{"title":"Red Meat, Poultry, and Fish Consumption and the Risk of Liver Cancer: A Prospective Cohort Study of 0.5 Million Chinese Adults.","authors":"Chun-Rui Wang, Dong Cai, Kun He, Jie-Jun Hu, Xin Dai, Qian Zhu, Guo-Chao Zhong","doi":"10.1158/1055-9965.EPI-24-1158","DOIUrl":"10.1158/1055-9965.EPI-24-1158","url":null,"abstract":"<p><strong>Background: </strong>Epidemiological evidence on meat consumption and liver cancer risk is limited and inconclusive; moreover, no prospective study has been conducted to investigate this association in China. Hence, we performed this study to examine the association of red meat, poultry, and fish consumption with the risk of liver cancer in a Chinese population.</p><p><strong>Methods: </strong>A total of 510,048 Chinese adults of ages 30 to 79 years were included and were followed up through December 31, 2016. Red meat, poultry, and fish consumption was evaluated using an interviewer-administered laptop-based questionnaire. HRs and 95% confidence intervals (CI) for liver cancer incidence were calculated using Cox regression.</p><p><strong>Results: </strong>Over a mean follow-up of 9.94 years, 1,906 liver cancer cases were observed. Each 50 g/day increase in red meat (HR 0.72; 95% CI, 0.49-1.05), poultry (HR 0.93; 95% CI, 0.83-1.03), and fish (HR 0.95; 95% CI, 0.85-1.05) consumption was not associated with the risk of liver cancer in the whole study population; however, subgroup analysis revealed an inverse association with poultry consumption in rural residents but not in urban residents (Pinteraction = 0.046). The initial associations did not change materially in a series of sensitivity analyses.</p><p><strong>Conclusions: </strong>Red meat and fish consumption is not associated with the risk of liver cancer in this Chinese population. The inverse association with poultry consumption in Chinese rural residents should be interpreted with caution.</p><p><strong>Impact: </strong>This is the first prospective study examining the association between meat consumption and the risk of liver cancer in the Chinese population.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"412-419"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chronic Health Conditions among LGBTQ+ Cancer Survivors: Letter.","authors":"Di Zhao, Jie Liu","doi":"10.1158/1055-9965.EPI-24-1737","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1737","url":null,"abstract":"","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"448"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Eslam Maher, Mohamed Kamal, Moatasem El-Ayadi, Amal Refaat, Abdelrahman Enayet, Mohamed El-Beltagy, Eman Eldebawy, Hala Taha, Madiha Awad, Mohamed S Zaghloul
{"title":"Epidemiology and Clinical Outcomes of Childhood Central Nervous System Cancers in a Large Low/Middle-Income Country Pediatric Oncology Center: A Report on 5,051 Kids.","authors":"Eslam Maher, Mohamed Kamal, Moatasem El-Ayadi, Amal Refaat, Abdelrahman Enayet, Mohamed El-Beltagy, Eman Eldebawy, Hala Taha, Madiha Awad, Mohamed S Zaghloul","doi":"10.1158/1055-9965.EPI-24-1188","DOIUrl":"10.1158/1055-9965.EPI-24-1188","url":null,"abstract":"<p><strong>Background: </strong>Central nervous system (CNS) tumors are the leading cause of cancer-related deaths in children. Although most cases come from low- and middle-income countries (LMIC) where their prognosis is worse, few epidemiologic studies are conducted in these regions.</p><p><strong>Methods: </strong>We conducted a registry-based cohort study for childhood CNS tumors at Children's Cancer Hospital, Egypt, over 15 years. Unified treatment protocols were implemented. Survival analyses were conducted using the Kaplan-Meier function. Cases were additionally annotated using the International Classification of Childhood Cancer-3 classification.</p><p><strong>Results: </strong>In total, 5,051 children ≤18 years of age were identified, accounting for 20% of all childhood cancers treated at Children's Cancer Hospital, Egypt. The most common tumor sites were the posterior fossa (36.8%) and brainstem (17.7%). Pathologies were predominantly astrocytic (n = 1,360; 26.9%) and embryonal (n = 1,003; 19.9%) in origin. The 5-year overall survival (OS) and event-free survival for all cases were 64.6% and 51.8%, respectively. More specifically, 1,421 low-grade gliomas were identified, with a 5-year OS of 91.1%. Medulloblastoma (n = 801) recorded a 5-year OS of 66%. The entity with the worst prognosis was diffuse intrinsic pontine glioma (n = 633), with a 5-year OS of 3.2%.</p><p><strong>Conclusions: </strong>We report on a large number of childhood CNS tumors from an LMIC. This study underscores the need to understand the burden of childhood brain tumors and its outcomes in resource-constrained settings.</p><p><strong>Impact: </strong>This study reports on the epidemiology and clinical outcomes of 5,000+ children with CNS tumors from a specialized LMIC center. Despite the lack of many sophisticated and advanced facilities, LMICs can improve the clinical end-results with experience and augmented efforts.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"420-427"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833909","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Frances E M Albers, S Ghazaleh Dashti, Brigid M Lynch
{"title":"Epidemiologic Studies of Biomarkers and Their Role in Carcinogenesis: The Need for a Formal Causal Inference Approach.","authors":"Frances E M Albers, S Ghazaleh Dashti, Brigid M Lynch","doi":"10.1158/1055-9965.EPI-24-1758","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1758","url":null,"abstract":"<p><p>In this issue of Cancer Epidemiology, Biomarkers & Prevention, Brantley and colleagues investigated the relationships between estrogen metabolites and postmenopausal breast cancer, using data from a nested case-control study within the Nurses' Health Study. One study aim was to investigate the extent to which estrogen metabolism patterns provided further insights into mechanisms in breast cancer development beyond the role of estradiol. In this editorial, we describe the challenges in interpreting results from observational studies of biomarkers and their role in carcinogenesis due to: (i) a general lack of clarity in the research question, (ii) the limits of current knowledge about the complex underlying causal structure involving interrelated biomarkers, and (iii) the limitations in existing data sources (e.g., biomarkers measured at a single time point). We propose that applying a formal causal inference framework in these studies could be a step forward in improving their rigor, by enabling researchers to be more explicit about the causal effects of interest and the assumptions made, and to advocate for the improvement of future studies. See related article by Brantley et al., p. 375.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"373-374"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Manzur Farazi, Xin Yang, Carson J Gehl, Gillian C Barnett, Neil G Burnet, Jenny Chang-Claude, Christopher C Parker, Alison M Dunning, David Azria, Ananya Choudhury, Tiziana Rancati, Dirk De Ruysscher, Petra Seibold, Elena Sperk, Christopher J Talbot, Liv Veldeman, Adam J Webb, Rebecca Elliott, Miguel E Aguado-Barrera, Ana M Carballo, Olivia Fuentes-Ríos, Antonio Gómez-Caamaño, Paula Peleteiro, Ana Vega, Harry Ostrer, Barry S Rosenstein, Shiro Saito, Matthew Parliament, Nawaid Usmani, Brian Marples, Yuhchyau Chen, Gary Morrow, Edward Messing, Michelle C Janelsins, William Hall, Catharine M L West, Paul L Auer, Sarah Kerns
{"title":"A Polygenic Risk Score for Late Bladder Toxicity Following Radiotherapy for Non-Metastatic Prostate Cancer.","authors":"Manzur Farazi, Xin Yang, Carson J Gehl, Gillian C Barnett, Neil G Burnet, Jenny Chang-Claude, Christopher C Parker, Alison M Dunning, David Azria, Ananya Choudhury, Tiziana Rancati, Dirk De Ruysscher, Petra Seibold, Elena Sperk, Christopher J Talbot, Liv Veldeman, Adam J Webb, Rebecca Elliott, Miguel E Aguado-Barrera, Ana M Carballo, Olivia Fuentes-Ríos, Antonio Gómez-Caamaño, Paula Peleteiro, Ana Vega, Harry Ostrer, Barry S Rosenstein, Shiro Saito, Matthew Parliament, Nawaid Usmani, Brian Marples, Yuhchyau Chen, Gary Morrow, Edward Messing, Michelle C Janelsins, William Hall, Catharine M L West, Paul L Auer, Sarah Kerns","doi":"10.1158/1055-9965.EPI-24-1228","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1228","url":null,"abstract":"<p><strong>Background: </strong>Late bladder toxicity is a concern for patients receiving prostate cancer radiotherapy and negatively impacts survivors. Few risk factors are known beyond the radiation dose and volume of bladder exposed. A polygenic risk score (PRS) could identify susceptible patients.</p><p><strong>Methods: </strong>A PRS was built using genome-wide association results from the Radiogenomics Consortium (N=3,988), then tested in the prospective REQUITE and URWCI studies (N=2,034). The primary outcome was time-to-patient-reported gross (≥ grade 2, G2) hematuria analyzed using Cox proportional hazards regression. Secondary outcomes were ≥G2 urinary retention and frequency. The PRS was externally validated for clinically-diagnosed irradiation cystitis in the UK Biobank (N=8,430). A gene-burden test evaluated rare coding variants.</p><p><strong>Results: </strong>A 115-variant PRS was associated with significantly increased risk of ≥G2 hematuria (hazard ratio [HR] per standard deviation [SD]=1.22, p=0.009) as well as urinary retention (HR-per-SD=1.18, p=0.016) and frequency (HR-per-SD=1.14, p=0.036). When binarized, men in the upper decile (PRShigh) had >2-fold increased risk of hematuria after adjusting for clinical risk factors (HR=2.12, p=0.002; Harrel's c-index 0.71 [95%CI=0.65 to 0.76]). A similar effect size was seen in the UK Biobank for clinically-diagnosed irradiation cystitis (OR=2.15, p=0.026). The burden test identified BOD1L1 as a putative novel radiosensitivity gene.</p><p><strong>Conclusions: </strong>This PRS identifies susceptible patients and could guide selection of those needing re-optimized treatment plans that spare the bladder beyond currently recommended constraints.</p><p><strong>Impact: </strong>PRS-guided treatment planning in radiation oncology could lower the incidence of clinically relevant bladder toxicity and reduce the impact of this outcome on prostate cancer survivors.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143540380","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kristen D Brantley, Regina G Ziegler, Neal E Craft, Susan E Hankinson, A Heather Eliassen
{"title":"Circulating Estrogen Metabolites and Risk of Breast Cancer among Postmenopausal Women in the Nurses' Health Study.","authors":"Kristen D Brantley, Regina G Ziegler, Neal E Craft, Susan E Hankinson, A Heather Eliassen","doi":"10.1158/1055-9965.EPI-24-0577","DOIUrl":"10.1158/1055-9965.EPI-24-0577","url":null,"abstract":"<p><strong>Background: </strong>Estradiol and estrone are well-established risk factors for postmenopausal breast cancer. Experimental evidence suggests that specific estrogen metabolites, produced via irreversible hydroxylation of estrone and estradiol at position 2 or 16, may independently influence carcinogenesis.</p><p><strong>Methods: </strong>We performed a nested case-control study of breast cancer (328 breast cancer cases; 639 controls) among postmenopausal women within the Nurses' Health Study to examine the role of estrogens and estrogen metabolites (jointly referred to as EM). Plasma concentrations of each EM (unconjugated + conjugated forms) were measured by LC-MS/MS. Multivariable conditional logistic regression, adjusting for breast cancer risk factors, estimated relative risks (RR) and 95% confidence intervals of breast cancer across quintiles of individual EM, EM pathways, and pathway ratios. Associations by estrogen receptor (ER) and progesterone receptor (PR) status were analyzed by unconditional logistic regression.</p><p><strong>Results: </strong>Estradiol and estrone were strongly associated with increased breast cancer risk [estradiol: RRQ5 vs. Q1 (95% confidence interval) = 2.64 (1.64-4.26); estrone: 2.78 (1.74-4.45); both P-trends <0.001]. The 2-hydroxylation pathway was strongly associated with risk [RRQ5 vs. Q1 = 3.09 (1.81-5.27); P-trend <0.001] and remained so after adjusting for unconjugated estradiol [RRQ5 vs. Q1 = 2.23 (1.25-3.96); P-trend = 0.01]. Although the 16-hydroxylation pathway was modestly associated with risk [RRQ5 vs. Q1 = 1.62 (1.03-2.54); P-trend = 0.01], the association was attenuated after unconjugated estradiol adjustment [RRQ5 vs. Q1 = 1.24 (0.77-1.99); P-trend = 0.19]. Similar positive associations with the 2-pathway and 16-pathway were observed for ER+/PR+ and ER-/PR- tumors.</p><p><strong>Conclusions: </strong>In this cohort of postmenopausal women, 2-hydroxylation of estrone and estradiol was associated with increased breast cancer risk, independent of unconjugated estradiol.</p><p><strong>Impact: </strong>These results highlight the need to revisit the role of estrogen metabolism in breast cancer etiology and prevention. See related In the Spotlight, p. 367.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"375-384"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11865363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142072103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Austin R Waters, Erin E Kent, Hazel B Nichols, Kelly Tan
{"title":"Chronic Health Conditions among LGBTQ+ Cancer Survivors: Reply.","authors":"Austin R Waters, Erin E Kent, Hazel B Nichols, Kelly Tan","doi":"10.1158/1055-9965.EPI-24-1788","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1788","url":null,"abstract":"","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":"34 3","pages":"449"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143536394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Joanna Aldoori, Michael A Zulyniak, Giles J Toogood, Mark A Hull
{"title":"Plasma n-3 Polyunsaturated Fatty Acid Levels and Colorectal Cancer Risk in the UK Biobank: Evidence of Nonlinearity, as Well as Tumor Site- and Sex-Specificity.","authors":"Joanna Aldoori, Michael A Zulyniak, Giles J Toogood, Mark A Hull","doi":"10.1158/1055-9965.EPI-24-1154","DOIUrl":"10.1158/1055-9965.EPI-24-1154","url":null,"abstract":"<p><strong>Background: </strong>The relationship between omega-3 polyunsaturated fatty acid (n-3 PUFA) intake and colorectal cancer risk is unclear. Blood n-3 PUFA concentration is a biomarker of dietary n-3 PUFA intake. We examined the relationship between plasma n-3 PUFA concentrations and colorectal cancer risk in UK Biobank (UKBB) participants.</p><p><strong>Methods: </strong>We analyzed the relationship between tertiles (T) of plasma total n-3 PUFAs and n-3 PUFA docosahexaenoic acid (DHA) levels, and overall colorectal cancer (also stratified by tumor location and sex) risk. Cox proportional hazards regression models were adjusted for clinical covariates. Nonlinearity was tested by restricted cubic splines.</p><p><strong>Results: </strong>There were 2,602 incident colorectal cancer cases in 234,598 UKBB participants with baseline plasma fatty acid data (mean follow-up 13.4 years). There was an inverse association between the plasma total n-3 PUFA level [T2 HR = 0.88 (95% confidence interval, 0.80-0.97) compared with the T1 reference; T3 = 0.91 (0.83-1.00)], as well as the plasma DHA concentration [T2 = 0.89 (0.80-0.98); T3 = 0.91 (0.82-1.00)], and colorectal cancer risk. The relationship was nonlinear [P for nonlinearity = 0.14 (total n-3 PUFAs) and 0.008 (DHA)], with a plateau effect at the highest n-3 PUFA concentrations. The relationship was more pronounced for proximal colon cancer [T2 = 0.82 (0.69-0.97); T3 = 0.76 (0.64-0.90) for DHA] and was evident for males [T2 = 0.84 (0.74-0.95); T3 = 0.89 (0.78-1.00)], but not for females.</p><p><strong>Conclusions: </strong>Higher plasma n-3 PUFAs are associated with reduced colorectal cancer risk in the UKBB.</p><p><strong>Impact: </strong>Nonlinearity, as well as tumor site and sex specificities, of the inverse relationship between plasma n-3 PUFA levels and colorectal cancer risk, if confirmed in other diverse populations, has significant implications for nutritional prevention guidelines.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":"394-404"},"PeriodicalIF":3.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Anna E Coghill, Nathan Van Bibber, Robert A Baiocchi, Susanne M Arnold, Gregory Riedlinger, Bryan P Schneider, Yonghong Zhang, Gita Suneja, Miguel Gomez Fontela, Daniel Abate-Daga, Jamie K Teer
{"title":"Elevated tumor mutation burden in patients with cancer with underlying HIV infection: data from the Oncology Research Information Exchange Network (ORIEN).","authors":"Anna E Coghill, Nathan Van Bibber, Robert A Baiocchi, Susanne M Arnold, Gregory Riedlinger, Bryan P Schneider, Yonghong Zhang, Gita Suneja, Miguel Gomez Fontela, Daniel Abate-Daga, Jamie K Teer","doi":"10.1158/1055-9965.EPI-24-1321","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1321","url":null,"abstract":"<p><strong>Background: </strong>People living with HIV (PWH) have improved life expectancy due to effective HIV therapy but still experience immune impairment (e.g., altered CD4/CD8 T-cells). We hypothesized that tumors diagnosed in PWH would have distinct molecular features.</p><p><strong>Methods: </strong>We utilized whole exome sequencing of paired tumor and germline DNA and RNA sequencing of tumors from 229 patients with cancer enrolled into ORIEN to classify: total tumor mutation burden (TMB), major histocompatibility complex (MHC) class I neoantigen count, and MHC class II neoantigen count.</p><p><strong>Results: </strong>Specimens from 229 patients with cancer (110 PWH and 119 without HIV) were evaluated. Average TMB for tumors diagnosed in PWH was 249, compared to 172 for those without HIV. After adjustment for age, sex, race, smoking, and cancer site, the association between HIV and TMB remained statistically significant (OR=1.72; 95% CI: 1.26-2.43). We further observed an association between HIV and higher class I neoantigen count (OR=1.62; 95% CI: 1.10-2.41) but no association with putative class II neoantigens. When considering cancer sites separately in unadjusted analyses, average TMB was elevated in PWH for thyroid (p<0.01) and bladder cancers (p=0.03), and sarcoma (p=0.04). Similarly, putative class I neoantigen count was elevated in PWH for head & neck (p<0.01) and thyroid (p=0.01) cancers, and sarcoma (p=0.04).</p><p><strong>Conclusion: </strong>Our findings indicate that tumors diagnosed in PWH harbor a higher TMB and a higher number of putative class I neoantigens.</p><p><strong>Impact: </strong>A higher TMB in PWH may portend a more favorable response to cancer treatment modalities such as immune checkpoint inhibitors.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Stephanie Byrne, Elina Hypponen, Beben Benyamin, Terry Boyle
{"title":"Greater adherence to lifestyle recommendations after cancer diagnosis is associated with lower mortality in the UK Biobank.","authors":"Stephanie Byrne, Elina Hypponen, Beben Benyamin, Terry Boyle","doi":"10.1158/1055-9965.EPI-24-1783","DOIUrl":"https://doi.org/10.1158/1055-9965.EPI-24-1783","url":null,"abstract":"<p><strong>Background: </strong>Research supporting the current recommendation to adhere to a healthy lifestyle following cancer diagnosis is limited. We investigated whether a healthy lifestyle after diagnosis is associated with a lower risk of mortality among those diagnosed with any malignant cancer, and breast, colorectal and prostate cancers.</p><p><strong>Methods: </strong>In 2006-2010, UK Biobank participants (aged 37-73 years) were assessed. Analyses were restricted to those with a malignant cancer diagnosis prior to baseline (n=20,805, including 5,845 breast, 1,943 colorectal and 2,715 prostate cancer cases). Participants were followed for all-cause and cancer-specific death up to November 2022. A lifestyle index was determined based on lifestyle recommendations for cancer prevention. Cox regression was used to examine associations with all-cause and cancer-specific mortality among those with any cancer, and separately for breast, colorectal and prostate cancers, adjusting for relevant confounders.</p><p><strong>Results: </strong>There were 4,328 deaths and 3,354 cancer-specific deaths in the 258,985 person-years of follow up. A higher lifestyle index, representing greater adherence to recommendations, was associated with a lower risk of all-cause mortality (any cancer - highest vs lowest lifestyle index tertile: HR[95%CI]=0.77[0.71,0.83]; breast: 0.75[0.64,0.88]; colorectal: 0.68[0.52,0.89]; prostate: 0.73[0.59,0.89]), and cancer-specific mortality in all populations examined (any cancer: 0.82[0.75,0.89]; breast: 0.88[0.71,1.09]; colorectal: 0.58[0.36,0.94]; prostate: 0.70[0.53,0.93]), although evidence was weaker for cancer-specific mortality among colorectal and breast cancer survivors.</p><p><strong>Conclusions: </strong>Our findings provide evidence to support the recommendation to follow a healthy lifestyle after cancer diagnosis to prolong life.</p><p><strong>Impact: </strong>Clinical guidelines and public health programs promoting a healthy lifestyle to cancer survivors may prolong life.</p>","PeriodicalId":9458,"journal":{"name":"Cancer Epidemiology Biomarkers & Prevention","volume":" ","pages":""},"PeriodicalIF":3.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522613","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}