B Gruber, Andrea Gsur, Li Li, Ludmila Vodickova, Robert C Grant, N Jewel Samadder, Nicholas J Timpson, Marc J Gunter, Benjamin Schuster-Böckler, James Yarmolinsky, Tom G Richardson, Heinz Freisling, Neil Murphy, Emma E Vincent
{"title":"Adiposity distribution and risks of 12 obesity-related cancers: a Mendelian randomization analysis.","authors":"Emma Hazelwood, Lucy J Goudswaard, Matthew A Lee, Marina Vabistsevits, Dimitri J Pournaras, Hermann Brenner, Daniel D Buchanan, Stephen B Gruber, Andrea Gsur, Li Li, Ludmila Vodickova, Robert C Grant, N Jewel Samadder, Nicholas J Timpson, Marc J Gunter, Benjamin Schuster-Böckler, James Yarmolinsky, Tom G Richardson, Heinz Freisling, Neil Murphy, Emma E Vincent","doi":"10.1093/jnci/djaf201","DOIUrl":"https://doi.org/10.1093/jnci/djaf201","url":null,"abstract":"<p><strong>Introduction: </strong>There is convincing evidence that overall adiposity increases the risks of several cancers. Whether the distribution of adiposity plays a similar role is unclear.</p><p><strong>Methods: </strong>We used 2-sample Mendelian randomization (MR) to examine causal relationships of 5 adiposity distribution traits (abdominal subcutaneous adipose tissue (ASAT); visceral adipose tissue (VAT); gluteofemoral adipose tissue (GFAT); liver fat; and pancreas fat) with the risks of 12 obesity-related cancers (endometrial, ovarian, breast, colorectal, pancreas, multiple myeloma, liver, kidney (renal cell), thyroid, gallbladder, esophageal adenocarcinoma, and meningioma).</p><p><strong>Results: </strong>Sample size across all genome-wide association studies (GWAS) ranged from 8407 to 728 896 (median: 57 249). We found evidence that higher genetically predicted ASAT increased the risks of endometrial cancer, liver cancer, and esophageal adenocarcinoma (odds ratios (OR) and 95% confidence intervals (CI) per standard deviation (SD) higher ASAT = 1.79 (1.18 to 2.71), 3.83 (1.39 to 10.53), and 2.34 (1.15 to 4.78), respectively). Conversely, we found evidence that higher genetically predicted GFAT decreased the risks of breast cancer and meningioma (ORs and 95% CIs per SD higher genetically predicted GFAT = 0.77 (0.62 to 0.97) and 0.53 (0.32 to 0.90), respectively). We also found evidence for an effect of higher genetically predicted VAT and liver fat on increased liver cancer risk (ORs and 95% CIs per SD higher genetically predicted adiposity trait = 4.29 (1.41 to 13.07) and 4.09 (2.29 to 7.28), respectively).</p><p><strong>Discussion: </strong>Our analyses provide novel insights into the relationship between adiposity distribution and cancer risk. These insights highlight the potential importance of adipose tissue distribution alongside maintaining a healthy weight for cancer prevention.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145130940","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":"Breastfeeding after breast cancer: a need for further mechanistic study.","authors":"Victoria L Seewaldt, Pepper J Schedin","doi":"10.1093/jnci/djaf240","DOIUrl":"https://doi.org/10.1093/jnci/djaf240","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091819","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}
Reinier G S Meester, Eric A Miller, Paul F Pinsky, Robert E Schoen, Uri Ladabaum
{"title":"Contrasts in colorectal cancer incidence and mortality in screening trials of sigmoidoscopy versus colonoscopy (NordICC).","authors":"Reinier G S Meester, Eric A Miller, Paul F Pinsky, Robert E Schoen, Uri Ladabaum","doi":"10.1093/jnci/djaf269","DOIUrl":"https://doi.org/10.1093/jnci/djaf269","url":null,"abstract":"<p><strong>Background: </strong>Interim 10-year results from the Nordic-European Initiative on Colorectal Cancer (NordICC), a randomized controlled trial (RCT) of screening colonoscopy, demonstrated a statistically significant reduction in colorectal cancer (CRC) incidence but not mortality, contrary to results from four flexible sigmoidoscopy (FS)-RCTs.</p><p><strong>Methods: </strong>We constructed CRC incidence and mortality Kaplan-Meier curves through 10 years to standardize comparisons across RCTs, and examined CRC screen-detection and stage. Novel analyses of one FS-RCT (Prostate, Lung, Colorectal, and Ovarian cancer screening trial [PLCO]) assessed year-by-year mortality in screen-detected CRCs.</p><p><strong>Results: </strong>At 10 years, all five RCTs demonstrated statistically significant CRC incidence reductions with screening (ratios = 0.77 [95%CI 0.70-0.84] to 0.82 [0.69-0.97] vs controls; P ≤ .011). Two FS-RCTs and NordICC showed no significant CRC mortality reduction (ratios = 0.84 [0.64-1.10] to 0.90 [0.69-1.18]; P = .10-0.23). In three FS-RCTs and NordICC, relative reductions were greater in CRC incidence than CRC mortality, but only NordICC reported higher CRC mortality with screening vs controls for the first 7 years. In contrast, PLCO observed fewer CRC deaths with screening by year 2 (ratio = 0.59, P = .03), and screen-detected CRCs were less often advanced (OR = 0.26; P < .001) or fatal (ratio = 0.50; P < .001).</p><p><strong>Conclusions: </strong>After 10 years, NordICC is similar to two FS-RCTs in observing statistically significant reductions in CRC incidence but not CRC mortality. However, only NordICC observed greater CRC mortality with screening vs controls for 7 years. Granular analyses of CRC cases and deaths in NordICC, paralleling our PLCO analyses, could provide insight into why CRC mortality results differ in NordICC vs FS-RCTs.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091842","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}
Hao-Chen Yang, Charles Chia-Chin Chuang, Che-Hsu Cheng, Po-Cheng Shih, James Cheng-Chung Wei
{"title":"RE: Trends in young-onset cancer incidence: a modeling perspective.","authors":"Hao-Chen Yang, Charles Chia-Chin Chuang, Che-Hsu Cheng, Po-Cheng Shih, James Cheng-Chung Wei","doi":"10.1093/jnci/djaf265","DOIUrl":"https://doi.org/10.1093/jnci/djaf265","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091851","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}
Michaela A Dinan, Kayla L Stratton, Wendy M Leisenring, Yutaka Yasui, Eric J Chow, Emily S Tonorezos, Chaya S Moskowitz, Jennifer M Yeh, David Noyd, Gregory T Armstrong, Kevin C Oeffinger
{"title":"Treatment exposure-based risk-stratification for care of survivors of childhood cancer: a report from the childhood cancer survivor study.","authors":"Michaela A Dinan, Kayla L Stratton, Wendy M Leisenring, Yutaka Yasui, Eric J Chow, Emily S Tonorezos, Chaya S Moskowitz, Jennifer M Yeh, David Noyd, Gregory T Armstrong, Kevin C Oeffinger","doi":"10.1093/jnci/djaf268","DOIUrl":"https://doi.org/10.1093/jnci/djaf268","url":null,"abstract":"<p><strong>Background: </strong>Treatment exposure-based risk-stratification of long-term cancer survivors may help inform health care in survivorship clinics. We used the large, diverse population of the Childhood Cancer Survivor Study (CCSS) to test a modified, exposure-based strata previously developed within United Kingdom to classify survivors with respect to risk of late morbidity and health-related mortality.</p><p><strong>Methods: </strong>Five-year survivors of childhood cancer were categorized into low, medium, and high-risk groups based on treatment exposures and diagnosis. Primary endpoints included cumulative health-related (ie, non-recurrence, non-external) late mortality and cumulative incidence of severe or fatal (CTCAE grade 3-5) chronic health conditions conditional on reaching age 20 without the outcome. Siblings were a comparison group for chronic health conditions. Cox proportional hazards models were adjusted for sex, race, ethnicity, and age at diagnosis.</p><p><strong>Results: </strong>Among 15,346 survivors diagnosed 1970-1999, the risk of developing a severe chronic condition by age 35 was 11.9% (95% CI 9.9-14.3%), 15.1% (13.7-16.6%) and 25.4% (24.3-26.5%) for low, medium, and high-risk survivors, respectively, and 6.9% (6.1-7.9%) for siblings. Multivariable analysis confirmed higher likelihood of developing a chronic condition in high (hazard ratio [HR] 2.9, 2.5- 3.4) and medium (HR 1.5, 1.3- 1.8) vs the low-risk group. Health-related mortality was similarly increased among high (HR 5.1, 3.8-7.0) and medium (HR 2.5, 1.8-3.4) risk groups, as well as Black vs Non-Hispanic White survivors (HR 1.7, 1.3-2.1).</p><p><strong>Conclusions: </strong>Exposure-based risk categorizations can provide generalized risk stratification regarding future chronic health conditions and early mortality and may be useful in guiding management of childhood cancer survivors.</p>","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091817","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":"Unstacking the deck in follicular lymphoma clinical trials.","authors":"Samuel Yamshon, John P Leonard","doi":"10.1093/jnci/djaf231","DOIUrl":"https://doi.org/10.1093/jnci/djaf231","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091859","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":"Clones and clots in lymphoma transplant survivors.","authors":"Rebecca L Kelly, Mitchell J Machiela","doi":"10.1093/jnci/djaf211","DOIUrl":"https://doi.org/10.1093/jnci/djaf211","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086325","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 Trak and Gökçe.","authors":"Ruixuan Chen, Guobao Wang, Sheng Nie","doi":"10.1093/jnci/djaf262","DOIUrl":"https://doi.org/10.1093/jnci/djaf262","url":null,"abstract":"","PeriodicalId":14809,"journal":{"name":"JNCI Journal of the National Cancer Institute","volume":" ","pages":""},"PeriodicalIF":7.2,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145029846","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}