Are unreported technical polychlorinated biphenyl formulations used in legacy building materials threatening indoor environments of a central Indian City despite the ban?

Qualitative evaluation of volatile organic compound emissions and quantitative risk assessment of benzene, toluene, ethylbenzene, xylenes, and styrene from household insecticides.

The association between breast cancer diagnosis and treatment and the risk of incident ischemic stroke remains unclear. We investigated ischemic stroke risk among breast cancer survivors and evaluated associations by age, follow-up duration, and type of cancer treatment. We conducted a nationwide, retrospective, matched cohort study using the Korean National Health Insurance Service database. Women aged 18 years and older with newly diagnosed breast cancer who underwent breast cancer surgery between January 2010 and December 2016 and had no prior stroke were identified. Each was matched 1:3 by birth year to cancer-free women. The primary outcome was first ischemic stroke, defined as hospitalization with International Classification of Disease, Tenth Revision codes I63/I64 plus inpatient brain CT or MRI. Subdistribution hazard ratios (sHRs) and 95% CIs were estimated using Fine-Gray models that accounted for death as a competing risk and adjusted for sociodemographic factors and cardiovascular and non-CV comorbidities. We analyzed 107,606 breast cancer surgery survivors (mean age, 50.0 years) and 322,818 matched cancer-free women. Over a mean 7.2-year follow-up, ischemic stroke occurred in 1,155 survivors (1.07%). Stroke risk was elevated shortly after breast cancer diagnosis (1-year sHR 1.59; 95% CI 1.34-1.89; 3-year sHR 1.17; 95% CI 1.05-1.30) compared with cancer-free women, with stronger associations at 3 and 6 months after diagnosis across all age groups. Over the long term, survivors had a slightly lower risk of stroke (sHR 0.94; 95% CI 0.88-1.00), and in a 1-year landmark analysis including only event-free individuals, the risk was lower (sHR 0.87, 95% CI 0.81-0.93). Among survivors, anthracycline use (sHR 1.25) and combined tamoxifen-aromatase inhibitor therapy (sHR 1.49) were associated with increased risk of stroke, whereas radiation therapy was associated with decreased risk (sHR 0.84). These associations attenuated and became nonsignificant beyond 1 year. Stroke risk was also higher among survivors with low income, hypertension, diabetes, or current smoking. The association between breast cancer and ischemic stroke risk is time dependent, with a short-term increase after diagnosis and treatment followed by a gradual decline over time. These findings highlight the need for proactive stroke risk management, including early CV assessment and ongoing monitoring for thromboembolic events during survivorship.

Diabetes mellitus is widely regarded as a risk factor for cancers. There is considerable controversy over whether maternal diabetes can cause cancer. This study aims to comprehensively assess and quantify the association between maternal diabetes and the risk of cancers in mother-offspring. The PubMed, Embase, and Web of Science databases were searched up to September 30, 2025, to explore the impact of maternal diabetes on cancer in mothers and their offspring. The primary outcome was the risk of cancers in the mother or offspring, presented as risk ratios (RRs) with 95% confidence intervals (CI). The I 2 statistic is used to assess heterogeneity among studies, thereby guiding the selection of random-effects or common-effects models. The 81 studies involving 44 917 447 mother-offspring. Maternal diabetes was associated with increased risks of any cancers in mothers and offspring. In studies adjusted for multiple confounders, the risk of offspring suffering from haematological malignancies (RR, 1.37; 95% CI, 1.23-1.52; I 2 = 1.0%) has significantly increased, especially leukaemia (1.34; 1.22-1.47; 0.0%). However, the risk of solid tumours (1.17; 1.09-1.24; 70.1%) in mothers increases significantly, especially, head and neck (1.34; 1.23-1.47; 35.1%), respiratory system (1.33; 1.05-1.67; 0.0%), gastrointestinal (1.30; 1.16-1.45; 45.5%), and gynecologic (1.16; 1.04-1.29; 64.1%). Maternal pre-gestational diabetes was more strongly associated with the risk of most cancers in offspring than gestational diabetes (1.60 [1.14-2.14] vs. 1.10 [1.02-1.18]; subgroup difference p = 0.0046). Maternal diabetes is associated with an increased risk of cancers in mothers and offspring. Further high-quality large-sample studies are needed to clarify and consolidate potential causal relationships.

Leukotriene receptor antagonist drugs as potential chemopreventive agents: A systematic review and meta-analysis of cancer risk in asthmatic patients.

Venous thromboembolism (VTE) has long been recognized as a harbinger of cancer. The epidemiology of VTE and cancer has evolved over the past decades, and contemporary data addressing the association between VTE and subsequent risk of cancer are needed. We aimed to investigate the short- (≤1 year) and long-term (>1 year) risk of cancer after incident VTE in a population-based cohort study. A total of 111,119 participants from Tromsø4-7 (1994-2016) and HUNT2-3 (1995-2008) surveys were followed through 2020, and all first-lifetime cancer and VTE events were recorded. Cox regression was used to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for cancer diagnosis in participants with VTE compared with those without VTE, with VTE being modeled as a time-varying exposure. Among the 2,506 individuals with incident VTE, 417 had a subsequent diagnosis of incident cancer during a median follow-up after VTE of 5.2 years. In models adjusted for age (as a time-scale), sex, body mass index, smoking, and comorbidities, the HRs for cancer were 4.57 (95% CI 3.89-5.37) at 0 to 1 year, 1.19 (95% CI 0.93-1.52) at 1 to 3 years, and 1.14 (95% CI 0.99-1.31) at >3 years after overall VTE when compared with individuals without VTE, and the risk estimates were particularly pronounced at 0 to 1 year after unprovoked VTE (HR 5.63, 95% CI 4.67-6.77). Our results indicate a transient and substantially increased risk of cancer diagnosis within 1 year after an incident VTE, and especially after unprovoked VTE.

Association of childhood maltreatment with risk of lung cancer: A mediation analysis from the UK biobank.

Post-liver transplant complications-cancer, infections, and renal dysfunction-impose substantial clinical and economic impact on recipients. This study evaluated clinical impacts and cost-effectiveness of adding everolimus (EVR) to a calcineurin inhibitor (CNI)-based regimen in liver transplant recipients, aiming to identify how co-occurring major complications affect cost-effectiveness. We conducted a cohort analysis and a cost-utility analysis, dividing recipients into CNI with and without EVR groups. We calculated adjusted hazard ratios (HRs) for the risk of cancer and posttransplant infection with EVR combination therapy using a Cox regression model. A Markov model that captured the co-occurrence of liver disease, infection, and renal dysfunction was constructed to estimate costs and quality-adjusted life years (QALYs) and compare the incremental cost-effectiveness ratio (ICER) of adding EVR to CNI. A hypothetical cohort of 10 000 liver transplant recipients aged 55 y was simulated during 30 y. The addition of EVR significantly reduced the risk of cancer (HR 0.435; 95% confidence interval 0.279-0.678) while increasing the infection risk in subsequent years (HR 1.468; 95% confidence interval 1.053-2.045). Cost-utility analysis demonstrated the CNI with EVR strategy was cost-effective, with an ICER of US$5298/QALY, well below the $25 000/QALY threshold. In analyses quantifying how co-occurring events shift value, the ICER was $9307/QALY when limited to liver disease, decreased to $4363/QALY with renal dysfunction included, and increased to $10 464/QALY when infection was added. Overall, CNI with EVR regimen in liver transplant remained cost-effective across co-occurring outcomes and perspectives, supporting risk-benefit balancing across cancer, posttransplant infection, and renal function.

The InAdvance Study addresses the critical need for comprehensive data and biospecimen collection from individuals at elevated risk for cancer. Despite the existence of numerous biobanks for patients with cancer and individuals at average risk for cancer, a gap persists in resources targeting individuals with an elevated risk for cancer. The InAdvance Study is longitudinally collecting biospecimens and health data from individuals with a range of cancer risk factors to facilitate collaborative research in cancer early detection and interception. Patient populations include those with precancerous or precursor lesions (e.g., oral precursor lesions and Barrett's esophagus), hereditary cancer risk, personal or family history of cancer, or a history of exposures associated with cancer risk. Additionally, we are enrolling patients receiving multicancer early detection (MCED) tests, family members of elevated risk participants, and controls. Key goals include optimized biospecimen collection through standardized procedures, participant enrollment and engagement through an online platform, and standardized scalable procedures. Data are compiled into a central repository, and researchers can request access through a streamlined data request process. Since April 2023, 1,415 participants have enrolled in the study. In total, 817 (58%) completed the baseline survey, and 816 (58%) gave a baseline blood sample. The InAdvance Study's comprehensive approach provides a framework for basic, population, and translational studies to elucidate the molecular and environmental factors that drive cancer development. Comprehensive data and biospecimen biorepositories are critical to informing strategies for early detection, risk stratification, early interception for risk mitigation, and improved outcomes for higher-risk populations.

Breast cancer screening is vital for early detection and improved health outcomes but requires robust health economic evaluations to guide implementation. This systematic review examines the methodology, quality, and results of health economic evaluations of screening strategies to support decision making and future research. A literature search was performed in PubMed, Embase, Web of Science, EconLit, and the HTA database. Health economic evaluations of breast cancer screening strategies using imaging modalities were included and screened independently by two reviewers. Data on study design, screening strategies, and outcomes were extracted and synthesized. Quality was assessed using the ISPOR checklist for model-based studies and the Consensus on Health Economics criteria (CHEC-extended) checklist for empirical data-based studies. All results were made publicly accessible via an interactive platform and the Open Science Framework, providing an open resource that facilitates transparency, reuse, and future updates. The review included 128 studies, comprising 96 model-based studies, 14 empirical data-based studies, 15 studies combining empirical data with extrapolation using a modeling approach, and 3 studies with unclear methods. Microsimulation and cohort simulation were used in 47 and 53 studies, respectively. Incremental cost-effectiveness ratios varied widely across studies depending on the screening modality, risk factors, age range of screening, and screening interval. Most studies found mammography to be cost effective compared with no screening, while some studies showed it as being not cost effective, especially for women at average risk of breast cancer, in young screening ages (40-49years), or with an annual interval. Ultrasound-based screening programs were generally cost effective compared with no screening in the women with average risk of breast cancer. Supplementing magnetic resonance imaging (MRI) with mammography was generally cost effective in women with dense breasts and a family history of breast or ovarian cancer but not cost effective in women with previous treatment using radiation therapy. The median quality score was 55% for model-based studies, with microsimulations having higher quality than cohort simulations. Empirical data-based studies with and without extrapolation had a similar median quality score of 65%. Mammography was generally reported as cost effective compared with no screening. Supplementing mammography with ultrasound and/or MRI could be cost effective depending on comparator, risk factors, age range, and screening interval. Suboptimal quality was commonly observed across published health economic evaluations. Future studies should prioritize enhancing overall quality, particularly in data, validation, and reporting.

To investigate the association between skeletal muscle mass loss and long-term outcomes in patients with intraductal papillary mucinous neoplasm (IPMN). This retrospective, single-center cohort study included 700 patients diagnosed with IPMN at Hokkaido University Hospital between April 2011 and April 2023. Skeletal muscle mass was assessed using the psoas muscle index (PMI) measured on a computed tomography scan at the initial visit. The primary outcome was the incidence of pancreatic cancer, and the secondary outcome was overall mortality. Cox proportional hazard models and competing risk analyses were used to identify independent risk factors. During a median follow-up of 71 months, 27 patients developed pancreatic cancer with an annual incidence rate of 0.63% (95% CI: 0.55%-1.86%). Patients with a low PMI had a significantly higher risk of pancreatic cancer than those with a high PMI (adjusted HR: 3.44, 95% CI: 1.62-7.32, P <0.01). Multivariate analysis identified a low PMI and a main pancreatic duct diameter ≥5mm as independent risk factors for the development of pancreatic cancer. Among the 69 deaths, 61 were comorbidity-related and 8 were pancreatic cancer-related. Low PMI (adjusted HR: 2.57, 95% CI: 1.60-4.12, P <0.01) and a high age-adjusted Charlson comorbidity index (aCCI) (adjusted HR: 9.06, 95% CI: 4.63-17.72, P <0.01) were independently associated with all-cause mortality. Competing risk analysis revealed that skeletal muscle mass loss was significantly associated with the incidence of pancreatic cancer in patients with a low aCCI score but not in those with a high aCCI score. Skeletal muscle mass loss was an independent risk factor for all-cause mortality, and it might be associated with the risk factor for the incidence of pancreatic cancer, particularly IPMN-derived carcinoma in patients with IPMN. Patients with a low PMI and minimal comorbidities might be better to undergo long-term surveillance due to their increased risk of pancreatic cancer.

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% confidence intervals (CIs). Compared to the lowest quintile, the highest quintile of adherence to gPVG was associated with an ORQ5vsQ1 = 0.61 (95% CI: 0.50-0.75; p-trend = < 0.001) and the hPVG was associated with an ORQ5vsQ1 = 0.66 (0.54-0.80; p-trend = < 0.001). The uPVG pattern was associated with an ORQ5vsQ1 = 1.27 (1.05-1.55; p-trend = 0.013). The inverse association for gPVG was more evident in men, ORQ5vsQ1 = 0.56 (0.43-0.73) than in women, ORQ5vsQ1 = 0.73 (0.53-1.01); for the hPVG pattern, a significant inverse association was only observed in women, ORQ5vsQ1 = 0.50 (0.36-0.69); and, for the uPVG pattern, the increased GC risk was only observed in women, ORQ5vsQ1 = 1.70 (1.25-2.32). Higher adherence to gPVG and hPVG dietary patterns is associated with lower GC risk, whereas higher adherence to uPVG is associated with increased risk. The inverse association observed for hPVG pattern and the positive association for uPVG were only observed in women. These differential effects of dietary patterns in men and women deserve to be further investigated.

Coal operations and cancer in the US: A systematic review.

Impact of Pre-LVAD Malignancy on Cancer Risk and Survival After LVAD Implant

High-grade vulvar intraepithelial neoplasia (VIN) is the precursor of vulvar squamous cell carcinoma (VSCC). High-grade VIN is categorized into human papillomavirus (HPV)-associated high-grade squamous intraepithelial lesion (HSIL) and HPV-independent VIN (HPVi-VIN). This study aimed to comprehensively characterize recurrence in a large VIN cohort with long-term follow-up. Recurrence was assessed in 578 HSIL and 46 HPVi-VIN patients by evaluating recurrence risk, number of recurrences, and related diagnostic/excisional procedures. Kaplan-Meier analysis estimated recurrence and VSCC risks, and Cox regression analysis was applied to identify risk factors for recurrence. The median follow-up time was 15 years for HSIL and 5.5 years for HPVi-VIN patients. Recurrence occurred in 50% of HSIL (288/578) and 63% of HPVi-VIN (29/46) patients. Cancer was present at first recurrence in 8.0% of HSIL (23/288) and 45% of HPVi-VIN (13/29). The 5-year recurrence risk was 36% for HSIL and 57% for HPVi-VIN (73% for p53 mutant, 25% for p53 wild-type). Among patients with recurrence, 39% of HSIL and 14% of HPVi-VIN had ≥3 recurrences during follow-up, requiring a median of 6.0 and 5.5 surgical procedures, respectively. For HSIL patients, the 5-year recurrence risk increased to 55% and 57% after the first and second recurrence, respectively, while the 5-year cancer risk increased from 4.5% at initial presentation to 7.4% and 12%, respectively. No independent risk factors for recurrence in HSIL were identified. Both HSIL and HPVi-VIN patients are at high risk of recurrence, with a higher cancer risk observed in those with recurrent HSIL or those with HPVi-VIN.

Increasing physical activity in rural Pennsylvanians: The PA moves trial study protocol for a cluster randomized controlled trial.

Metabolic bariatric surgery (MBS) reduces overall cancer incidence, yet colorectal cancer (CRC) risk diverges by procedure. Roux-en-Y gastric bypass (RYGB) has been associated with increased long-term CRC risk (HR 1.55 at 10-14 years), whereas sleeve gastrectomy (SG) shows no equivalent elevation, though shorter follow-up (mean 4.5 vs. 8.5 years) precludes definitive conclusions. This review develops a biologically plausible mechanistic framework for these divergent outcomes. RYGB-induced anatomical bypass and accelerated transit are proposed to drive distal substrate overload, with an associated shift of the colonic microbiome toward proteolytic fermentation. The proposed genotoxic luminal environment is characterized by convergent actions of secondary bile acids, tyramine, and hydrogen sulfide, compounded by butyrate depletion. By preserving gastrointestinal continuity, SG is hypothesized to avoid these alterations. These considerations support integrating baseline CRC risk into surgical selection and procedure-specific surveillance after RYGB.

A DNA Methylation-based algorithm Improves Lung Cancer risk prediction in the Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial.

The Multiethnic Cohort Study (MEC) is a US prospective cohort of more than 215,000 participants, designed to investigate variation in risk factors and disease across diverse racial and ethnic groups. More than 74,000 participants contributed biospecimens for genetic studies. We describe this subcohort and demonstrate the types of analyses it enables. The MEC recruited adults aged 45 to 75 in California and Hawaii between 1993 and 1996. Cancer diagnoses were identified via state tumor registries. The MEC Genetics Database includes 73,139 participants with germline genotype data. We evaluated genetic similarity, its relationship with self-reported race/ethnicity, and baseline characteristics, including neighborhood socioeconomic status (nSES). Using breast, colorectal, and prostate cancer as examples, we conducted genome-wide association studies (GWAS), assessed nongenetic risk factors, and performed time-to-event analyses. Participants included 10,962 African Americans, 24,234 Japanese Americans, 17,242 Latinos, 5,488 Native Hawaiians, 14,649 Whites, and 564 others. Principal component analysis showed substantial diversity. Multiethnic GWAS replicated known variants with effective control of population stratification. Polygenic risk score (PRS) effects varied across groups. Time-to-event models revealed associations between cancer incidence and nSES, population descriptors, and genetic similarity. The MEC Genetics Database enables multiancestry analyses of genetic and nongenetic cancer risk, supporting research on disparities, polygenic traits, and integrated risk prediction. Example analyses using these resources show the relationship between population descriptors, PRSs, and common cancer risk factors that require special consideration in genetic analyses.

Accurate identification of individuals at high risk of gastric cancer (GC) remains a major challenge for effective screening. We aimed to identify plasma proteomic signatures and develop a risk prediction model for GC risk stratification. Plasma proteomic profiling was performed using liquid chromatography-tandem mass spectrometry in a case-control discovery set (100 GC cases and 94 controls). Candidate proteins were evaluated in 52,552 UK Biobank participants with a median follow-up of 13.63 years, during which 92 incident GC cases were identified. Risk models integrating clinical, genetic, and proteomic factors were developed using LASSO-penalized Cox regression with stability selection and internally validated using bootstrap resampling. Among 2306 differentially expressed proteins in discovery, 25 were replicated in validation at nominal significance (P < 0.05) with consistent directions. Two proteins (CTSD and GGH) remained significant after false discovery rate correction. A primary proteomic model (clinical factors plus five proteins) improved discrimination versus clinical model (optimism-corrected C-index: 0.745 vs. 0.732, P = 0.046). Risk stratification revealed a clear GC risk gradient: hazard ratios were 6.08 (95% CI 2.15-17.20) for moderate-risk and 23.88 (95% CI 8.66-65.87) for high-risk groups. The risk score was also associated with GC risk as continuous variable (HR per standard deviation: 1.09, 95% CI 1.08-1.11). The 15-year cumulative incidence ranged from 0.02 to 0.56% across risk groups. Decision curve analysis indicated improved clinical utility. Plasma proteomic signatures may improve GC risk stratification beyond traditional clinical factors and could support more targeted screening strategies. Further validation is warranted.