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PURPOSE: Gastric cancer (GC) is among the leading causes of cancer mortality worldwide. The objective of this study was to investigate the association between dietary fiber intake and GC. METHODS: We pooled data from 11 population or hospital-based case-control studies included in the Stomach Cancer Pooling (StoP) Project, for a total of 4865 histologically confirmed cases and 10,626 controls. Intake of dietary fibers and other dietary factors was collected using food frequency questionnaires. We calculated the odds ratios (OR) and 95% confidence intervals (CI) of the association between dietary fiber intake and GC by using a multivariable logistic regression model adjusted for study site, sex, age, caloric intake, smoking, fruit and vegetable intake, and socioeconomic status. We conducted stratified analyses by these factors, as well as GC anatomical site and histological type. RESULTS: The OR of GC for an increase of one quartile of fiber intake was 0.91 (95% CI: 0.85, 0.97), that for the highest compared to the lowest quartile of dietary fiber intake was 0.72 (95% CI: 0.59, 0.88). Results were similar irrespective of anatomical site and histological type. CONCLUSION: Our analysis supports the hypothesis that dietary fiber intake may exert a protective effect on GC.

BACKGROUND: Previous studies suggest that dietary vitamin C is inversely associated with gastric cancer (GC), but most of them did not consider intake of fruit and vegetables. Thus, we aimed to evaluate this association within the Stomach cancer Pooling (StoP) Project, a consortium of epidemiological studies on GC. METHODS: Fourteen case-control studies were included in the analysis (5362 cases, 11,497 controls). We estimated odds ratios (ORs) and corresponding 95% confidence intervals (CIs) for the association between dietary intake of vitamin C and GC, adjusted for relevant confounders and for intake of fruit and vegetables. The dose-response relationship was evaluated using mixed-effects logistic models with second-order fractional polynomials. RESULTS: Individuals in the highest quartile of dietary vitamin C intake had reduced odds of GC compared with those in the lowest quartile (OR: 0.64; 95% CI: 0.58, 0.72). Additional adjustment for fruit and vegetables intake led to an OR of 0.85 (95% CI: 0.73, 0.98). A significant inverse association was observed for noncardia GC, as well as for both intestinal and diffuse types of the disease. The results of the dose-response analysis showed decreasing ORs of GC up to 150-200 mg/day of vitamin C (OR: 0.54; 95% CI: 0.41, 0.71), whereas ORs for higher intakes were close to 1.0. CONCLUSIONS: The findings of our pooled study suggest that vitamin C is inversely associated with GC, with a potentially beneficial effect also for intakes above the currently recommended daily intake (90 mg for men and 75 mg for women).

BackgroundCocaine is an illegal recreational drug used worldwide, yet little is known about whether cocaine inhalation (smoking/snorting) increases the risk of head and neck cancer (HNC).MethodsThe analyses were conducted by pooling data from three case-control studies with 1639 cases and 2506 controls from the International Head and Neck Cancer Epidemiology Consortium. Epidemiologic data, including cocaine use histories, were obtained in face-to-face interviews. Odds ratios (ORs) and corresponding 95% confidence intervals (CIs) were estimated using hierarchical logistic regression models.ResultsControlling for cumulative tobacco and alcohol use, we observed a weak positive association between cocaine use and HNC (ORever vs. never  = 1.35, 95% CI: 0.96, 1.90). In stratified analysis, while we did not detect associations among never tobacco or alcohol users due to the limited sample size, the association with cocaine use was observed among tobacco users and alcohol drinkers. ORs for ever and high cumulative use (>18 times) versus never use were 1.40 (95% CI: 0.98, 2.00) and 1.66 (95% CI: 1.03, 2.69) among tobacco users, and 1.34 (95% CI: 0.93, 1.92) and 1.59 (95% CI: 1.00, 2.51) among alcohol drinkers, respectively.ConclusionIn this pooled analysis, we observed a weak positive association between cocaine inhalation and HNC risk. Our findings provide preliminary evidence of the potential carcinogenic effect of cocaine on HNC. Because of study limitations, including limited number of cocaine users, confounding, and heterogeneity across studies, future investigations will require larger studies with more detailed information on cocaine use history.

Background: While much research has been done to identify individual workplace lung carcinogens, little is known about joint effects on risk when workers are exposed to multiple agents. Objectives: We investigated the pairwise joint effects of occupational exposures to asbestos, respirable crystalline silica, metals (i.e., nickel, chromium-VI), and polycyclic aromatic hydrocarbons (PAH) on lung cancer risk, overall and by major histologic subtype, while accounting for cigarette smoking. Methods: In the international 14-center SYNERGY project, occupational exposures were assigned to 16,901 lung cancer cases and 20,965 control subjects using a quantitative job-exposure matrix (SYN-JEM). Odds ratios (ORs) and 95% confidence intervals (CIs) were computed for ever vs. never exposure using logistic regression models stratified by sex and adjusted for study center, age, and smoking habits. Joint effects among pairs of agents were assessed on multiplicative and additive scales, the latter by calculating the relative excess risk due to interaction (RERI). Results: All pairwise joint effects of lung carcinogens in men were associated with an increased risk of lung cancer. However, asbestos/metals and metals/PAH resulted in less than additive effects; while the chromium-VI/silica pair showed marginally synergistic effect in relation to adenocarcinoma (RERI: 0.24; CI: 0.02, 0.46; p = 0.05). In women, several pairwise joint effects were observed for small cell lung cancer including exposure to PAH/silica (OR = 5.12; CI: 1.77, 8.48), and to asbestos/silica (OR = 4.32; CI: 1.35, 7.29), where exposure to PAH/silica resulted in a synergistic effect (RERI: 3.45; CI: 0.10, 6.8). Discussion: Small or no deviation from additive or multiplicative effects was observed, but co-exposure to the selected lung carcinogens resulted generally in higher risk than exposure to individual agents, highlighting the importance to reduce and control exposure to carcinogens in workplaces and the general environment. https://doi.org/10.1289/EHP13380, Introduction Occupational carcinogens represent a significant threat on worker's health, and exposed workers may be (simultaneously) exposed to more than one carcinogen. The European CAREX project estimated that 23% of [...]

Objectives: To determine the associations between waterpipe use, duration, and intensity of use with prevalence and incidence of metabolic syndrome and its components (increased waist circumference, triglycerides, fasting glucose, blood pressure and decreased high-density lipoprotein cholesterol). Methods: We conducted cross-sectional and prospective analyses using data from the Pars Cohort Study in southern Iran, encompassing 9,264 participants at the baseline, and 5,002 randomly selected in a repeated follow-up. We used multivariate logistic regression models adjusted for age, sex, education, wealth score, physical activity and cigarette pack-years to report odds ratios (OR) and 95% confidence intervals (CI). Results: Among 9,264 participants, 3,119 (33.7%) had metabolic syndrome, and 3,482 (37.6%) had ever smoked waterpipe, with both more common in women than in men. In adjusted models, former waterpipe use was significantly associated with prevalence (OR = 1.43, 95% CI: 1.23–1.68) and incidence (OR = 1.57, 95% CI: 1.19–2.06) of the metabolic syndrome while current waterpipe use was not. Past use was associated with increased risk in all components of metabolic syndrome; current use was associated with increases in all except high blood glucose and hypertension. Past waterpipe users had higher waterpipe use intensity (before quitting) in comparison with current users (2.3 vs. 2.0 waterpipes per day, p < 0.01) and had started waterpipe smoking at a younger age (27.2 vs. 30.1 years, p < 0.01). Conclusion: Waterpipe use was associated with metabolic syndrome and its components, especially among former users potentially due to higher intensity and earlier initiation of use. [ABSTRACT FROM AUTHOR]

Numerous studies have reported lower overall cancer mortality rates among immigrants compared to native populations. However, limited information exists regarding cancer mortality among immigrants based on specific birth countries and cancer types. We used population‐based registries and followed 10 million individuals aged 20 years or older in Sweden between 1992 and 2016. The Cox proportional hazard model was used to explore the disparities in cancer mortality by country of birth and cancer type, stratified by gender. Age‐standardized mortality rates were also computed using the world standard population. Hazard ratio (HR) of all‐site cancer was slightly lower among immigrants (males: HRm = 0.97: 95% confidence interval: 0.95, 0.98; females: HRf = 0.93: 0.91, 0.94) than Swedish‐born population. However, the immigrants showed higher mortality for infection‐related cancers, including liver (HRf = 1.10: 1.01, 1.19; HRm = 1.10: 1.02, 1.17), stomach (HRf = 1.39: 1.31, 1.49; HRm = 1.33: 1.26, 1.41) cancers, and tobacco‐related cancers, including lung (HRm = 1.44: 1.40, 1.49), and laryngeal cancers (HRm = 1.47: 1.24, 1.75). The HR of mesothelioma was also significantly higher in immigrants (HRf = 1.44: 1.10, 1.90). Mortality from lung cancer was specifically higher in men from Nordic (HRm = 1.41: 1.27, 1.55) and non‐Nordic Europe (HRm = 1.49: 1.43, 1.55) countries and lower in Asian (HRm = 0.78: 0.66, 0.93) and South American men (HRm = 0.70: 0.57, 0.87). In conclusion, there are large variations in cancer mortality by country of birth, and cancer type and require regular surveillance. Our detailed analyses lead to some novel findings such as excess mortality rate of mesothelioma and laryngeal cancers in Immigrants in Sweden. A targeted cancer prevention program among immigrants in Sweden is needed. [ABSTRACT FROM AUTHOR]

Objective: Despite the implementation of the WHO Framework Convention on Tobacco Control (FCTC) program in Iran, the regulation of second-hand smoke (SHS) exposure—an often-overlooked hazard—, still requires improvement. We employed a multi-center case-control study to investigate the association between exposure to secondhand smoke (SHS) from various tobacco products (cigarettes, water-pipes, pipes, and chopogh), opium use, and the risk of lung cancer. Method: We included 627 lung cancer cases and 3477 controls. Exposure to SHS tobacco and SHS opium was collected through a questionnaire. We used mixed-model logistic regressions to estimate odds ratios (ORs) and 95% confidence intervals (CI). Result: Among the overall population exposed to second-hand tobacco smoke (SHTS), the odds ratio (OR) compared to those never exposed was 1.35 (95% CI: 1.08–1.71). Never smokers who were ever exposed to second-hand tobacco smoke (SHTS) had 1.69-fold risk of lung cancer compared to those who were never exposed (95% CI: 1.13–2.52). Exposure to SHTS between 2–3 per day (OR = 2.27, 95% CI: 1.13–4.53) and more than three hours per day (OR = 2.29, 95% CI: 1.20–4.37) can increase the risk of lung cancer compared with the no exposure group (P-trend <0.01). We did not observe any association between exposure to second-hand opium smoke (SHOS) and the risk of lung cancer, either in the overall population or among never-smokers. Conclusion: Our study estimates the impact of second-hand tobacco smoke (SHTS) on lung cancer risk in both the overall population and never-smokers. Additional studies are required to evaluate the association between exposure to second-hand smoke from opium and other type of tobacco, including water-pipe and the risk of lung cancer. [ABSTRACT FROM AUTHOR]

Esophageal cancer (EC), which includes squamous cell carcinoma (ESCC) and adenocarcinoma (EAC), is an important cancer with poor prognosis and high mortality rate. Several occupational exposures have been associated with EC. We aim to investigate the association between occupational asbestos exposure and EC risk, considering types of asbestos and histology of the disease. We included studies mentioned in the list of references in previous reviews and pooled analyses, and we conducted an independent search in PubMed and Scopus. Forest plots of relative risks (RR) were constructed based on the association between occupational asbestos and EC risk. Random‐effects models were used to address heterogeneity between 48 independent cohort and case‐control studies. We found an association between occupational asbestos exposure and EC (meta‐relative risk [RR] = 1.20, 95% confidence interval [CI] = 1.09‐1.32; I2 = 58.8%, p‐heterogeneity [het] <.001). The results of stratification by job (p‐het =.20) indicate an increased RR among asbestos product workers (RR = 1.39, 95% CI = 1.07‐1.81), asbestos applicators (RR = 1.41, 95% CI = 1.20‐1.67), and construction workers (RR = 1.12, 95% CI = 1.02‐1.24). There was no heterogeneity in meta‐RR according to outcome (p =.29), geographic region (p =.69), year of publication (p =.59), quality score (p =.73), asbestos type (p =.93), study design (p =.87), and gender (p =.88), control for potential confounders (p =.20), year of first employment (p =.94) and exposure level (p =.43). The stratification analysis by histology type found an increased RR for both ESCC 1.33(1.03‐1.71) and EAC 1.45(1.03‐2.04) (p‐het =.68). We didn't find evidence of publication bias (p =.07). The results of our study suggest that occupational asbestos exposure is associated with an increased risk of EC in both histology types. [ABSTRACT FROM AUTHOR]

Background: This study aimed to explore the association between occupational exposure to diesel exhaust (DE) and gynaecological and breast cancers. Methods: A systematic review was performed to identify cohort studies reporting results on the association between occupational exposure to DE and risk of gynaecological and breast cancers. STROBE guidelines and PECOS criteria were followed. We identified 6 studies for breast cancer (BC), 4 for cervical cancer (CC), 4 for endometrial cancer (EC) and 7 for ovarian cancer (OC). Random-effects meta-analyses were conducted on the relationship between DE exposure and BC, CC, EC, and OC risk; 95% Confidence Intervals (CI) and prediction intervals (PI) were reported. We investigated between-study heterogeneity and potential publication bias using Egger's test. Results: No associations were observed between occupational DE exposure and risk of BC [RR=0.93; CI: 0.77-1.13; PI:0.50-1.73, I2=80.31% (CI: 21.72-95.05%)], EC [RR=0.89; CI: 0.75-1.05; PI:0. 61-1.30, I2=0.78% (CI: 0-85.57%)], and OC [RR=1.08; CI: 0.89-1.32, PI: 0.76-1.56, I2=11.87% (CI: 0-74.42%)]. A weak association was observed for CC [RR=1.41; CI: 1.17-1.17; PI:0.85-2.30, I2=6.44% (CI: 0-86.40%)]. No between-study heterogeneity or publication bias was detected. Conclusions: This study identified an association between DE exposure and CC, which was not adjusted for potential confounders. No evidence of an association was found with BC, EC, and OC. [ABSTRACT FROM AUTHOR]

Background: Our objective was to study the association between occupational exposure to diesel exhaust (DE) and skin cancer. Methods: A systematic review following STROBE guidelines and PECOS criteria was conducted to identify cohort studies describing the association between occupational DE exposure and the risk of skin cancer. We extracted 12 independent risk estimates for melanoma skin cancer (MSC), 8 for non-melanoma skin cancer (NMSC), and 3 for skin cancer not otherwise specified (SC-NOS). Random effects meta-analyses were performed, site-specific and stratified by geographic region and quality score. 95% confidence intervals (CI) were reported. Between-study heterogeneity and potential publication bias were investigated. Results: There was no overall evidence of an increased risk of MSC [RR=0.90, 95% CI: 0.73-1.11; I²=92.86%, 95% CI: 82.83-97.03%], NMSC [RR=1.04, 95% CI: 0.88-1.23; I²=60.79%, 95% CI: 0-87.34%] or SC-NOS [RR=0.72, 95% CI: 0.54-0.97; I²=26.60%, 95% CI: 0-94.87%] in workers exposed to DE. No difference between low-quality and high-quality studies was found. A stratified analysis by geographical region did not reveal any significant differences. There was no evidence of publication bias. Conclusions: No evidence of an association between skin cancer and occupational DE exposure was found. Residual confounding and other sources of bias cannot be ruled out. [ABSTRACT FROM AUTHOR]

Rationale: Benzene has been classified as carcinogenic to humans, but there is limited evidence linking benzene exposure to lung cancer. Objectives: We aimed to examine the relationship between occupational benzene exposure and lung cancer. Methods: Subjects from 14 case-control studies across Europe and Canada were pooled. We used a quantitative job-exposure matrix to estimate benzene exposure. Logistic regression models assessed lung cancer risk across different exposure indices. We adjusted for smoking and five main occupational lung carcinogens and stratified analyses by smoking status and lung cancer subtypes. Measurements and Main Results: Analyses included 28,048 subjects (12,329 cases, 15,719 control subjects). Lung cancer odds ratios ranged from 1.12 (95% confidence interval, 1.03–1.22) to 1.32 (95% confidence interval, 1.18–1.48) (Ptrend = 0.002) for groups with the lowest and highest cumulative occupational exposures, respectively, compared with unexposed subjects. We observed an increasing trend of lung cancer with longer duration of exposure (Ptrend < 0.001) and a decreasing trend with longer time since last exposure (Ptrend = 0.02). These effects were seen for all lung cancer subtypes, regardless of smoking status, and were not influenced by specific occupational groups, exposures, or studies. Conclusions: We found consistent and robust associations between different dimensions of occupational benzene exposure and lung cancer after adjusting for smoking and main occupational lung carcinogens. These associations were observed across different subgroups, including nonsmokers. Our findings support the hypothesis that occupational benzene exposure increases the risk of developing lung cancer. Consequently, there is a need to revisit published epidemiological and molecular data on the pulmonary carcinogenicity of benzene. [ABSTRACT FROM AUTHOR]

Background: Poor oral health has been linked to various systemic diseases, including multiple cancer types, but studies of its association with lung cancer have been inconclusive. Methods: We examined the relationship between dental status and lung cancer incidence and mortality in the Golestan Cohort Study, a large, prospective cohort of 50,045 adults in northeastern Iran. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between three dental health measures (i.e., number of missing teeth; the sum of decayed, missing, or filled teeth (DMFT); and toothbrushing frequency) and lung cancer incidence or mortality with adjustment for multiple potential confounders, including cigarette smoking and opium use. We created tertiles of the number of lost teeth/DMFT score in excess of the loess adjusted, age- and sex-specific predicted numbers, with subjects with the expected number of lost teeth/DMFT or fewer as the reference group. Results: During a median follow-up of 14 years, there were 119 incident lung cancer cases and 98 lung cancer deaths. Higher DMFT scores were associated with a progressively increased risk of lung cancer (linear trend, p = 0.011). Compared with individuals with the expected DMFT score or less, the HRs were 1.27 (95% CI: 0.73, 2.22), 2.15 (95% CI: 1.34, 3.43), and 1.52 (95% CI: 0.81, 2.84) for the first to the third tertiles of DMFT, respectively. The highest tertile of tooth loss also had an increased risk of lung cancer, with a HR of 1.68 (95% CI: 1.04, 2.70) compared with subjects with the expected number of lost teeth or fewer (linear trend, p = 0.043). The results were similar for lung cancer mortality and did not change substantially when the analysis was restricted to never users of cigarettes or opium. We found no associations between toothbrushing frequency and lung cancer incidence or mortality. Conclusion: Poor dental health indicated by tooth loss or DMFT, but not lack of toothbrushing, was associated with increased lung cancer incidence and mortality in this rural Middle Eastern population. [ABSTRACT FROM AUTHOR]

Background: Understanding the trend of the severe acute respiratory syndrome Coronavirus 2 (SARS-CoV-2) is becoming crucial. Previous studies focused on predicting COVID-19 trends, but few papers have considered models for disease estimation and progression based on large real-world data. Methods: We used de-identified data from 60,938 employees of a major financial institution in Italy with daily COVID-19 status information between 31 March 2020 and 31 August 2021. We consider six statuses: (i) concluded case, (ii) confirmed case, (iii) close con- tact, (iv) possible-probable contact, (v) possible contact, and (vi) no-COVID-19 or infection. We conducted a logistic regression to assess the odds ratio (OR) of transition to confirmed COVID-19 case at each time point. We also fitted a general model for disease progression via the multi-state transition probability model at each time point, with lags of 7 and 15 days. Results: Employment in a branch versus in a central office was the strongest predictor of case or contact status, while no association was detected with gender or age. The geographic prevalence of possible-probable contacts and close contacts was predictive of the subsequent risk of confirmed cases. The status with the highest prob- ability of becoming a confirmed case was concluded case (12%) in April 2020, possible-probable contact (16%) in November 2020, and close contact (4%) in August 2021. The model based on transition probabilities predicted well the rate of confirmed cases observed 7 or 15 days later. Conclusion: Data from industry-based surveillance systems may effectively predict the risk of subsequent infection. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusions Aspirin and statins have been suggested to have potential chemopreventive effects against gastric cancer (GC), although the results of previous studies have been inconsistent. This study therefore aimed to investigate the association between the use of aspirin and statins and GC.A pooled analysis of seven case‐control studies within the Stomach Cancer Pooling Project, including 3220 cases and 9752 controls, was conducted. Two‐stage modeling analyses were used to estimate the association between aspirin and statin use and GC after adjusting for potential confounders.The pooled odds ratio (OR) of GC for aspirin users versus nonusers was 0.72 (95% confidence interval [CI], 0.54–0.95). The protective effect of aspirin appeared stronger in individuals without a GC family history (OR, 0.60; 95% CI, 0.37–0.95), albeit with borderline heterogeneity between those with and without a family history (p = .064). The OR of GC decreased with increasing duration of aspirin use, with an OR of 0.41 (95% CI, 0.18–0.95) for durations of ≥15 years. An inverse, nonsignificant association with the risk of GC was observed for the use of statins alone (OR, 0.79; 95% CI, 0.52–1.18).These findings suggest that aspirin use, particularly long‐term use, is associated with a reduced risk of GC, whereas a similar association was not observed with statins, possibly because of the low frequency of use. [ABSTRACT FROM AUTHOR]

We updated to December 2023 the main findings of the stomach cancer pooling (StoP) project including about 13 000 cases and 31 000 controls from 29 case-control and 5 nested studies. The StoP project quantified more precisely than previously available the positive associations of tobacco smoking, high alcohol consumption, meat intake, selected occupations (e.g. agricultural and miners), gastric ulcer and family history with gastric cancer and the inverse associations with socioeconomic status and selected aspects of diet (fruits, including citrus fruits, vegetables, including allium and mushrooms, and polyphenols). No consistent associations were found with coffee, yoghurt and leisure-time physical activity, metformin or proton pump inhibitors use., (Copyright © 2024 The Author(s). Published by Wolters Kluwer Health, Inc.)

There has been growing evidence suggesting that diabetes may be associated with increased liver cancer risk. However, studies conducted in Asian countries are limited. This project considered data of 968,738 adults pooled from 20 cohort studies of Asia Cohort Consortium to examine the association between baseline diabetes and liver cancer incidence and mortality. Cox proportional hazard model and competing risk approach was used for pooled data. Two-stage meta-analysis across studies was also done. There were 839,194 subjects with valid data regarding liver cancer incidence (5654 liver cancer cases [48.29/100,000 person-years]), follow-up time and baseline diabetes (44,781 with diabetes [5.3%]). There were 747,198 subjects with valid data regarding liver cancer mortality (5020 liver cancer deaths [44.03/100,000 person-years]), follow-up time and baseline diabetes (43,243 with diabetes [5.8%]). Hazard ratio (HR) (95% confidence interval [95%CI]) of liver cancer diagnosis in those with vs. without baseline diabetes was 1.97 (1.79, 2.16) (p < .0001) after adjusting for baseline age, gender, body mass index, tobacco smoking, alcohol use, and heterogeneity across studies (n = 586,072; events = 4620). Baseline diabetes was associated with increased cumulative incidence of death due to liver cancer (adjusted HR (95%CI) = 1.97 (1.79, 2.18); p < .0001) (n = 595,193; events = 4110). A two-stage meta-analytic approach showed similar results. This paper adds important population-based evidence to current literature regarding the increased incidence and mortality of liver cancer in adults with diabetes. The analysis of data pooled from 20 studies of different Asian countries and the meta-analysis across studies with large number of subjects makes the results robust., (© 2024 UICC.)

Objective: Head and neck (HN) cancer comprises the neoplasms originating from the oral cavity, pharynx and larynx. We aimed at reviewing the available literature on the effect of smoking cessation on HN cancer risk., Method: We conducted a systematic search in Medline, PubMed and Embase to June 2022. We abstracted or calculated relative risks (RR) and 95% CIs of HN cancer after cessation of tobacco smoking (both former smoking status and duration of quitting) and combined them using random effects meta-analyses. Papers included were case-control or cohort studies available in the English language. Studies investigating smoking cessation after cancer diagnosis, case reports, intervention studies or animal studies were excluded. Quality and susceptibility to bias of each included study were evaluated using the Newcastle-Ottawa Scale. Publication bias was assessed using funnel plot and Egger's test., Results: A total of 65 studies were included in the review, including 5 cohort and 60 case-control studies. The RR of HN cancer for former smokers compared with current smokers was 0.40 (95% CI 0.35 to 0.46). In an analysis by cancer site, the RR of oral cancer was 0.44 (95% CI 0.35 to 0.55), that of pharyngeal cancer 0.44 (95% CI 0.32 to 0.60) and that of laryngeal cancer 0.38 (95% CI 0.29 to 0.50). The dose-response meta-analysis was based on 37 studies. The RR per 10-year increase in smoking cessation was 0.47 (95% CI 0.43 to 0.52)., Conclusions: The risk of HN cancer declines within the first 5 years of quitting smoking. Quitting smoking is an essential element of HN cancer prevention., Trial Registration Number: The protocol has been deposited in the PROSPERO repository (CRD42022338262)., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2024. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.)

Clonal hematopoiesis of indeterminate potential (CHIP) is the presence of somatic mutations in myeloid and lymphoid malignancy genes in the blood cells of individuals without a hematologic malignancy. Inflammation is hypothesized to be a key mediator in the progression of CHIP to hematologic malignancy and patients with CHIP have a high prevalence of inflammatory diseases. This study aimed to identify the prevalence and characteristics of CHIP in patients with inflammatory bowel disease (IBD). We analyzed whole exome sequencing data from 587 Crohn's disease (CD), 441 ulcerative colitis (UC), and 293 non-IBD controls to assess CHIP prevalence and used logistic regression to study associations with clinical outcomes. Older UC patients (age>45) harbored increased myeloid-CHIP mutations compared to younger patients (age≤45) ( p =0.01). Lymphoid-CHIP was more prevalent in older IBD patients ( p =0.007). Young CD patients were found to have myeloid-CHIP with high-risk features. IBD patients with CHIP exhibited unique mutational profiles compared to controls. Steroid use was associated with increased CHIP ( p =0.05), while anti-TNF therapy was associated with decreased myeloid-CHIP ( p =0.03). Pathway enrichment analyses indicated overlap between CHIP genes, IBD phenotypes, and inflammatory pathways. Our findings underscore a connection between IBD and CHIP pathophysiology. Patients with IBD and CHIP had unique risk profiles especially among older UC patients and younger CD patients. These findings suggest distinct evolutionary pathways for CHIP in IBD and necessitate awareness among IBD providers and hematologists to identify patients potentially at risk for CHIP-related complications including malignancy, cardiovascular disease and acceleration of their inflammatory disease., Competing Interests: J.M reports receiving consulting fees from Incyte, SOBI, Novartis, Geron, AbbVie, Bristol Myers Squibb, GSK, MorphoSys, Galecto, Disc, Pfizer, Merck, Keros and PharmaEssentia; receiving research support from Incyte, SOBI, Geron, BMS, PharmaEssentia, AbbVie, Novartis, Kartos and Ajax. R.H reports receiving consulting fees from Potagonaist Therapeutics and Silence Therapeutics; receiving research support from Kymera, Karyopharm, Cellinkos, Kartos, and Dexcel Therapeutics. L.J.C. reports receiving consulting fees from Orchard Therapeutics and ORGANOIDSCIENCES; receiving research grants from Bristol Myers Squibb; receiving payment for lectures from Ferring Pharmaceuticals and Takeda. B.K.M reports receiving consulting fees from Cellarity. All other authors have no disclosures. No authors have any conflicts of interest to declare.

Incidence of esophageal and gastric cancer has been linked to low B-vitamin status. We conducted matched nested case-control studies of incident esophageal squamous cell carcinoma (ESCC; 340 case-control pairs) and gastric cancer (GC; 352 case-control pairs) within the Golestan Cohort Study. The primary exposure was plasma biomarkers: riboflavin and flavin mononucleotide (FMN) (vitamin B2), pyridoxal phosphate (PLP) (B6), cobalamin (B12), para-aminobenzoylglutamate (pABG) (folate), and total homocysteine (tHcy); and indicators for deficiency: 3-hydroxykyurenine-ratio (HK-r for vitamin B6) and methylmalonic acid (MMA for B12). We estimated odds ratios (ORs) and 95% confidence intervals (CIs) using conditional logistic regression adjusting for matching factors and potential confounders. High proportions of participants had low B-vitamin and high tHcy levels. None of the measured vitamin B levels was associated with the risk of ESCC and GC, but elevated level of MMA was marginally associated with ESCC (OR = 1.42, 95% CI = 0.99-2.04) and associated with GC (OR = 1.53, 95% CI = 1.05-2.22). Risk of GC was higher for the highest versus lowest quartile of HK-r (OR = 1.95, 95%CI = 1.19-3.21) and for elevated versus non-elevated HK-r level (OR = 1.59, 95% CI = 1.13-2.25). Risk of ESCC (OR = 2.81, 95% CI = 1.54-5.13) and gastric cancer (OR = 2.09, 95%CI = 1.17-3.73) was higher for the highest versus lowest quartile of tHcy. In conclusion, insufficient vitamin B12 was associated with higher risk of ESCC and GC, and insufficient vitamin B6 status was associated with higher risk of GC in this population with prevalent low plasma B-vitamin status. Higher level of tHcy, a global indicator of OCM function, was associated with higher risk of ESCC and GC., (© 2024 The Author(s). International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC. This article has been contributed to by U.S. Government employees and their work is in the public domain in the USA.)