Background:Although tobacco smoking is one of the established risk factors for liver cancer, results from epidemiological studies remain inconclusive on the relationship between second-hand smoke (SHS) and liver cancer, particularly among nonsmokers.Objectives:This study aimed to examine the association between SHS and liver cancer, and to assess its potential interaction with major risk factors such as hepatitis B virus (HBV) infection.Methods:A population-based case-control study was conducted in Jiangsu, China, from 2003 to 2010, including 2011 newly diagnosed primary liver cancer cases and 7933 population-based controls. Data on SHS exposure at home and in the workplace, along with other major liver cancer risk factors such as alcohol consumption, were collected through self-reported questionnaires. SHS exposure was assessed as a dichotomous variable, categorizing participants as either exposed or unexposed to SHS. HBV infection status was determined by testing serum samples for serum hepatitis B virus surface antigen. Multivariable unconditional logistic regression models were used to examine the association between SHS and risk of liver cancer. Besides stratified analyses, interactions on additive and multiplicative scales were further evaluated between SHS and other risk factors for liver cancer.Results:Exposure to SHS was associated with liver cancer, shown as adjusted odds ratios (ORs) of 1.84 (95% confidence interval [CI]: 1.56, 2.18) in the overall population and 2.11 (95% CI: 1.67, 2.65) among never smokers. Stratified analyses showed that the association between SHS and liver cancer was stronger among HBV-positive participants (OR: 2.09, 95% CI: 1.48, 2.93) compared with HBV-negative participants (OR: 1.87, 95% CI: 1.54, 2.27) (P = 0.02). Both super-additive and super-multiplicative interactions were observed between SHS and HBV infection, with relative excess risk due to interaction (RERI) of 12.56 (95% CI: 6.60, 18.53) and ratio of ORs of 1.55 (95% CI: 1.07, 2.23) in the total population, and RERI of 12.87 (95% CI: 4.93, 20.81) and ratio of ORs of 1.78 (95% CI: 1.06, 2.99) among never smokers.Conclusion:SHS is independently associated with liver cancer, and this association is further modified by HBV infection, leading to a substantially elevated risk, particularly among nonsmokers.

OBJECTIVE:In the United States, racial and ethnic minorities have higher risk of developing type 2 diabetes (T2D) than Whites. One hypothesis is that some minorities (e.g., Hispanics, Asians) have more visceral fat than Whites in a sex-specific manner. We aimed to test this hypothesis by examining to what degree racial differences in T2D were explained by visceral fat in males and females. METHODS:This prospective cohort included 1457 participants (51.2% females) from the Multi-Ethnic Study of Atherosclerosis (MESA) cohort who had visceral fat measured by computed tomography and followed for incident T2D from 2002-2005 to 2020. We assessed associations of race and T2D risk using Cox proportional hazards regressions and estimated associations explained by visceral fat using natural mediation effects, stratified by sex. RESULTS:Controlling for confounders, compared with White participants, T2D risk was higher in Hispanic females (HR 1.77, 95% CI 1.17-2.69), Chinese females (1.91, 1.15-3.15), Black females (1.59, 1.02-2.49), and Hispanic males (1.82, 1.20-2.76). Estimates for Black males (1.48, 0.92-2.38) and Chinese males (0.86, 0.48-1.55) were not statistically significant. By sex, Hispanic females [mean difference (SE): 22.72 (5.68)] had higher visceral fat (cm2) than White females, while Chinese [-77.56 (8.47)] and Black [-57.57 (8.11)] males had lower visceral fat (cm2) than White males. Visceral fat explained 23.1% of T2D risk between Hispanic and White females, but not for other racial and sex subgroups. CONCLUSION:Visceral fat explained one-fifth of racial and ethnic differences in T2D comparing Hispanic females to White females and may contribute to Hispanic females' higher T2D risk.

INTRODUCTION:The relationship between insufficient sleep and prostate cancer incidence is unclear. Our goal was to investigate the association of sleep duration, restless sleep, and prostate cancer incidence and aggressiveness, and whether race influences any sleep-prostate cancer association. METHODS:The Southern Community Cohort Study (SCCS) recruited study participants from 12 Southeastern states from 2002 to 2009. The cohort included nearly 35,000 males, predominantly African American (AA, 67%). Sleep exposures were measured via a baseline questionnaire at enrollment, which captured weekday and weekend sleep duration, weighted average sleep duration, and restless sleep. We used Cox proportional hazards models and multinomial logistic regression models to estimate associations between sleep and prostate cancer incidence and aggressiveness. RESULTS:During follow-up (median 10.9 years), 1345 men developed prostate cancer. Shorter sleep duration (< 6 h), in comparison to optimal duration (7-8 h), was suggestively associated with a decreased risk of prostate cancer in the overall cohort (adjusted hazard ratio (HR) = 0.83, (95% confidence interval (CI): 0.68-1.01) for sleep average; HR = 0.79, 95% CI: 0.65-0.95 for sleep weekdays; and HR = 0.81, 95% CI: 0.66-0.99 for sleep weekends), and among Black men (HR = 0.77, 95% CI: 0.62-0.97 for sleep average; HR = 0.76, 95% CI: 0.61-0.94 for sleep weekdays; and HR = 0.74, 95% CI: 0.59-0.94 for sleep weekends) when stratified by racial groups. Sleep duration and restless sleep were not associated with prostate cancer aggressiveness overall. CONCLUSION:Shorter sleep duration was suggestively associated with a decreased risk of prostate cancer, but sleep duration was not associated with aggressive prostate cancer. Stratified analysis suggests a reduction of prostate cancer risk among Non-Hispanic Black men with < 6 h of sleep, compared to those sleeping 7-8 h. This is an intriguing finding, and further research is needed to assess the impact of confounding factors on racial differences in prostate cancer development.

OBJECTIVE:The purpose of this study was to estimate the lifetime risk of alcohol-attributable mortality and morbidity in the United States based on a person's average lifetime weekly alcohol consumption to assess the impact of per-occasion alcohol consumption on health. METHOD:Lifetime risks were estimated using a cause-specific modeling approach that combined exposure data from national health surveys, relative risks, population data from the U.S. Census Bureau, mortality data from the Centers for Disease Control and Prevention, and morbidity data from the Institute for Health Metrics and Evaluation. A narrative review assessed the health impact of per-occasion alcohol consumption on health. RESULTS:At low levels of consumption, no protective net effect of alcohol consumption on health was observed. Elevated mortality and morbidity risks were associated with alcohol consumption starting at relatively low levels. Males consuming >6.5 (95% CI [<1, 13.5]) and females consuming >7.0 (95% CI [<1, 11.5]) drinks per week had life-time alcohol-attributable mortality risks >1:1,000. At >8.5 (95% CI [2.5, 13]) drinks per week for both males and females, these risks increased to >1:100. At 14 drinks per week for males (the upper limit of the former Dietary Guidelines for males), the risk of an alcohol-caused death was 1:25 (4%). Drinking patterns also impacted risk. Above 1 drink per occasion, higher consumption was associated with progressively increased risks of breast cancer, cardiovascular disease, and injury. CONCLUSIONS:Alcohol consumption, including at what may be perceived as "moderate" levels, is associated with increased mortality and morbidity risks. These results support tightening alcohol use guidance in the United States, for both males and females, to no more than 1 drink per day.

Premalignant lesions provide a crucial window of opportunity for cancer chemoprevention. Green tea, particularly its major catechin, epigallocatechin-3-gallate (EGCG), has demonstrated potential as a chemopreventive agent. Notably, a green tea ointment (Sinecatechins, or Veregen®) is the first and only botanical drug derived from green tea approved by the U.S. Food and Drug Administration for the treatment of HPV-related epithelial lesions. This approval underscores its clinical translational relevance, even though these lesions are caused by HPV types 6 and 11, which are considered low risk for malignancy. This review summarizes current mechanistic and clinical evidence supporting the role of green tea in suppressing the progression of premalignant lesions, with a specific focus on its ability to modulate the epithelial-mesenchymal transition (EMT). We first review the major constituents, bioavailability, and bioactivities of green tea, followed by the role of EMT in various stages of cancer progression, from early carcinogenesis to premalignant progression, and ultimately to cancer invasion and metastasis. EMT as a potential therapeutic as well as chemopreventive target is also discussed. We then summarize the association of the EMT pathway with the chemopreventive effect of green tea on premalignant lesions in several organ systems, including oral, cervical, colorectal, prostate, and skin. Although the existing in vitro, in vivo, and small-scale human studies are encouraging, definitive, large-scale, randomized, and prospective clinical trials that measure EMT-associated biomarkers are necessary to confirm the efficacy of green tea-based interventions as a strategy for managing premalignant lesions and EMT modulation.

BACKGROUND:According to the International Agency for Research on Cancer, certain hydrocarbons are known or suspected carcinogens. OBJECTIVE:Our study aimed to estimate cancer risks in children and adolescents associated with paternal exposure to groups of aliphatic/alicyclic, aromatic, and chlorinated hydrocarbons, and the individual chemicals, toluene, methylene chloride, trichloroethylene, and 1,1,1-trichloroethane, from 3 months preconception to birth. METHODS:For this population-based case-control study of Danish children and adolescents (born 1968-2013) < 20 years of age when diagnosed with cancer 1968-2016, 10,442 cancer cases were matched to 261,050 cancer-free controls (25:1 matching ratio by sex and birth year). Paternal occupational exposure to hydrocarbons was generated by job-exposure matrices to span the time 3 months before conception until the child's birthdate. We employed unconditional logistic regression to estimate cancer risks in children and adolescents whose fathers were exposed to hydrocarbons, compared to those born to unexposed employed fathers and examined associations by exposure status (any or high/low vs. unexposed). RESULTS:We found consistent associations for several hydrocarbon solvents and glioma, acute myeloid leukemia (AML), and osteosarcoma in children and adolescents. The risk of glioma was highest in children and adolescents whose fathers were highly exposed to chlorinated hydrocarbons (low exposure: adjusted Odds Ratio (aOR): 1.24; 95% Confidence Interval (CI): 0.88, 1.74; high exposure: aOR: 1.68; 95% CI: 1.10, 2.57), while AML risk was increased when fathers were highly exposed to aliphatic/alicyclic hydrocarbons (low: aOR: 1.08; 95% CI: 0.68, 1.71; high: aOR: 1.87; 95% CI: 1.25, 2.78). The risk of osteosarcoma increased in children and adolescents with fathers highly exposed to 1,1,1-trichloroethane (low: aOR: 1.27; 95% CI: 0.65, 2.45; high: aOR: 2.14; 95% CI: 1.20, 3.82). SIGNIFICANCE:Our findings in Denmark suggest that paternal hydrocarbon exposure in the preconception and pregnancy periods may increase the risk of certain cancers in their children and adolescents. IMPACT:This study comprehensively evaluates paternal occupational exposure to solvents in relation to childhood cancer using nationwide registry data. By leveraging high-quality Danish occupational histories and robust exposure assessment methods, we contribute to narrowing the research gap in paternal environmental contributions to early-life carcinogenesis. Our findings provide new insights into preconception paternal risk factors and highlight the need for future prevention strategies.

PurposeThe relationship between whole and refined grain intake and gastric cancer risk has been investigated, but findings remain inconclusive. We aimed to evaluate and quantify the association of whole and refined grain consumption with gastric cancer risk through an individual participant pooled analysis of studies participating in the Stomach cancer Pooling (StoP) Project.MethodsTwenty case-control studies (including 7,943 cases and 19,729 controls) contributed to the analysis of refined grains, and 13 of these (5,658 cases and 15,802 controls) contributed to the analysis of whole grains. Study-specific odds ratios (ORs) were estimated using multivariable logistic regression models and pooled through a two-stage approach based on fixed-effects models.ResultsFor whole grains, compared with no consumption, the OR was 0.92 (95% confidence interval, CI: 0.84-1.01) for any consumption, and 0.86 (95% CI: 0.77-0.96) for a consumption equal or above the study-specific median. There was an increasing risk of gastric cancer with increasing consumption of refined grains, with an OR for the highest versus the lowest tertile of 1.39 (95% CI: 1.28-1.50) when considering staple grain foods only and 1.52 (95% CI: 1.39-1.65) when also considering grain-based sweets and desserts.ConclusionOur findings indicate that whole grain consumption is inversely associated, and refined grain consumption directly associated with gastric cancer risk. These findings support current dietary recommendations favoring whole grains over refined grains.

Previous research suggests that dairy consumption may reduce colorectal cancer (CRC) risk, potentially due to key nutrients found in dairy products. However, most of these studies were performed in mainly White populations, limiting our understanding of dairy and CRC risk in other races and ethnicities. We examined associations between dairy intake and CRC risk in 192,644 participants across five racial and ethnic groups from the Multiethnic Cohort (MEC) Study. Dietary intake was assessed using a validated food frequency questionnaire, and Cox proportional hazards models were used to estimate the associations of dairy products, milk, lactose, calcium, and vitamin D with CRC risk. Analyses were further stratified by race and ethnicity, sex, and tumor subsite. Over an average follow-up of 20 years, 5743 CRC cases were identified. Higher intakes of total dairy products (hazard ratios [HR]Q5vsQ1 = 0.85, 95% confidence interval [CI] 0.77-0.93, ptrend = .001) and milk (HRQ5vsQ1 = 0.82, 95% CI 0.75-0.90, ptrend <.001) were associated with reduced CRC risk. Intakes of calcium (HRQ5vsQ1 = 0.80, 95% CI 0.71-0.91, ptrend = .001), vitamin D (HRQ5vsQ1 = 0.87, 95% CI 0.75-1.02, ptrend = .258), and lactose (HRQ5vsQ1 = 0.85, 95% CI 0.77-0.93, ptrend = .001) also showed inverse associations with CRC. Stratified analyses revealed stronger benefits from dairy and milk consumption among Latino participants. Tumor site analyses indicated notably stronger protection against cancers in the colon, particularly the left colon. Our findings support a protective role of dairy products and their key nutrients against CRC across diverse racial and ethnic populations. These results underscore the potential importance of dairy consumption in CRC prevention and call for further research into the biological mechanisms underlying these associations.

BACKGROUND:Cancer remains the second leading cause of death in the United States, with persistent racial/ethnic and socioeconomic disparities. Expanding healthcare access is a key strategy for addressing these inequities. We considered Medicaid expansion as a natural experiment to assess whether broader access is associated with changes in cancer mortality overall and by U.S. region, gender, and race/ethnicity. METHODS:Using 2005-2019 state-level data from the U.S. Census, CDC WONDER, Kaiser Family Foundation, and America's Health Rankings, we compared age-adjusted cancer mortality (per 100,000 adults aged 25-64) between 27 expansion and 24 non-expansion states. We applied a person-time weighted generalized synthetic control method, adjusting for demographic, socioeconomic, and healthcare access variables. This improves robustness to violations of the parallel trends assumption that may have limited prior analyses. RESULTS:Expansion was associated with an overall reduction in cancer mortality (mean difference [MD]: -2.06; 95% CI: -4.24 to 0.11). Subgroup analyses revealed reductions in cancer mortality among women (MD: -3.02; 95% CI: -5.28 to -0.77), non-Hispanic Whites (MD: -2.27; 95% CI: -4.15 to -0.38), and Northeastern states (MD: -4.46; 95% CI: -7.40 to -0.89). CONCLUSIONS:Findings suggest Medicaid expansion had a heterogeneous impact on cancer mortality. While reductions were evident overall, particularly among White individuals, women, and those in the Northeast, imprecise estimates limited evidence of benefit for racial/ethnic minorities, men, and other regions, where disparities are more pronounced. This may also reflect inequities in healthcare access, quality, utilization, and risk factor distribution (e.g., smoking). Future research should assess long-term impacts across broader outcomes and populations.

Among Asian, Native Hawaiian, and Pacific Islanders (ANHPI) in the United States, cancer and cardiovascular disease are the leading causes of death. Colorectal cancer (CRC) is the third most common cancer among ANHPIs, with improving survival rates. However, the risk of cardiovascular disease (CVD) events among ANHPI CRC survivors is unknown, especially within disaggregated ANHPI race and ethnicity groups. We estimated the risk of CVD events among ANHPI CRC survivors within the SEER-Medicare database. Composite CVD, heart failure, ischemic heart disease, and stroke/transient ischemic attack were identified using International Classification of Diseases (ICD) diagnostic codes. Cox proportional hazard models were used to estimate hazard ratios (HR) and 95

This study investigates maternal residential proximity to oil and gas development (OGD) in pregnancy and the risk of multiple childhood cancers in California. Cases (N = 9487) were identified from California Cancer Registry and controls (N = 183834) were randomly selected from the California Birth Registry (20:1 frequency-matched by birth year: 1998-2016), restricting both to births within 10 km of OGD. Exposure was defined as residing within 1 km or 3 km of any well at birth; ‘low’ and ‘high’ exposures were defined by the median well count within each distance. Unconditional logistic regression models estimated cancer risks comparing each exposed group to the unexposed (residing 3-10 km from any well). The risks of several cancers among children of mothers exposed to any well increased: medulloblastoma (within 3 km: adjusted Odds Ratio (aOR): 1.40; 95% confidence interval (CI): 1.08, 1.82; low, aOR = 1.27; 95% CI = 0.93, 1.74; high, aOR = 1.55; 95% CI = 1.14, 2.11); rhabdomyosarcoma (within 3 km: aOR = 1.64; 95% CI = 1.28, 2.09) with similar estimates across low and high exposure levels; and teratoma (within 3 km: aOR = 1.42; 95% CI = 0.99, 2.05; low, aOR = 1.35; 95% CI = 0.88, 2.07; high, aOR = 1.51; 95% CI = 0.98, 2.33). The results were consistent across both buffer sizes (1 km and 3 km) and estimates were similar for any well and inactive wells. No clear associations were observed for other major childhood cancers including leukemias and lymphomas. Our study suggests that OGD may increase the risk of developing several rare childhood cancers.

Introduction Oesophageal cancer is a highly lethal malignancy with geographic disparity and a heavy burden in developing countries. While smoking and alcohol are established risk factors, emerging evidence suggests that indoor air pollution (IAP) may also play a role through the inhalation of aerosols along the aerodigestive tract, but its relationship with oesophageal cancer remains poorly understood. Previous studies have focused on how IAP is associated with lung cancer, and evidence on oesophageal cancer is sparse, underpowered and inconclusive. Methods This population-based case–control study was conducted in the Jiangsu Province, China, from 2003 to 2010. We analysed 2969 cases and 8019 controls using unconditional logistic regression, adjusting for potential confounders. In addition to the six individual household air pollution sources, we also studied their combined effect by calculating the unweighted and weighted sum of these IAP sources to improve comparability. Furthermore, we conducted subgroup analyses by sex and smoking status, as well as by sex exclusively among non-smokers. Results In both the overall sample and subgroups, higher exposure to various individual or combined IAP sources was associated with a dose-response increase in oesophageal cancer risk (weighted risk score (WRS) semi-Bayesian (SB)-adjusted OR (aOR): 2.70; 95% CI 2.36 to 3.07). Solid fuels appeared to have the strongest association (SB-aOR: 1.76; 95% CI 1.56 to 1.98), followed by coal used for cooking, passive smoking and poor ventilation in the kitchen and bedrooms. The vulnerability to different sources varied by sex and smoking status, and females among non-smokers consistently experienced a more profound impact from combined IAP exposure using WRS. Conclusions Exposure to common IAP is associated with an increased risk of oesophageal cancer among the Chinese population, with variations in susceptibility observed across sex and depending on smoking status.

This study investigated risk factors associated with HNC by subsite including oral cavity cancer (OCC), oropharyngeal cancer (OPC), and laryngeal cancer (LC) among former smokers in the International Head and Neck Cancer Epidemiology Consortium (INHANCE). Case-control study including former smokers from the pooled INHANCE data, with information on sociodemographic, smoking, and alcohol history. Associations were assessed using logistic regression with 95% confidence intervals (CI). The study included 2143 cases with HNC and 5799 controls. Cancer cases were categorized by their respective subsites: 954 LC (44.5%), 685 OPC (32.0%), 504 OCC (23.5%). The risk of developing OCC was 2.8-fold higher [CI: 1.9-4.1], LC 2.6-fold higher [CI: 1.9-3.5], and OPC 2.1-fold higher [CI: 1.5-2.8] in individuals who smoked > 50 pack-years, compared to < 10 pack-years. The risk of OCC/OPC/LC increased with tobacco consumption in North-America, whereas in Western/Southern-Europe and South-America the association plateaued beyond 31-50 pack-years. Cessation after age 55 increased the risk of LC by 3.0-fold [CI: 2.2-4.2], and OCC by 2.2-fold [CI: 1.4-3.3] versus cessation age ≤ 45 years. Consuming ≥ 5 drinks/day was associated with 5-fold higher risk of OPC [CI: 3.7-6.6], 4.4-fold higher risk of OCC [CI: 3.2-6.1] and 3.1-fold higher risk of LC [CI: 2.4-3.9] compared to 0-0.9 drinks/day. The risk of HNC among former smokers is not homogeneous across regions and that there were distinct patterns for OCC, OPC, and LC. The amount of tobacco and alcohol consumption are key risk factors, with alcohol being more important for OCC/OPC, and tobacco being more strongly associated with LC risk.

Pro-vegetarian (PVG) diets may reduce gastric cancer (GC) risk, but evidence remains limited. We aimed to evaluate the association between three predefined PVG patterns—general (gPVG), healthful (hPVG), and unhealthful (uPVG)—and GC risk stratifying by sex in the context of the Stomach Cancer Pooling (StoP) Project Consortium. We analysed data from six case–control studies from the StoP Consortium. The final sample included 1,857 incidents, histologically confirmed GC cases and 5,646 controls. Food intakes were assessed using country-specific food frequency questionnaires, which allowed the estimation of PVG patterns using established scoring methods. Adherence to PVG dietary patterns was classified into quintiles. Logistic mixed models with random intercepts for each study were used to estimate odds ratios (ORs) and 95

INTRODUCTION:Approximately 12.4% of patients with lung cancer experience depression after cancer diagnosis. Asian, Native Hawaiian, and Pacific Islanders (ANHPIs) constitute a large group with heterogeneity. The aim of this study is to examine the racial differences in depression risk, comparing overall ANHPI and ANHPI ethnic groups to non-Hispanic White (NHW) patients with lung cancer. METHOD:We utilized the Surveillance, Epidemiology and End Results (SEER)-Medicare and SEER-Consumer Assessment of Healthcare Providers and System (CAHPS) dataset. We included patients with primary lung cancer who were aged 66 and older, diagnosed from 2000 to 2017 with full coverage of Medicare Part A and B. One ANHPI patient with lung cancer was matched to three NHW patients with lung cancer based on sex, diagnosis age, and diagnosis year. We used the Cox proportional hazards model to estimate the differences in depression incidence among ANHPI and NHW patients with lung cancer. RESULTS:Overall ANHPI, Chinese, Japanese, Filipino, Asian Indian or Pakistani, and other Asian patients with lung cancer had a lower incidence of depression than NHW patients with lung cancer. Korean patients with lung cancer (HR 1.62, 95% CI 1.05-2.51) had a higher incidence of depression when compared to Chinese patients with lung cancer. ANHPI and NHW males had a lower incidence of depression compared to female lung cancer patients. CONCLUSION:Korean patients with lung cancer may have a higher incidence of depression than Chinese comparisons. More research to investigate the heterogeneity and underdiagnosis of depression risk among older ANHPI groups is needed.

Supplementary Figure from Family History and Risk of Bladder Cancer: An Analysis Accounting for First- and Second-degree Relatives

ABSTRACT Background There may be heterogeneity in lung cancer‐related outcomes for individuals who are Asian, Native Hawaiian, and Pacific Islanders (ANHPI). Objectives The aims of this study were to investigate possible disparities in cardiovascular disease (CVD) risk between ANHPI and Non‐Hispanic White (NHW) lung cancer survivors and evaluate potential CVD risk factors. Methods A total of 3920 ANHPI and 11,760 NHW lung cancer patients aged 66 years and older were identified from the Surveillance, Epidemiology, and End Results (SEER)‐Medicare registry from 1999 to 2017. Cox proportional hazards models were used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (95% CIs) for incident CVD, comparing ANHPI lung cancer patients and their race/ethnicity subgroups to NHW lung cancer patients. Results Compared to NHW lung cancer patients, ANHPI lung cancer patients had a lower risk of developing heart failure (HR, 0.64, 95% CI, 0.53–0.76) and ischemic heart disease (HR, 0.76, 95% CI, 0.60–0.95). Additionally, compared to Chinese lung cancer patients, Pacific Islander, South Asian, and Southeast Asian lung cancer patients had a higher risk of heart failure. Conclusion While ANHPI lung cancer patients had lower risks of heart failure and ischemic heart disease than NHW lung cancer patients, heterogeneity in risk was observed among ANHPI subgroups. Further research is needed to investigate the reasons for the higher risk of several CVDs among Pacific Islander, South Asian, and Southeast Asian lung cancer patients.

This study aimed to evaluate the prognostic factors influencing the survival of patients with lung cancer identified from a lung cancer screening cohort in the community. A total of 25,310 eligible participants were enrolled in this population-based prospective cohort study, derived from a community lung cancer screening program started from 2013 to 2017. Survival analyses were conducted using the Kaplan–Meier method and the log-rank test. Cox proportional hazards regression models were utilized to identify prognostic factors, including demographic characteristics, risk factors, low-dose CT (LDCT) screening, and treatment information. The screening cohort identified a total of 429 patients with lung cancer (276 men, 153 women) during the study period. The 1-year, 3-year, and 5-year survival rates were 74.4

BACKGROUND:Although colorectal cancer survival rates are improving, the risk of incident type 2 diabetes mellitus (T2D) among Asian, Native Hawaiian, and Pacific Islander (ANHPI) ethnic groups is poorly understood. This study aims to identify high-risk groups and quantify the risk across different periods. METHODS:Using the SEER-Medicare database, colorectal cancer survivors who were ANHPI were matched to non-Hispanic White (NHW) survivors at a ratio of 1:3. Multivariable Cox regression models computed HRs and 95% confidence intervals (CI) for incident T2D. RESULTS:The study included 6,463 NHW and 2,901 ANHPI colorectal cancer survivors diagnosed between 2000 and 2017. Among them, 715 NHW and 484 ANHPI developed T2D during 39,097 and 10,769 person-years of follow-up, respectively. ANHPI colorectal cancer survivors had an elevated T2D risk compared with NHW across all follow-up periods (HRoverall: 1.84, 95% CI, 1.51-2.25; HR1-5 years: 1.83, 95% CI, 1.45-2.30). Southeast and East Asians demonstrated the highest T2D risks. Colon cancer was linked to early postdiagnosis T2D risk, whereas rectal cancer was associated with later risk. No significant association was observed for Native Hawaiians and Pacific Islanders. CONCLUSIONS:ANHPI colorectal cancer survivors face a greater risk of T2D, particularly among Southeast and East Asians. These findings highlight the need for evidence-based survivorship strategies to prevent T2D and reduce ethnic disparities. IMPACT:This is the first study to examine T2D risk among ANHPI colorectal cancer survivors, providing critical insights to inform tailored diabetes prevention and survivorship care.

Though indoor air pollution (IAP) is associated with elevated lung cancer risk, an integrated measure is imperative to thoroughly investigate this association. The interplay between sex and IAP on lung cancer remains unclear. We conducted a population-based case-control study in Jiangsu Province, China, from 2003 to 2010, with 2871 lung cancer cases and 8019 controls. Exposures and covariates information were collected via in-person interviews using a standardized questionnaire. An integrated weighted risk score (WRS), accounting for the effect sizes of each source of IAP, was introduced. Unconditional logistic regression was employed to estimate adjusted odds ratios (aORs) and their 95% confidence intervals (CIs). Interactions between sex and IAP by tobacco smoking status were evaluated. Environmental tobacco smoking (ETS) (aOR = 1.54, 95% CI: 1.40, 1.69), poor ventilation (aOR = 1.18, 95% CI: 1.07, 1.30), and coal used for cooking (aOR = 1.27, 95% CI: 1.15, 1.41) were associated with lung cancer. Dose-response relationships between lung cancer and WRS were observed, with p for trend less than 0.001. aOR for individuals at the highest quartile of the WRS of IAP was 1.74 (95% CI: 1.52, 2.00) compared to the lowest quartile. The associations were more profound among never-smokers than ever-smokers. Females tended to be more vulnerable to IAP, and sex interacted with IAP beyond multiplicativity on the odds scale. IAP is associated with lung cancer, with a stronger impact among never-smokers. An interaction between IAP and sex was observed. These results underscore the importance of controlling IAP, especially ETS in order to reduce the risk of lung cancer.