Pub Date : 2026-01-21DOI: 10.1016/j.canep.2026.102997
Nina Afshar , Darren Qiang , Simon Cheah , Roger L. Milne
Background
Inequalities in adult cancer survival by sex, socio-economic position, and rural-urban residence are well established; however, evidence for childhood cancers, particularly site-specific survival, remains limited and inconsistent. This study investigated whether these inequalities exist among children diagnosed with central nervous system (CNS) cancers or neuroblastoma.
Methods
We conducted a population-based study using Victorian Cancer Registry data including 1324 children aged 0–14 years when diagnosed with CNS cancers (n = 933) or neuroblastoma (n = 391) in 1982–2021. Follow-up was conducted through linkage with death registries up to the end of 2021. Multivariable Cox regression models were used to estimate hazard ratios (HRs) for all-cause mortality in relation to sex, area-level socio-economic disadvantage, and remoteness of residence.
Results
There was weak evidence of higher mortality in males than females for both CNS cancers (HR=1.16; 95 % CI: 0.96–1.41) and neuroblastoma (HR=1.29; 95 % CI: 0.92–1.80). Survival was poorer among children living in the most disadvantaged areas (highest quintile): 54 % higher mortality for CNS cancers (HR=1.54; 95 % CI: 1.09–2.18) and 89 % higher for neuroblastoma (HR=1.89; 95 % CI: 0.99–3.61) compared to those in the least disadvantaged areas (lowest quintile). Children with neuroblastoma living outside major cities had higher mortality (HR=1.43; 95 % CI: 1.01–2.02) than those in major cities, which was attenuated (HR=1.32; 95 % CI: 0.92–1.88) after adjustment for socio-economic disadvantage.
Conclusion
Children with CNS cancers and neuroblastoma living in socio-economically disadvantaged areas experienced poorer survival outcomes. There was weaker evidence for poorer survival in males and those living outside major cities. These findings underscore the need for targeted strategies to address survival inequalities in these childhood cancers.
{"title":"Inequalities in survival among children with central nervous system cancers and neuroblastoma: A population-based study","authors":"Nina Afshar , Darren Qiang , Simon Cheah , Roger L. Milne","doi":"10.1016/j.canep.2026.102997","DOIUrl":"10.1016/j.canep.2026.102997","url":null,"abstract":"<div><h3>Background</h3><div>Inequalities in adult cancer survival by sex, socio-economic position, and rural-urban residence are well established; however, evidence for childhood cancers, particularly site-specific survival, remains limited and inconsistent. This study investigated whether these inequalities exist among children diagnosed with central nervous system (CNS) cancers or neuroblastoma.</div></div><div><h3>Methods</h3><div>We conducted a population-based study using Victorian Cancer Registry data including 1324 children aged 0–14 years when diagnosed with CNS cancers (n = 933) or neuroblastoma (n = 391) in 1982–2021. Follow-up was conducted through linkage with death registries up to the end of 2021. Multivariable Cox regression models were used to estimate hazard ratios (HRs) for all-cause mortality in relation to sex, area-level socio-economic disadvantage, and remoteness of residence.</div></div><div><h3>Results</h3><div>There was weak evidence of higher mortality in males than females for both CNS cancers (HR=1.16; 95 % CI: 0.96–1.41) and neuroblastoma (HR=1.29; 95 % CI: 0.92–1.80). Survival was poorer among children living in the most disadvantaged areas (highest quintile): 54 % higher mortality for CNS cancers (HR=1.54; 95 % CI: 1.09–2.18) and 89 % higher for neuroblastoma (HR=1.89; 95 % CI: 0.99–3.61) compared to those in the least disadvantaged areas (lowest quintile). Children with neuroblastoma living outside major cities had higher mortality (HR=1.43; 95 % CI: 1.01–2.02) than those in major cities, which was attenuated (HR=1.32; 95 % CI: 0.92–1.88) after adjustment for socio-economic disadvantage.</div></div><div><h3>Conclusion</h3><div>Children with CNS cancers and neuroblastoma living in socio-economically disadvantaged areas experienced poorer survival outcomes. There was weaker evidence for poorer survival in males and those living outside major cities. These findings underscore the need for targeted strategies to address survival inequalities in these childhood cancers.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 102997"},"PeriodicalIF":2.3,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024974","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}
Emerging evidence suggests a complex bidirectional relationship between cardiovascular disease (CVD) and cancer. However, population-level data characterizing the burden of cardiovascular comorbidities at the time of cancer-attributable death remains limited. We analyzed the association between the presence of cardiovascular disease on death certificates and cancer mortality patterns across demographic groups using national mortality data from 1999 to 2020.
Methods
Using CDC WONDER multiple cause-of-death data, we analyzed records of adults ≥ 18 years with cancer as the underlying cause of death. CVD comorbidity was defined as any cardiovascular condition (ICD-10 I00-I99) listed as a contributing cause. We calculated age-adjusted mortality rates (AAMR) per 100,000 population and rate ratios, stratified by demographics and cancer types.
Results
Among 13,847,293 cancer deaths, 4521,847 (32.6 %) had cardiovascular disease listed as a contributing cause. The overall AAMR for cancer deaths with CVD was 47.75 per 100,000 (95 % CI: 47.66–47.85). Males showed higher rates than females (62.26 vs 37.22 per 100,000, rate ratio 1.67). Non-Hispanic Black populations had the highest burden (57.10 per 100,000), while Asian/Pacific Islander populations had the lowest (30.80 per 100,000). For lung cancer, mortality rates were substantially higher when CVD was present, with rate ratios ranging from 1.70 to 2.43; however, this association is likely attributable to profound unmeasured confounding by shared risk factors such as smoking.
Conclusions
Cardiovascular disease is listed as a contributing factor in nearly one-third of all cancer deaths, with distinct demographic patterns. These findings highlight the significant burden of cardiovascular comorbidities documented on death certificates at the end of life for cancer patients.
{"title":"Cardiovascular disease as a contributing cause of cancer mortality: A population-based analysis of United States death certificate data (1999–2020)","authors":"Sanchit Mehta , Lovy Arora , Netra Agarwal , Asha Khubchandani","doi":"10.1016/j.canep.2026.102991","DOIUrl":"10.1016/j.canep.2026.102991","url":null,"abstract":"<div><h3>Background</h3><div>Emerging evidence suggests a complex bidirectional relationship between cardiovascular disease (CVD) and cancer. However, population-level data characterizing the burden of cardiovascular comorbidities at the time of cancer-attributable death remains limited. We analyzed the association between the presence of cardiovascular disease on death certificates and cancer mortality patterns across demographic groups using national mortality data from 1999 to 2020.</div></div><div><h3>Methods</h3><div>Using CDC WONDER multiple cause-of-death data, we analyzed records of adults ≥ 18 years with cancer as the underlying cause of death. CVD comorbidity was defined as any cardiovascular condition (ICD-10 I00-I99) listed as a contributing cause. We calculated age-adjusted mortality rates (AAMR) per 100,000 population and rate ratios, stratified by demographics and cancer types.</div></div><div><h3>Results</h3><div>Among 13,847,293 cancer deaths, 4521,847 (32.6 %) had cardiovascular disease listed as a contributing cause. The overall AAMR for cancer deaths with CVD was 47.75 per 100,000 (95 % CI: 47.66–47.85). Males showed higher rates than females (62.26 vs 37.22 per 100,000, rate ratio 1.67). Non-Hispanic Black populations had the highest burden (57.10 per 100,000), while Asian/Pacific Islander populations had the lowest (30.80 per 100,000). For lung cancer, mortality rates were substantially higher when CVD was present, with rate ratios ranging from 1.70 to 2.43; however, this association is likely attributable to profound unmeasured confounding by shared risk factors such as smoking.</div></div><div><h3>Conclusions</h3><div>Cardiovascular disease is listed as a contributing factor in nearly one-third of all cancer deaths, with distinct demographic patterns. These findings highlight the significant burden of cardiovascular comorbidities documented on death certificates at the end of life for cancer patients.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 102991"},"PeriodicalIF":2.3,"publicationDate":"2026-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146024976","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":"Comment on “Association between blood cholesterol profile and risk of lung cancer: A meta-analysis of prospective cohort studies”","authors":"Sushma Narsing Katkuri, Zarine Khan, Rhushvi Thakkar, Archana Dhyani, Hariharan Srinivasan","doi":"10.1016/j.canep.2026.103000","DOIUrl":"10.1016/j.canep.2026.103000","url":null,"abstract":"","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 103000"},"PeriodicalIF":2.3,"publicationDate":"2026-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146020735","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}
Pub Date : 2026-01-16DOI: 10.1016/j.canep.2026.102987
Jaehee Jung , Hyunha Kang , Eunjung Choo , Hye-Young Kang , Chang Wook Jeong , Ha-Lim Jeon , Hankil Lee
Introduction
The incidence of prostate cancer (PC) is rapidly increasing with population aging. With the emergence of new androgen receptor-targeting agents beyond androgen deprivation therapy, the treatment paradigm for PC is expected to shift. This study aimed to analyze the epidemiological characteristics and treatment patterns of patients with PC in Korea over the past decade, with a particular focus on drug utilization.
Materials and methods
We conducted a prevalence-based cross-sectional study on all Korean patients who received medical care for PC between 2011 and 2021. Patient characteristics, including age, comorbidities, metastatic status, drug classes, and treatment patterns, were analyzed.
Results
In 2021, the prevalence of PC was 532 per 100,000 adult men, an increase of 170.45 %, from 220 per 100,000 adult men in 2011. The mean age of patients with PC in 2021 was 73.07 years, with more than 80 % aged 65 years or older. Comorbidities, such as diabetes, pulmonary diseases, and mild liver disease, were common. Androgen deprivation therapy remained the most common pharmacological treatment; however, the proportion of its use gradually decreased over time, and the introduction of androgen receptor-targeting agents led to a steady increase in their use.
Conclusions
This study provides real-world evidence of the epidemiology and therapeutic patterns of PC, thereby enhancing the understanding of the current clinical landscape in Korea.
{"title":"Prostate cancer in Korea: Nationwide trends in prevalence and medication use during 2011–2021","authors":"Jaehee Jung , Hyunha Kang , Eunjung Choo , Hye-Young Kang , Chang Wook Jeong , Ha-Lim Jeon , Hankil Lee","doi":"10.1016/j.canep.2026.102987","DOIUrl":"10.1016/j.canep.2026.102987","url":null,"abstract":"<div><h3>Introduction</h3><div>The incidence of prostate cancer (PC) is rapidly increasing with population aging. With the emergence of new androgen receptor-targeting agents beyond androgen deprivation therapy, the treatment paradigm for PC is expected to shift. This study aimed to analyze the epidemiological characteristics and treatment patterns of patients with PC in Korea over the past decade, with a particular focus on drug utilization.</div></div><div><h3>Materials and methods</h3><div>We conducted a prevalence-based cross-sectional study on all Korean patients who received medical care for PC between 2011 and 2021. Patient characteristics, including age, comorbidities, metastatic status, drug classes, and treatment patterns, were analyzed.</div></div><div><h3>Results</h3><div>In 2021, the prevalence of PC was 532 per 100,000 adult men, an increase of 170.45 %, from 220 per 100,000 adult men in 2011. The mean age of patients with PC in 2021 was 73.07 years, with more than 80 % aged 65 years or older. Comorbidities, such as diabetes, pulmonary diseases, and mild liver disease, were common. Androgen deprivation therapy remained the most common pharmacological treatment; however, the proportion of its use gradually decreased over time, and the introduction of androgen receptor-targeting agents led to a steady increase in their use.</div></div><div><h3>Conclusions</h3><div>This study provides real-world evidence of the epidemiology and therapeutic patterns of PC, thereby enhancing the understanding of the current clinical landscape in Korea.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 102987"},"PeriodicalIF":2.3,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145981928","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}
Pub Date : 2026-01-16DOI: 10.1016/j.canep.2026.102988
Christèle Asmar , Raphaël Asmar , Maria Al Rachid , Carole Kesrouani , Viviane Trak-Smayra , Hampig Raphaël Kourié , Joseph Gharios
Background
Neuroendocrine neoplasms (NENs) are rare tumors, making up 0.5 % of all cancers, with around 65 % found in the gastroenteropancreatic (GEP) system, with increasing occurrence globally in recent years. The World Health Organization (WHO) classifies GEP-NENs into two main groups: neuroendocrine tumors and neuroendocrine carcinomas according to the new 2022 classification.
Aim
To provide updated epidemiological data on GEP-NENs diagnosed at a tertiary referral center in Beirut, Lebanon, using the WHO 2022 classification, and to describe changes in incidence, demographics, and tumor characteristics compared with previously reported data.
Methods
This retrospective study included patients treated at Hotel Dieu de France, from January 2013 to June 2024, with histologically confirmed GEP-NENs and complete medical records available. GEP-NENs were categorized based on their primary site and pathology reports reanalyzed according to the WHO 2022 classification. Data were then collected on patient demographics, primary tumor site, tumor grade and presence of metastasis at diagnosis.
Results
Among 194 NENs diagnosed during the study period, 74 were GEP-NENs (25.2 %). The mean age at diagnosis was 59.8 years, with a male-to-female ratio of 1.61. Of patients with available grading data, 39.0 % were classified as NET G1, 34.4 % as NET G2, and 26.6 % as high-grade disease (NET G3 and NEC combined). Compared with data from the previous decade, a lower proportion of G1 tumors and higher proportions of G2 and G3 tumors were observed, along with higher frequencies of pancreatic and hepatic primaries and lower rates of colonic and duodenal primaries. NET G3 and NECs were most frequently located in the liver, ampulla of Vater, and colon. All colorectal GEP-NENs identified were metastatic at diagnosis.
Conclusion
GEP-NENs in this cohort were more frequently diagnosed with higher histological grades and metastatic disease compared to the previous decade, a pattern observed during a period marked by major socioeconomic disruption and the COVID-19 pandemic.
{"title":"Unicentric retrospective study of gastroenteropancreatic neuroendocrine tumors: Updated epidemiological insights","authors":"Christèle Asmar , Raphaël Asmar , Maria Al Rachid , Carole Kesrouani , Viviane Trak-Smayra , Hampig Raphaël Kourié , Joseph Gharios","doi":"10.1016/j.canep.2026.102988","DOIUrl":"10.1016/j.canep.2026.102988","url":null,"abstract":"<div><h3>Background</h3><div>Neuroendocrine neoplasms (NENs) are rare tumors, making up 0.5 % of all cancers, with around 65 % found in the gastroenteropancreatic (GEP) system, with increasing occurrence globally in recent years. The World Health Organization (WHO) classifies GEP-NENs into two main groups: neuroendocrine tumors and neuroendocrine carcinomas according to the new 2022 classification.</div></div><div><h3>Aim</h3><div>To provide updated epidemiological data on GEP-NENs diagnosed at a tertiary referral center in Beirut, Lebanon, using the WHO 2022 classification, and to describe changes in incidence, demographics, and tumor characteristics compared with previously reported data.</div></div><div><h3>Methods</h3><div>This retrospective study included patients treated at Hotel Dieu de France, from January 2013 to June 2024, with histologically confirmed GEP-NENs and complete medical records available. GEP-NENs were categorized based on their primary site and pathology reports reanalyzed according to the WHO 2022 classification. Data were then collected on patient demographics, primary tumor site, tumor grade and presence of metastasis at diagnosis.</div></div><div><h3>Results</h3><div>Among 194 NENs diagnosed during the study period, 74 were GEP-NENs (25.2 %). The mean age at diagnosis was 59.8 years, with a male-to-female ratio of 1.61. Of patients with available grading data, 39.0 % were classified as NET G1, 34.4 % as NET G2, and 26.6 % as high-grade disease (NET G3 and NEC combined). Compared with data from the previous decade, a lower proportion of G1 tumors and higher proportions of G2 and G3 tumors were observed, along with higher frequencies of pancreatic and hepatic primaries and lower rates of colonic and duodenal primaries. NET G3 and NECs were most frequently located in the liver, ampulla of Vater, and colon. All colorectal GEP-NENs identified were metastatic at diagnosis.</div></div><div><h3>Conclusion</h3><div>GEP-NENs in this cohort were more frequently diagnosed with higher histological grades and metastatic disease compared to the previous decade, a pattern observed during a period marked by major socioeconomic disruption and the COVID-19 pandemic.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 102988"},"PeriodicalIF":2.3,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145981929","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}
Pub Date : 2026-01-16DOI: 10.1016/j.canep.2026.102994
Jie Cai , Hongda Chen , Yuhan Zhang , Bin Lu , Ming Lu , Chenyu Luo , Lei You , Min Dai
Background
Pancreatic cancer (PC) is a malignant tumor without effective screening methods in the general population. This study aimed to develop a PC risk score to identify men at high risk for PC for early intervention.
Methods
Based on a prospective cohort study conducted in China in 2006, 90,402 men with at least two fasting blood glucose (FBG) measurements were included in this study. The PC risk model was developed using Cox regression, including the risk factors for age, total cholesterol, FBG and body mass index (BMI) change rate. The power of discrimination was examined using Harrell’s C-index and time-dependent area under curves (AUCs).
Results
During the 10-year follow-up period, 82 men developed PC (total person-years: 821,346). Age, total cholesterol level, FBG and BMI change rate were included in the final PC risk model, with a C-index of 0.754 (95 % CI 0.709–0.799). After internal validation, the AUCs of the model in different years (2, 5, 8, and 10 years) were > 0.700 in all men and in men without diabetes. In the derived scoring system (score range:-2–10), there was an approximately 40 % increased risk (Hazard ratio, 1.415; 95 % CI, 1.291–1.550) with every 1-point increase. Participants with the top 20 % scores (6–10 points) had a 30-fold increased risk of PC compared with individuals in the lowest score group (-2 – -1 points).
Conclusions
A scoring system for identifying high-risk men with PC was developed, which may be helpful for early detection and intervention of PC in the future.
{"title":"Risk score development for pancreatic cancer in Chinese men: A population-based cohort study","authors":"Jie Cai , Hongda Chen , Yuhan Zhang , Bin Lu , Ming Lu , Chenyu Luo , Lei You , Min Dai","doi":"10.1016/j.canep.2026.102994","DOIUrl":"10.1016/j.canep.2026.102994","url":null,"abstract":"<div><h3>Background</h3><div>Pancreatic cancer (PC) is a malignant tumor without effective screening methods in the general population. This study aimed to develop a PC risk score to identify men at high risk for PC for early intervention.</div></div><div><h3>Methods</h3><div>Based on a prospective cohort study conducted in China in 2006, 90,402 men with at least two fasting blood glucose (FBG) measurements were included in this study. The PC risk model was developed using Cox regression, including the risk factors for age, total cholesterol, FBG and body mass index (BMI) change rate. The power of discrimination was examined using Harrell’s C-index and time-dependent area under curves (AUCs).</div></div><div><h3>Results</h3><div>During the 10-year follow-up period, 82 men developed PC (total person-years: 821,346). Age, total cholesterol level, FBG and BMI change rate were included in the final PC risk model, with a C-index of 0.754 (95 % CI 0.709–0.799). After internal validation, the AUCs of the model in different years (2, 5, 8, and 10 years) were > 0.700 in all men and in men without diabetes. In the derived scoring system (score range:-2–10), there was an approximately 40 % increased risk (Hazard ratio, 1.415; 95 % CI, 1.291–1.550) with every 1-point increase. Participants with the top 20 % scores (6–10 points) had a 30-fold increased risk of PC compared with individuals in the lowest score group (-2 – -1 points).</div></div><div><h3>Conclusions</h3><div>A scoring system for identifying high-risk men with PC was developed, which may be helpful for early detection and intervention of PC in the future.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"101 ","pages":"Article 102994"},"PeriodicalIF":2.3,"publicationDate":"2026-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145981930","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}
Pub Date : 2026-01-08DOI: 10.1016/j.canep.2026.102986
Thomas Lawler , Zoe L. Walts , Lauren Giurini , Mark Steinwandel , Wei Zheng , Shaneda Warren Andersen
Background
Higher serum insulin-like growth factor 1 (IGF-1) has been linked to colorectal cancer (CRC), with evidence supporting increased risk for colon but not rectal tumors. Few studies have included substantial numbers of non-Hispanic Black individuals, who have elevated population-level CRC risk. We investigated associations between IGF-1 and CRC in the Southern Community Cohort Study. We also report associations with IGF binding protein 3 (IGFBP-3), the primary IGF-1 transporter, and the IGF-1/IGFBP-3 ratio (a surrogate marker for biologically available IGF-1).
Methods
Participants with incident CRC (N = 297) were individually matched with controls (N = 604) on age, race, and sex. The majority of the cohort reports Black racial identity (75 %). Serum IGF-1 and IGFBP-3 were measured at enrollment. Logistic regression was used to estimate odds ratios (ORs) with 95 % confidence intervals (CIs) for CRC, colon and rectal cancers.
Results
For higher IGF-1 (tertile 3vs1), the OR for CRC was 1.45 (CI 0.95–2.21). Higher IGF-1 was associated with greater odds for colon cancer (OR 1.64, CI 1.01–2.64) but not rectal cancer (OR 0.93, CI 0.43–1.97). The associations with CRC and colon cancer were consistent among participants who fasted prior to serum draw (N = 356, CRC: OR 1.89, CI 0.95–3.78; colon cancer: OR 2.08, CI 0.96–4.51). No associations were observed for IGFBP-3 or the IGF-1/IGFBP-3 ratio in the full sample.
Conclusion
Higher IGF-1 was associated with increased odds for colon cancer, but not rectal cancer, among predominantly non-Hispanic Black individuals with lower socioeconomic status, consistent with findings from predominantly non-Hispanic White cohorts.
高血清胰岛素样生长因子1 （IGF-1）与结直肠癌（CRC）有关，有证据支持结肠肿瘤风险增加，而非直肠肿瘤。很少有研究包括大量非西班牙裔黑人，他们有较高的人群CRC风险。我们在南部社区队列研究中调查了IGF-1与CRC之间的关系。我们还报道了与IGF结合蛋白3 （IGFBP-3）、主要IGF-1转运蛋白和IGF-1/IGFBP-3比率（生物可用性IGF-1的替代标记物）的关联。方法将发生CRC的参与者（N = 297）与对照组（N = 604）在年龄、种族和性别上进行单独匹配。大多数队列报告黑人种族身份（75% %）。入组时测定血清IGF-1和IGFBP-3。采用Logistic回归估计CRC、结肠癌和直肠癌的比值比（ORs），置信区间为95% %。结果高IGF-1组CRC的OR为1.45 （CI 0.95 ~ 2.21）。较高的IGF-1与结肠癌（OR 1.64, CI 1.01-2.64）相关，但与直肠癌（OR 0.93, CI 0.43-1.97）无关。在血清抽血前禁食的参与者中，结直肠癌和结肠癌的相关性是一致的（N = 356，结直肠癌：OR 1.89, CI 0.95-3.78；结肠癌：OR 2.08, CI 0.96-4.51）。在整个样本中没有观察到IGFBP-3或IGF-1/IGFBP-3比值的关联。结论：在社会经济地位较低的非西班牙裔黑人中，较高的IGF-1与结肠癌的发病率增加有关，但与直肠癌无关，这与非西班牙裔白人人群的研究结果一致。
{"title":"Associations between insulin-like growth factor 1, IGF-binding protein 3, and colorectal cancer","authors":"Thomas Lawler , Zoe L. Walts , Lauren Giurini , Mark Steinwandel , Wei Zheng , Shaneda Warren Andersen","doi":"10.1016/j.canep.2026.102986","DOIUrl":"10.1016/j.canep.2026.102986","url":null,"abstract":"<div><h3>Background</h3><div>Higher serum insulin-like growth factor 1 (IGF-1) has been linked to colorectal cancer (CRC), with evidence supporting increased risk for colon but not rectal tumors. Few studies have included substantial numbers of non-Hispanic Black individuals, who have elevated population-level CRC risk. We investigated associations between IGF-1 and CRC in the Southern Community Cohort Study. We also report associations with IGF binding protein 3 (IGFBP-3), the primary IGF-1 transporter, and the IGF-1/IGFBP-3 ratio (a surrogate marker for biologically available IGF-1).</div></div><div><h3>Methods</h3><div>Participants with incident CRC (N = 297) were individually matched with controls (N = 604) on age, race, and sex. The majority of the cohort reports Black racial identity (75 %). Serum IGF-1 and IGFBP-3 were measured at enrollment. Logistic regression was used to estimate odds ratios (ORs) with 95 % confidence intervals (CIs) for CRC, colon and rectal cancers.</div></div><div><h3>Results</h3><div>For higher IGF-1 (tertile 3vs1), the OR for CRC was 1.45 (CI 0.95–2.21). Higher IGF-1 was associated with greater odds for colon cancer (OR 1.64, CI 1.01–2.64) but not rectal cancer (OR 0.93, CI 0.43–1.97). The associations with CRC and colon cancer were consistent among participants who fasted prior to serum draw (N = 356, CRC: OR 1.89, CI 0.95–3.78; colon cancer: OR 2.08, CI 0.96–4.51). No associations were observed for IGFBP-3 or the IGF-1/IGFBP-3 ratio in the full sample.</div></div><div><h3>Conclusion</h3><div>Higher IGF-1 was associated with increased odds for colon cancer, but not rectal cancer, among predominantly non-Hispanic Black individuals with lower socioeconomic status, consistent with findings from predominantly non-Hispanic White cohorts.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"100 ","pages":"Article 102986"},"PeriodicalIF":2.3,"publicationDate":"2026-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145924709","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}
Pub Date : 2026-01-03DOI: 10.1016/j.canep.2025.102985
Yu Long , Yuting Zhu , Meiyin Lin , Qinming Li , Jun Liang , Chunyang Wang , Ruijie Zeng , Dongling Luo , Lijun Zhang , Yuyin Ma , Chongyang Duan , Yue Zhu , Hao Chen , Jianhua Liu
Background
Although tobacco exposure is an established risk factor for colorectal cancer (CRC), the specific impact of early-life exposure (from prenatal to adolescence) and its joints with genetic susceptibility remains uncertain. This population-based study aimed to investigate the joint effects of early-life tobacco exposure and polygenic risk on CRC.
Methods
Data from UK Biobank participants were analyzed to assess tobacco exposure during two periods: prenatal exposure (n = 429,847) and age of smoking initiation (n = 430,672). Using Cox proportional hazards models, the associations between early-life tobacco exposure and CRC incidence were explored. Additionally, we evaluated the mediating role of accelerated biological aging in the link between early-life tobacco exposure and CRC, and further integrated the polygenic risk score (PRS) to assess the joint effects of genetic on CRC risk.
Results
Early-life tobacco exposure exhibited age-at-initiation-dependent CRC risk associations. Smoking initiation in adolescence [hazard ratios (HR) = 1.13, 95 % confidence intervals (CI): 1.06–1.22], and adulthood (HR = 1.19, 95 % CI: 1.10–1.30) all significantly increased risk (P < 0.001), while in utero exposure and smoking initiation childhood (HR:1.06, 95 % CI: 0.94–1.19, P = 0.372) showed a suggestive but non-significant trend (HR:1.05, 95 % CI: 1.00–1.11, P = 0.066). In the joint analysis, high-PRS individuals with prenatal tobacco exposure had an elevated CRC risk compared to those with low PRS and no exposure (HR 1.28, 95 % CI: 1.16–1.42, P < 0.001). Furthermore, among high-PRS individuals, smoking initiation at any age (childhood, adolescence, or adulthood) increased CRC risk relative to never-smokers with low PRS. Mediation analysis indicated that accelerated biological aging may contribute to the association between smoking initiation at different ages and increased CRC risk.
Conclusion
Early-life tobacco exposure elevated CRC risk, especially in genetically susceptible individuals. These findings underscored the importance of early tobacco prevention and enhanced screening for high genetic-risk populations.
{"title":"Early-life tobacco exposure, genetic susceptibility and incident colorectal cancer risk in UK biobank: A prospective cohort analysis","authors":"Yu Long , Yuting Zhu , Meiyin Lin , Qinming Li , Jun Liang , Chunyang Wang , Ruijie Zeng , Dongling Luo , Lijun Zhang , Yuyin Ma , Chongyang Duan , Yue Zhu , Hao Chen , Jianhua Liu","doi":"10.1016/j.canep.2025.102985","DOIUrl":"10.1016/j.canep.2025.102985","url":null,"abstract":"<div><h3>Background</h3><div>Although tobacco exposure is an established risk factor for colorectal cancer (CRC), the specific impact of early-life exposure (from prenatal to adolescence) and its joints with genetic susceptibility remains uncertain. This population-based study aimed to investigate the joint effects of early-life tobacco exposure and polygenic risk on CRC.</div></div><div><h3>Methods</h3><div>Data from UK Biobank participants were analyzed to assess tobacco exposure during two periods: prenatal exposure (n = 429,847) and age of smoking initiation (n = 430,672). Using Cox proportional hazards models, the associations between early-life tobacco exposure and CRC incidence were explored. Additionally, we evaluated the mediating role of accelerated biological aging in the link between early-life tobacco exposure and CRC, and further integrated the polygenic risk score (PRS) to assess the joint effects of genetic on CRC risk.</div></div><div><h3>Results</h3><div>Early-life tobacco exposure exhibited age-at-initiation-dependent CRC risk associations. Smoking initiation in adolescence [hazard ratios (HR) = 1.13, 95 % confidence intervals (CI): 1.06–1.22], and adulthood (HR = 1.19, 95 % CI: 1.10–1.30) all significantly increased risk (<em>P</em> < 0.001), while in utero exposure and smoking initiation childhood (HR:1.06, 95 % CI: 0.94–1.19, <em>P</em> = 0.372) showed a suggestive but non-significant trend (HR:1.05, 95 % CI: 1.00–1.11, <em>P</em> = 0.066). In the joint analysis, high-PRS individuals with prenatal tobacco exposure had an elevated CRC risk compared to those with low PRS and no exposure (HR 1.28, 95 % CI: 1.16–1.42, P < 0.001). Furthermore, among high-PRS individuals, smoking initiation at any age (childhood, adolescence, or adulthood) increased CRC risk relative to never-smokers with low PRS. Mediation analysis indicated that accelerated biological aging may contribute to the association between smoking initiation at different ages and increased CRC risk.</div></div><div><h3>Conclusion</h3><div>Early-life tobacco exposure elevated CRC risk, especially in genetically susceptible individuals. These findings underscored the importance of early tobacco prevention and enhanced screening for high genetic-risk populations.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"100 ","pages":"Article 102985"},"PeriodicalIF":2.3,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883748","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}
Pub Date : 2026-01-03DOI: 10.1016/j.canep.2025.102984
Stuart J. Case , Lindsay Sabik , Haley Grant
Introduction
Cancer survivors endure unique immune system suppression as a result of their cancer treatment, potentially making them susceptible to long COVID in ways that differ from the general population. The purpose of this study is to assess what factors are associated with long COVID among cancer survivors.
Methods
Observational, cross-sectional data from the 2023 Behavioral Risk Factor Surveillance System (BRFSS) survey were analyzed. The main outcome of interest was the prevalence of long COVID among cancer survivors who had tested positive for COVID-19. Bivariate analyses were conducted comparing those who did and did not have long COVID, and logistic regression models were used to determine the sociodemographic variables and individual health factors associated with long COVID among cancer survivors.
Results
In this sample, 15.2 % of cancer survivors who had tested positive for COVID-19 indicated they had long COVID. Cancer survivors who were male, older, received flu and COVID-19 vaccinations, and did not have diabetes or asthma had significantly lower odds of having long COVID.
Conclusion
This study provides insight into what sociodemographic and health-related factors are associated with the presence of long COVID, including age, sex, vaccination status, and comorbid conditions. Future longitudinal studies are warranted to establish causal patterns.
{"title":"Factors associated with long COVID among cancer survivors: A population-based analysis","authors":"Stuart J. Case , Lindsay Sabik , Haley Grant","doi":"10.1016/j.canep.2025.102984","DOIUrl":"10.1016/j.canep.2025.102984","url":null,"abstract":"<div><h3>Introduction</h3><div>Cancer survivors endure unique immune system suppression as a result of their cancer treatment, potentially making them susceptible to long COVID in ways that differ from the general population. The purpose of this study is to assess what factors are associated with long COVID among cancer survivors.</div></div><div><h3>Methods</h3><div>Observational, cross-sectional data from the 2023 Behavioral Risk Factor Surveillance System (BRFSS) survey were analyzed. The main outcome of interest was the prevalence of long COVID among cancer survivors who had tested positive for COVID-19. Bivariate analyses were conducted comparing those who did and did not have long COVID, and logistic regression models were used to determine the sociodemographic variables and individual health factors associated with long COVID among cancer survivors.</div></div><div><h3>Results</h3><div>In this sample, 15.2 % of cancer survivors who had tested positive for COVID-19 indicated they had long COVID. Cancer survivors who were male, older, received flu and COVID-19 vaccinations, and did not have diabetes or asthma had significantly lower odds of having long COVID.</div></div><div><h3>Conclusion</h3><div>This study provides insight into what sociodemographic and health-related factors are associated with the presence of long COVID, including age, sex, vaccination status, and comorbid conditions. Future longitudinal studies are warranted to establish causal patterns.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"100 ","pages":"Article 102984"},"PeriodicalIF":2.3,"publicationDate":"2026-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145883747","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}
Pub Date : 2025-12-27DOI: 10.1016/j.canep.2025.102983
Yehudit Peerless , Gal Strauss , Ofer Margalit , Einat Shacham-Shmueli , Yu-Xiao Yang , Ben Boursi
Background
Colorectal cancer (CRC) is a major cause of cancer-related morbidity and mortality. Tumor sidedness influences treatment decisions for metastatic disease due to differences in biology and therapeutic response. Metformin, an anti-diabetic medication, may reduce CRC risk. This study aims to evaluate the relationship between metformin exposure and CRC risk based on tumor-sidedness.
Methods
A nested case-control study was conducted using the Veterans Administration (VA) database (1999–2020). The cohort included individuals with diabetes mellitus and at least 3 years of follow-up. CRC cases were identified and classified by tumor sidedness. Controls were selected via incidence-density sampling, matched on age, sex, index-date, and first VA encounter. Exposure of interest was cumulative metformin use prior to the index-date. Conditional logistic regression was used to estimate adjusted odds-ratios (ORs) and 95 % confidence intervals (CIs). The analysis was adjusted for race, BMI, smoking, aspirin, statins, and other anti-diabetic medications.
Results
The study included 31,078 CRC cases and 310,621 matched controls among diabetic individuals. Metformin exposure showed no effect on right-sided CRC incidence (adjusted OR 1.03, 95 %CI 0.92–1.16 for 1–3 years; 0.96, 95 %CI 0.83–1.12 for 3–5 years). In contrast, in patients with left-sided CRC metformin use was associated with a reduced risk of CRC (adjusted OR 0.90, 95 %CI 0.82–0.98 for 1–3 years; 0.87, 95 %CI 0.77–0.98 for 3–5 years).
Conclusions
Metformin was associated with a decrease in the incidence of left-sided CRC. These results suggest the influence of tumor sidedness, not only on treatment effect, but on prevention strategies as well.
{"title":"The effect of metformin exposure on colorectal cancer incidence according to tumor sidedness","authors":"Yehudit Peerless , Gal Strauss , Ofer Margalit , Einat Shacham-Shmueli , Yu-Xiao Yang , Ben Boursi","doi":"10.1016/j.canep.2025.102983","DOIUrl":"10.1016/j.canep.2025.102983","url":null,"abstract":"<div><h3>Background</h3><div>Colorectal cancer (CRC) is a major cause of cancer-related morbidity and mortality. Tumor sidedness influences treatment decisions for metastatic disease due to differences in biology and therapeutic response. Metformin, an anti-diabetic medication, may reduce CRC risk. This study aims to evaluate the relationship between metformin exposure and CRC risk based on tumor-sidedness.</div></div><div><h3>Methods</h3><div>A nested case-control study was conducted using the Veterans Administration (VA) database (1999–2020). The cohort included individuals with diabetes mellitus and at least 3 years of follow-up. CRC cases were identified and classified by tumor sidedness. Controls were selected via incidence-density sampling, matched on age, sex, index-date, and first VA encounter. Exposure of interest was cumulative metformin use prior to the index-date. Conditional logistic regression was used to estimate adjusted odds-ratios (ORs) and 95 % confidence intervals (CIs). The analysis was adjusted for race, BMI, smoking, aspirin, statins, and other anti-diabetic medications.</div></div><div><h3>Results</h3><div>The study included 31,078 CRC cases and 310,621 matched controls among diabetic individuals. Metformin exposure showed no effect on right-sided CRC incidence (adjusted OR 1.03, 95 %CI 0.92–1.16 for 1–3 years; 0.96, 95 %CI 0.83–1.12 for 3–5 years). In contrast, in patients with left-sided CRC metformin use was associated with a reduced risk of CRC (adjusted OR 0.90, 95 %CI 0.82–0.98 for 1–3 years; 0.87, 95 %CI 0.77–0.98 for 3–5 years).</div></div><div><h3>Conclusions</h3><div>Metformin was associated with a decrease in the incidence of left-sided CRC. These results suggest the influence of tumor sidedness, not only on treatment effect, but on prevention strategies as well.</div></div>","PeriodicalId":56322,"journal":{"name":"Cancer Epidemiology","volume":"100 ","pages":"Article 102983"},"PeriodicalIF":2.3,"publicationDate":"2025-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145839684","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}
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