Studies have shown that reproductive factors can influence hormone levels in females, potentially affecting the risk of developing lung cancer. However, it remains unclear whether this association is modified by genetic variants.

Age-matched case-control study.

Reproductive factors included menopausal status, age at menopause, hormone use, hysterectomy and oophorectomy. Odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between reproductive factors and lung cancer risk were estimated using a multivariable conditional logistic regression model. A polygenic risk score (PRS) was calculated using a clumping plus thresholding approach. Gene-environment interactions between reproductive factors and PRS on lung cancer risk were evaluated.

Our analysis included a total of 2910 female participants (1455 cases and 1455 controls). Compared to women with no surgical history, those who had undergone hysterectomy (OR = 1.41, 95 % CI = 1.10-1.82) or oophorectomy (OR = 1.52, 95% CI = 1.15-2.02) were associated with an increased risk of lung cancer. A PRS for lung cancer derived from 7 genetic variants showed a linear association with lung cancer risk (Ptrend < 0.001). After adjusting for false discovery rate (FDR), we found a borderline non-significant interaction between hormone use and PRS on lung cancer risk (Pinteraction-FDR = 0.05).

Women with a history of hysterectomy or oophorectomy had a higher risk of lung cancer compared to those without such surgical history, highlighting the need for targeted prevention strategies in this high-risk population. No significant effect modification by the lung cancer PRS was observed in the associations between reproductive factors and lung cancer risk. Larger prospective studies are warranted to validate these findings.

Hepatocellular carcinoma (HCC) is a major concern for public health. Fatty liver disease, related to alcohol misuse or metabolic syndrome, has become the leading cause of chronic liver disease and HCC. The strong association between type 2 diabetes mellitus and HCC can be partly attributed to the development of metabolic dysfunction-associated steatotic liver disease (MASLD). There is a strong interest in strategies that may mitigate HCC risk and reduce HCC incidence in this growing population of at-risk individuals. In this review, we describe the pathogenesis of HCC in patients with MASLD and discuss potential emerging pharmacological and lifestyle interventions for MASLD-related HCC. HCC risk has been observed to be lower with healthy lifestyle behaviors, such as healthy dietary patterns (eg, high consumption of vegetables, whole grains, fish and poultry, yogurt, and olive oil, and low consumption of red and processed meats and dietary sugar) and increased physical activity. Selecting an appropriate pharmacologic approach for individuals with MASLD may also decrease the occurrence of HCC. Metformin, PPAR activators, sodium-glucose cotransporter 2 inhibitors, dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor agonists, aspirin, and statins have all shown promise to reduce the risk of HCC, although guidelines do not recommend their use for the sole purpose of chemoprevention at this time, given a dearth of data defining their risk-benefit ratio.

Rationale: The association between fine particulate matter (particulate matter ⩽2.5 μm in aerodynamic diameter, PM2.5) and lung cancer incidence in nonsmokers (LCINS) remains inconsistent. Objectives: To investigate the association between long-term PM2.5 exposure and LCINS in a Chinese population and to assess the modifying effect of genetic factors. Methods: Time-dependent Cox proportional hazard models were used to evaluate the hazard ratios (HRs) and 95% confidence intervals (CIs) of PM2.5 with LCINS risk and LCINS-related mortality. The polygenic risk score was constructed to further explore the interactions between genetic risk and PM2.5 exposure. In addition, the population attributable fraction of PM2.5 to lung cancer risk and mortality was calculated. Measurements and Main Results: The results demonstrated significant associations between PM2.5 exposure and LCINS incidence (HR, 1.10 per 10 μg/m3; 95% CI, 1.04-1.17 per 10 μg/m3) and mortality (HR, 1.17 per 10 μg/m3; 95% CI, 1.08-1.27 per 10 μg/m3). Compared with the lowest-risk group, individuals exposed to the high PM2.5 concentration (⩾50.9 μg/m3) and high genetic risk (top 30%) exhibited the highest LCINS incidence (HR, 2.01; 95% CI, 1.39-2.87) and mortality (HR, 2.30; 95% CI, 1.38-3.82). A significant additive interaction between PM2.5 and genetic risk on LCINS incidence was observed. Approximately 33.6% of LCINS cases and 48.5% of LCINS-related deaths in China could be prevented if PM2.5 concentrations were reduced to meet World Health Organization guidelines. Conclusions: Long-term exposure to outdoor PM2.5 increases LCINS risk and LCINS-related mortality, especially in populations with high genetic risk. Strengthening air pollution control measures in China has the potential to significantly reduce the burden of LCINS.

Bilateral risk-reducing mastectomies (RRMs) have been proven to decrease the risk of breast cancer in patients at high risk owing to family history or having pathogenic genetic mutations. However, few resources with consolidated data have detailed the patient experience following surgery. This systematic review features patient-reported outcomes for patients with no breast cancer history in the year after their bilateral RRM.

The databases MEDLINE, Embase, and Scopus were used to identify studies. Studies were then evaluated by multiple authors, and their quality was assessed by using the Methodological Index for Non-Randomized Studies score.

Our search identified 1858 unique studies, of which 11 met our inclusion criteria. Only two of these studies included patients who did not receive postmastectomy reconstruction. The included studies were either retrospective cohort studies or prospective studies. General satisfaction with the outcome of RRM and the decision to undergo RRM was high across many of the studies, with low levels of regret. There was also a noticeable trend of improved psychosocial outcomes following RRM. For postoperative sexual well-being, body image, aesthetic satisfactions, and somatosensory function, there were a mix of positive and negative outcomes.

The patients who elected to manage their breast cancer risk with bilateral RRM (mostly with reconstruction) tend to be satisfied with their decision and the surgical outcomes. This may be related to decreased cancer-related anxiety. Postmastectomy psychosocial well-being tends to improve while physical health after surgery varies by patient.

The cancer burden continues to escalate in China. This study was designed to quantify the burden of deaths attributable to modifiable risk factors for major cancers in China from 2012 to 2035, and to provide evidence-based recommendations for cancer management. Using nationally representative data on risk factors and cancer mortality, a comparative risk assessment approach was employed to calculate the temporal trend of population-attributable fractions (PAFs) for 15 modifiable risk factors associated with major cancers in China. The PAF for modifiable risk factors decreased from 64.5% (95% uncertainty interval [UI]: 46.2%-75.3%) in 2012 to 59.3% (95% UI: 40.6%-71.2%) in 2035. Attributable deaths increased from 1,309,990 (95% UI: 938,217-1,529,170) in 2012 to 1,313,418 (95% UI: 898,411-1,577,189) in 2035, while attributable disability-adjusted life years (DALYs) rose from 28,488,120 (95% UI: 20,471,859-33,308,237) to 33,017,705 (95% UI: 22,730,814-39,564,735). Between 2012 and 2035, the top three risk factors contributing to cancer burden shifted from smoking, insufficient fruit intake and particulate matter <2.5 μm in diameter (PM2.5) exposure to smoking, physical inactivity, and inadequate fruit intake. Controlling modifiable risk factors at recommended levels by 2020 could have prevented around 890,000 deaths and 2.2 million DALYs by 2035. The proportion of cancer burden due to modifiable risk factors is projected to decrease, but the absolute number continues to rise. Adhering to an optimal lifestyle could prevent ~40% of cancer deaths by 2035. Key modifiable risk factors including smoking, physical inactivity, and insufficient intake of fruits require high attention.

To investigate associations between daily physical activity, activity intensity and step counts with incident cancer risk.

Prospective analysis of UK Biobank participants who wore wrist-based accelerometers for 7 days, followed for cancer incidence (mean follow-up 5.8 years, SD 1.3). Time-series machine-learning models derived total physical activity, sedentary behaviour (SB), light-intensity physical activity (LIPA), moderate-vigorous-intensity physical activity (MVPA) and step counts. The outcome was a composite of 13 cancers previously associated with low physical activity in questionnaire-based studies. Cox proportional hazard models estimated HRs and 95% CIs, adjusted for demographic, health and lifestyle factors. We also explored associations of LIPA, MVPA and SB with cancer risk.

Among 85 394 participants (median age 63 (IQR 56-68)), 2633 were diagnosed with cancer during follow-up. Compared with individuals in the lowest quintile of total physical activity (<21.6 milligravity units), those in the highest (34.3+) had a 26% lower cancer risk (HR=0.74 (95% CI 0.65 to 0.84)). After mutual adjustment, LIPA (HR=0.94 (95% CI 0.90 to 0.98)) and MVPA (HR=0.87 (95% CI 0.79 to 0.94)) were associated with lower risk, but SB was not. Similar associations were observed for substituting 1 hour/day of SB with LIPA or MVPA. Daily step counts were inversely associated with cancer, with the dose-response beginning to plateau at around 9 000 steps/day (HR=0.89 (95% CI 0.83 to 0.96) 7000 vs 5000 steps; HR=0.84 (95% CI 0.76 to 0.93) 9000 vs 5000 steps). There was no significant association between stepping intensity (peak 30-minute cadence) and cancer after adjusting for step count.

Total physical activity, LIPA, MVPA and step counts were inversely associated with incident cancer.

This study examined the influence of knowledge and attitudes on smoking cessation behaviors among Koreans-including both individuals who have quit smoking and those who continue to smoke-using an extended KAP (knowledge, attitude, and practice) model.

Data for this study were drawn from the Korean National Cancer Prevention Awareness and Practice Survey conducted between 2014 and 2023, encompassing 12,400 participants. After excluding responses lacking data on KAP questions and individuals who had never smoked, the final analytic sample comprised 4,794 participants. To evaluate the associations among knowledge (that smoking causes cancer), attitudes (regarding smoking cessation for cancer prevention), and practice (the decision to stop smoking), we employed multiple logistic regression and mediation analyses to assess both the direct and indirect effects of these variables on smoking behavior.

Most participants demonstrated awareness that smoking causes cancer. In assessing the associations among knowledge, attitude, and practice, a decline in odds ratios was observed in 2023 compared with 2021. Attitudes toward smoking cessation for cancer prevention exerted a direct influence on the decision to quit smoking, with effect sizes of 0.23 in 2014, - 0.10 in 2016, 0.50 in 2018, 0.42 in 2021, and 0.40 in 2023. Furthermore, knowledge about smoking indirectly influenced the decision to quit smoking via its effect on attitudes toward cessation, with indirect effects of 0.12 in 2018, 0.10 in 2021, and 0.09 in 2023. Notably, knowledge did not directly affect practice; thus, attitudes toward smoking cessation emerged as the primary mediator between knowledge and the decision to quit smoking.

Our findings indicate that the decision to quit smoking is significantly influenced by individuals' attitudes toward smoking. Consequently, smoking cessation policies and interventions should integrate strategies that address attitudes in tandem with knowledge and practice components among Koreans. Moreover, the gradual weakening of the relationships among knowledge, attitudes, and practices over time underscores the need to reinforce these associations through innovative smoking cessation policies.

Social media (SM) has emerged as a tool for health-related usage among US adults, including cancer screening promotion. Here, we aimed to assess the differences in health-related SM use between US and foreign-born adults and the relationship between health-related SM use and colorectal (CRC) screening practices.

Using data from the fifth edition of the National Cancer Institute's Health Information National Trends Survey (HINTS 5), cycle 2, we compared the differences in health-related SM use between US and foreign-born adults and the effects of SM use on CRC screening by country of birth. We included adults aged 50-75 and excluded participants with a history of CRC. The primary endpoint was CRC screening, which was determined by self-reported CRC screening using colonoscopy, sigmoidoscopy, or stool occult blood testing.

Our study included 1,812 adults, of whom 236 (13.0%) were foreign-born. Most participants (72.1%) reported undergoing CRC screening. Interestingly, we found no discernible difference in health-related SM use [odds ratio [OR] 0.91; 95% CI (0.49, 1.69)] between US and foreign-born adults. Furthermore, our analysis revealed that SM use did not influence CRC screening practices among either group (US-born: 0.88 [95% CI: 0.50, 1.52], foreign-born 0.52 [0.10, 2.51]).

Contrary to previous studies, which showed a positive relationship between SM use and satisfactory health-related practices, we found that although foreign-born adults use SM as much as US-born adults, there was no significant relationship between SM use and CRC screening.

Cancer burden can be reduced by controlling modifiable risk factors, including diet. We provided an evidence-based assessment of cancer cases and deaths attributable to diet in Italy in 2020. We considered dietary factor-cancer type pairs for which the World Cancer Research Fund/American Institute for Cancer Research - Continuous Update Project reported either 'convincing' or 'probable' evidence of causal association. Relative risks were retrieved from recent meta-analyses and dietary intakes (around 2005) from a national food consumption survey. Sex-specific population attributable fractions (PAFs) were computed by comparing the distribution of dietary intakes in the Italian population against counterfactual scenarios based on dietary recommendations. Using data from national cancer and mortality registries in 2020, we estimated the number of attributable cancer cases and deaths, assuming ~15-year lag period. Unhealthy diet accounted for 6.3% (95% CI: 2.5%-9.9%) of all cancer cases in men and 4.5% (95% CI: 1.7%-7.4%) in women. PAFs of colorectal cancer were 10.5% and 7.0% for any intake of processed meat, 3.3% and 2.0% for high red meat, 4.8% and 4.3% for low dairy products, and 7.9% and 9.0% for low fiber intakes in men and women, respectively. PAFs for low intake of non-starchy vegetables and fruit ranged from 0.8% to 16.5% in men and 0.6%-17.8% in women for cancers of the aerodigestive tract. The estimated cancer burden associated with unfavorable dietary habits in Italy is considerable, but appears lower than for other high-income countries, reflecting the typically Mediterranean diet.

Gastrointestinal (GI) cancers are highly prevalent and considered a major global health challenge. Their approach has undergone a remarkable transformation over the past years due to the development of new technologies that enabled better outcomes regarding their diagnosis and management. These include artificial intelligence, robotics, next-generation sequencing and personalized medicine. Nonetheless, the integration of these advances into everyday clinical practice remains complex and challenging as we are still trying to figure out if these innovations tangibly improve oncological outcomes or if the current state of art should remain as the gold standard for the treatment of these patients. Additionally, there are also some issues regarding ethical subjects, data privacy, finances and governance. Precision surgery concept has evolved considerably over the past decades, especially for oncological patients. It aims to customize medical treatments and to operate on those patients who most likely will benefit from a specific surgical procedure. In the future, to improve GI oncological outcomes, a delicate balance between technological advances adoption and evidence-based care should be chased. As we move forward, the question will be to harness the power of innovation while keeping up the highest standards of patient care.

The gut microbiome, specifically enterotoxigenic Bacteroides fragilis (ETBF), has been reported to play a role in colorectal cancer development. We aimed to conduct a systematic review and meta-analysis of published studies to compare the prevalence of ETBF in patients with colorectal cancer and healthy controls as well as in various stages of colorectal cancer.

PubMed, EMBASE, and The Cochrane Library were systematically searched for studies published until May 2024. We utilized studies either comparing the prevalence of ETBF in patients with colorectal cancer and healthy control or examining its prevalence across different stages of colorectal cancer. The prevalence of ETBF colonization in biological samples from individuals with colorectal cancer compared to that in healthy controls or adjacent normal tissue as well as the association between the prevalence of ETBF and various stages of colorectal cancer were plotted using a random-effect or fixed-effect model.

Fourteen relevant articles were identified. Meta-analyses revealed that patients with colorectal cancer had a higher likelihood of having ETBF than healthy controls (odds ratio [OR]: 2.54, 95% confidence interval [CI]: 1.63-3.98, I2 = 55%). Additionally, ETBF detection was lower in stage I/II than in stage III/IV colorectal cancer (OR: 0.61, 95% CI: 0.41-0.91, I2 = 41%).

The prevalence of ETBF was consistently higher in the tissue and fecal samples of patients with colorectal cancer than in those of controls. A difference in ETBF prevalence between stage I/II and stage III/IV colorectal cancer was noted, but further analysis revealed that the conclusion is unreliable.

https://www.crd.york.ac.uk/prospero/, identifier CRD 42024548325.

Background/Objectives: Colorectal cancer (CRC) is one of the most common and deadly types of cancer. Compared with the classical histopathological approach, this study discusses the application of 1H NMR and FT-IR techniques for the fast evaluation degree of healing of patients with CRC after surgical intervention. Methods: Native and deproteinized blood plasma collected from 10 patients with confirmed CRC and 20 healthy volunteers were analyzed using 1H NMR T2 distributions and FT-IR spectra measured for samples collected before and 7 days after surgery. The average FT-IR spectrum from 20 healthy volunteers is also presented. Principal component analysis (PCA) was performed on the FT-IR spectra. The results were used for further statistical analysis using receiver operating characteristic (ROC) and area under the curve (AUC) and to produce a series of prediction maps using a machine learning library. Results: Both experimental methods combined with analysis methods demonstrated that the native blood plasma samples can be better used to predict the CRC patients' evolution 7 days after surgery. Three patients showed a significant evolution by 1H NMR T2 distribution, correlated to the observation of FT-IR-PCA analysis. Maps of medical state probability were generated using a trained machine learning-based ANN. Conclusions: The experimental measurements combined with an advanced statistical analysis and machine learning were successfully used and show that the healing process of patients with CRC is not linear, from the preoperative state to the state associated with healthy volunteers, but passes through a distinct healing state.

The existing evidence has shown a positive association between alcohol consumption and an increased risk of colorectal cancer (CRC). However, the evidence is primarily based on studies of CRC in all ages, and the role of alcohol in early onset colorectal cancer (EOCRC) remains to be determined. The aim of this study was to investigate an association between the increasing incidence of EOCRC and alcohol consumption.

We systematically searched PubMed, EMBASE, Cochrane and Web of Science up to June 2024 for studies that evaluated the association of alcohol intake with EOCRC risk and report specific results (e.g. relative risk, OR or hazard ratio and corresponding 95% CI). Based on the varying designs of the included studies, the corresponding effect values were extracted and categorized into high alcohol consumption and low alcohol consumption groups; a random-effects model was adopted to estimate the pooled effect sizes for analysis. Furthermore, subgroup analyses and publication bias assessments were conducted.

Three cohort studies and eight case-control studies were eligible and included. The results were pooled in meta-analyses, which yielded a heightened risk of EOCRC for increased alcohol intake (OR = 1.56, 95% CI 1.28-1.89, I2 = 89.3%). In the subgroup analysis, no significant differences were found in the association between alcohol consumption and the risk of developing EOCRC across gender, location or tumour site. The results of sensitivity analysis and publication bias indicated that the conclusion was robust.

This meta-analysis provides possible evidence for an association between alcohol consumption and risk of EOCRC. More research is needed in the future to confirm these findings.

This study sought to identify effective health warnings about alcohol consumption and breast cancer risk among young adult female participants.

We tested a pool of health warnings in a national pilot study. We used the most effective designs from the pilot in the main experiment where young (ages 21-29) U.S. adult female participants (N = 1038) reporting past 30-day alcohol consumption were randomly assigned into 1 of 4 conditions where they viewed a health warning about (1) mortality, (2) mastectomy, (3) hair loss, or (4) control (non-health warning message). Participants were then randomly assigned to view 1 of 2 message types within each condition: text-only or pictorial. Warnings were shown apart from products. Outcomes were message reactions (attention to and cognitive elaboration of warnings, fear, hope, and perceived message effectiveness), attitudes and beliefs (perceived severity and susceptibility to alcohol harms, and perceived response and self-efficacy to prevent alcohol harms), and behavioral intentions to stop or to reduce alcohol consumption in the next month.

Multivariate analysis of covariance (MANCOVA) models testing between warning conditions showed estimated marginal means (EMM) for every health warning condition were significantly higher than the control for attention (control = 5.80 vs. mortality = 6.63, mastectomy = 6.81, hair loss = 6.83, all ps < 0.05), fear (control = 2.45 vs. mortality = 4.11, mastectomy = 4.16, hair loss = 4.02, ps < 0.05), perceived message effectiveness (control = 3.44 vs. mortality = 5.75, mastectomy = 5.82, hair loss = 6.09, ps < 0.05), and perceived severity of alcohol harms (control = 5.51 vs. mortality = 6.25, mastectomy = 6.09, hair loss = 6.35, ps < 0.05). There were no significant differences between the health warnings about cancer effects for perceived message effectiveness. EMMs for intentions to reduce alcohol consumption in the next month were significantly higher in the mortality (6.44) and hair loss (6.35) conditions versus control (5.61, ps < 0.05).

Exposure to health warnings about alcohol consumption and breast cancer risk (vs. control) resulted in greater attention, fear, perceived message effectiveness, perceived severity of alcohol harms, and intentions to reduce alcohol consumption.

Equol, a naturally occurring phytoestrogen derived from the fermentation of soy and soy-based products by gut bacteria, is recognized for its diverse health benefits. While there is speculation about its association with cancer prevention, the scientific community has yet to reach a consensus due to the variability in research findings. Our study aims to shed light on this topic by examining the correlation between urine equol concentrations and the cancer risk among the American population. The National Health and Nutrition Examination Survey (NHANES) is a national survey of U.S. civilians in which cancer participants are enrolled in a database by a sample questionnaire. This study included 2797 Americans aged 40 years and older in the NHANES database (2005-2010). The relationship between urine equol concentration and cancer was analysed using weighted logistic regression models, stratified analysis, smoothed curve fitting and threshold effect analysis were also performed. Among the 2797 participants in our study, 390 individuals received a cancer diagnosis. Our findings indicate a positive correlation between urine equol levels and the risk of cancer. Notably, individuals in the highest quartile of equol excretion exhibited a significantly elevated risk of cancer, with a 25.4% increase compared to those in the lowest quartile (POR = 1.254, 95% CI: 1.252, 1.256), after fully adjusting for confounders. Similar results were observed in other adjusted models. A non-linear relationship in the shape of an inverted U-shape can be observed by smoothed curve fitting, and the inflection point is 25.5. Urinary equol concentrations below 25.5 ng/ml were positively associated with cancer risk, while equol concentrations above 25.5 ng/ml showed a slight negative trend in cancer risk. However, further prospective studies are needed to provide more robust evidence and confirmed in large clinical trials.

The numbers of new cancer cases and deaths in China were the largest in the world, causing a huge social and economic burden. We attempt to use more intuitive indicators to measure the probabilities of being diagnosed of or dying from cancer in China and compare these probabilities with those in Japan and the United States (US). We obtained the cancer data from GLOBOCAN 2022 for China, Japan, and the US and the all-cause mortality and population data from the United Nations. The lifetime risks of developing and dying from cancer were estimated with adjusted actual life expectancy, multiple primaries, and death-competing risks from causes other than cancers. Approximately 27.61% of Chinese people developed cancer and 1 in 5 persons were likely to die from cancer. The highest-risk cancer among men and women was lung cancer in China, but in the US and Japan, prostate cancer among men and breast cancer among women posed the highest risk. Lung cancer presented the highest likelihood of death, but women in Japan had the highest likelihood of dying from colorectal cancer. China had a lower lifetime risk of developing cancer compared with Japan and the US, but a higher probability of dying from cancer than the US. Although the probability of developing cancer was not as high as that in Japan and the US, China was still faced with enormous pressure due to its huge population and contradictory cancer patterns. Estimating lifetime risks can provide essential information to formulate appropriate cancer prevention and control plans.

Cancer-related deaths and environmental issues pose significant global challenges. The Planetary Health Diet (PHD) is a healthy dietary pattern that simultaneously promotes human health and ecology. This study aims to investigate the association between the Planetary Health Diet Index (PHDI) and mortality among cancer survivors, as well as the mediating role of inflammation between PHDI and all-cause mortality.

This study analyzed data from 3,442 cancer survivors enrolled in the United States National Health and Nutrition Examination Survey between 1999 and 2018. To investigate the association between PHDI and mortality, we applied weighted multivariate Cox proportional hazards regression, restricted cubic spline analysis, subgroup analysis, and sensitivity analysis. The mediating effects of the Systemic Immune-Inflammation Index (SII) and Neutrophil-to-Lymphocyte Ratio (NLR) were assessed using the bootstrap method with 1000 simulations.

In the fully adjusted model, each 10-point PHDI increase correlated with a 9% decrease in all-cause mortality (HR, 0.91; 95% CI, 0.86-0.95), a 10% decrease in cancer mortality (HR, 0.90; 95% CI, 0.83-0.99), and a 10% decrease in non-cancer mortality (HR, 0.90; 95% CI, 0.85-0.96). The PHDI was significantly inversely correlated with SII and NLR, which were positively related to all-cause mortality. The mediation proportions of SII and NLR between the PHDI and all-cause mortality were 6.52% and 8.52%, respectively.

Adherence to the PHD is associated with reduced all-cause, cancer, and non-cancer mortality among cancer survivors. Additionally, SII and NLR may mediate the relationship between PHDI and all-cause mortality.

Physical activity plays key roles in colorectal cancer survivorship; however, the impact of different clinicodemographic outcomes on cross-sectional and longitudinal objectively measured physical activity 12 and 24 months post-diagnosis are unclear.

ColoCare study participants (n = 165) wore an Actigraph GT3x accelerometer for 4-10 consecutive days to objectively assess activity levels 12 and 24 months after colorectal cancer diagnosis and resection. Associations between these clinical/demographic exposures and physical activity outcomes and longitudinal changes were determined using t-test, ANOVA F-test, and linear regression modeling, adjusting for common confounders (e.g., sex, age, stage).

Key physical activity and sedentary behavior variables significantly differed by demographic status, including minutes of weekly exercise by sex and age (age < 50: 364 min ± 303 min; age 50-70: 232 min ± 263 min; age > 70: 93 min ± 135 min, p < 0.001) and (%) daily sedentary time by age (age < 50: 64 ± 10%; age 50-70: 67 ± 7%; age > 70: 71 ± 7%, p = 0.003). Within the multivariate model, age was the primary measure consistently associated with activity differences. Participants who wore accelerometers 12- and 24-month post-resection (n = 52) significantly increased weekly exercise minutes (214 min ± 208 min vs. 288 min ± 316 min, p = 0.04).

Age is the primary clinicodemographic determinant separating physical activity levels in colorectal cancer survivors, and increases in exercise from 12 to 24 months are likely due to consolidation of sporadic daily physical activity into bouts of exercise.

Colorectal cancer survivors experience different volumes and changes in accelerometer-derived physical activity based on some (e.g., age) but not all (e.g., stage) clinicodemographic variables.

Smoking remains highly prevalent among Indigenous populations in the U.S., contributing to cardiovascular and cancer health disparities. Tailored smoking cessation interventions can reduce these disparities among Indigenous people, but the current evidence regarding the effectiveness of such extant interventions is unclear. This review aimed to collate evidence about the smoking cessation interventions tested among Indigenous groups in the U.S.

The study systematically searched PubMed, EMBASE, and Web of Science in September 2023 for experimental or quasi-experimental studies of smoking cessation interventions among Indigenous adults in the U.S. The Cochrane guidelines assessed study bias. Outcomes included self-reported and bio-verified smoking abstinence.

The review included eight studies, comprising 7 randomized control trials (RCTs) and 1 quasi-experimental trial evaluating multi-component interventions. The interventions included counseling, education, cultural tailoring, pharmacotherapy, mobile medical apps, and social media. The smoking abstinence outcomes varied. Four RCTs found no significant differences in self-reported or bio-verified abstinence between groups. Two RCTs showed significantly higher self-reported abstinence with culturally tailored interventions, while two postpartum RCTs found no difference between groups. The one-group quasi-experimental study showed a retention rate of 71 % and an abstinence rate of 31 % at 6-month follow-up. While results appear promising for tailored, multi-faceted approaches, abstinence differences between interventions and control groups overall remain inconsistent.

This review suggests that culturally tailored, technology-assisted smoking cessation interventions that strategically utilize pharmacotherapies may hold promise for U.S. Indigenous populations. However, the review emphasizes the need to test large-scale interventions that utilize more personalized strategies and community-based participatory approaches as well as the need for experimental trials that bio-verify abstinence.

The occurrence and development of cancer are deeply intertwined with chronic inflammatory processes. Epigallocatechin gallate (EGCG), the most pharmacologically potent catechin derived from tea, has garnered attention for its anti-inflammatory and anti-carcinogenic properties. However, the molecular mechanisms through which EGCG modulates tobacco smoke (TS)-induced inflammatory responses in lung carcinogenesis remain incompletely elucidated.

To unravel the molecular mechanisms by which EGCG mitigates TS-induced inflammatory processes in lung carcinogenesis.

Network pharmacology analysis was conducted to explore the potential target genes of EGCG involved in the inhibition of TS-induced lung cancer inflammation. In vitro and in vivo experiments were conducted to demonstrate EGCG's chemopreventive potential against lung carcinogenesis.

Utilizing data from the US adults, it was uncovered that tea consumption could suppress the inflammatory response in patients with various cancer types. CCL5 (chemokine (CC motif) ligand 5) could function as a core regulator of TS-induced lung cancer cell proliferation, and EGCG exerted beneficial effects. The following experiments revealed that TS upregulated CCL5 expression in H1299 and H226 cells. CCL5 recombinant protein elevated both ROS production and Nrf2 expression to promote lung cancer cell proliferation. EGCG could suppress CCL5-stimulated lung cancer cell proliferation by downregulating Nrf2 expression. In the mouse model, EGCG reduced tumor weight and volume, diminished the levels of CCL5, Ki67, Cyclin D1, PCNA, and Nrf2, and elevated the expression of Keap1 relative to the control group.

EGCG targets CCL5 to inhibit the proliferation of TS-induced lung cancer cells and may serve as a new treatment strategy.

Previous estimates of the number of cancers attributable to physical inactivity in the United States have typically focused on only three malignancies (colon, endometrial, and postmenopausal breast cancer). Contemporary epidemiologic evidence suggests that physical inactivity could contribute to up to 15 types of cancer, and a dose-response effect has been demonstrated for 13 of these. This study estimated the number of cancers diagnosed in the United States in 2015 due to physical inactivity for these 13 sites.

Data from the 2005 National Health Interview Survey were used to estimate physical activity prevalence and, with the assumption of a 10-year latency period, 2015 cancer incidence data from the National Program of Cancer Registries and Surveillance, Epidemiology, and End Results Incidence US Cancer Statistics Public Use Database.

The potential impact fraction was estimated to be 4.1%, which meant that 30,951 of 761,625 incident cancers at the 13 sites could have been prevented in the United States in 2015 if adults had increased physical activity by one category in 2005 (approximately 7.5 additional metabolic equivalent task hours per week [MET-h/week]). Theoretically, 85,415 of 761,625 incident cancers at the 13 sites (population attributable fraction, 11.2%) could have been prevented if all adults had achieved the highest level of physical activity (>30 MET-h/week).

When estimates are based on updated epidemiologic evidence regarding physical inactivity and cancer risk, substantially more cancers are attributable to physical inactivity than previously reported. A greater focus on physical activity promotion is warranted for cancer control in the United States.

Oxidative stress and reactive oxygen species play a pivotal role in carcinogenesis. Recent studies have indicated a potential reduction in cancer incidence associated with antioxidant intake; however, these results remain controversial. We performed 2-sample Mendelian randomization (MR) analysis to explore the causal relationship between dietary antioxidant vitamins (retinol, carotene, vitamin C, and vitamin E), oxidative stress injury biomarkers (GST, CAT, SOD, and GPX), and the risk of colorectal cancer (CRC). The genetic instrumental variants (IVs) that had previously shown significant association with dietary antioxidant vitamins and oxidative stress injury biomarkers were screened from the UK Biobank and relevant published studies. The genome-wide association study (GWAS) data for total colorectal, colon, and rectal cancer were obtained from the FinnGen cohort. The primary MR analysis employed the inverse-variance-weighted (IVW) method. Furthermore, sensitivity analysis was performed to assess heterogeneity and horizontal pleiotropy. The results revealed no significant causal associations between dietary antioxidant vitamins, oxidative stress injury biomarkers, and the risk of CRC. The odds ratios (ORs) were as follows: 1.22 (95% confidence interval (CI): 0.65-2.28, P = .53) for retinol, 0.77 (95% CI: 0.50-1.18, P = .24) for carotene, 0.82 (95% CI: 0.42-1.63, P = .58) for vitamin C, and 1.20 (95% CI: 0.86-1.68, P = .28) for vitamin E. Regarding oxidative stress injury biomarkers, the ORs were 0.99 (95% CI: 0.93-1.06, P = .88) for GST, 0.99 (95% CI: 0.93-1.05, P = .65) for CAT, 1.02 (95% CI: 0.95-1.09, P = .57) for SOD, and 1.01 (95% CI: 0.95-1.07, P = .76) for GPX. Likewise, stratified analysis by tumor site revealed no beneficial effects in colon and rectal cancers. Our findings indicate that elevated levels of diet-related antioxidant vitamins, as well as biomarkers of oxidative stress injury, do not provide a protective effect against CRC risk.

Association of cigarette use with risk of prostate cancer remains unclear. We performed this study to examine whether cigarette use is associated with increased risk of prostate cancer.

This cross-sectional study used data from the 1999 to 2020 National Health and Nutrition Examination Survey (NHANES), a population-based nationally representative survey designed to assess the health and nutritional status of US adults and children. Males were eligible if they were aged ≥ 20 years at the time of participation. Cigarette use (ever use, categorized into former use and current use) was defined as having smoked at least 100 cigarettes in life. Smoking duration, cigarettes smoked per day, and smoking pack-years were calculated in former smokers and current smokers. The primary outcome was self-reported diagnosis of prostate cancer by participants. Logistic regression was used to calculate the adjusted odd ratios (aOR) and 95% CI for the associations of cigarette use with risk of prostate cancer, adjusting for demographic characteristics. Subgroup analyses by age group were conducted. Data were analyzed from June 4 to November 30, 2023.

Of the 107 622 participants in 1999-2020 NHANES, 28 170 were included in the analysis. The mean (SD) age of the 28 170 participants was 46.4 (16.4) years, 68.0% were non-Hispanic White. Compared with never smokers, ever (aOR, 2.41 [95% CI, 1.15-5.06]) and former smokers (aOR, 3.56 [95% CI, 1.62-7.85]) had a higher risk of prostate cancer. This higher risk in former (aOR, 3.82 [95% CI, 1.69-8.64]) and ever smokers (aOR, 2.82 [95% CI, 1.27-6.25]) was also found in participants aged 20-59 years. Dose-response analysis showed a positive association between smoking duration (aOR, 1.07 [95% CI, 1.03-1.11]), cigarettes smoked per day (aOR, 1.03 [95% CI, 1.00-1.07]), smoking pack-years (aOR, 1.02 [95% CI, 1.01-1.03]) and risk of prostate cancer in current smokers.

This study suggests that cigarette use was associated with an increased risk of prostate cancer in US males, especially among those aged 20-59 years. Further research utilizing prospective study design and modeling family history is needed to confirm the findings.

The association between tomato/lycopene intake and blood levels of lycopene with the risk of specific cancers were assessed in previous meta-analyses; however, no study evaluated the risk of overall cancer incidence/mortality. Therefore, the present systematic review and dose-response meta-analysis aimed to summarize available findings from prospective studies to examine the association between tomato/lycopene intake and lycopene levels with the risk of total and specific cancers and cancer-related mortality.

A comprehensive literature search was done using Scopus, PubMed, ISI Web of Science, and Google Scholar until July 2023.

In total, 121 prospective studies were included in the systematic review and 119 in the meta-analysis. During the follow-up period of 2-32 years, a total of 108,574 cancer cases and 10,375 deaths occurred. High intakes and high levels of lycopene compared to low amounts were, respectively, associated with 5% (Pooled RR: 0.95, 95% CI: 0.92-0.98, I2 = 26.4%, p = 0.002) and 11% (Pooled RR: 0.89, 95% CI: 0.84-0.95, I2 = 15.0%, p < 0.001) reduction in overall cancer risk. Also, each 10 μg/dL increase in blood levels of lycopene was associated with a 5% lower risk of overall cancer. Moreover, we found a linear inverse association between dietary lycopene intake and prostate cancer risk (Pooled RR 0.99, 95% CI 0.97-1.00, I2 = 0, p = 0.045). Regarding cancer mortality, negative relationships were found with total tomato intake (Pooled RR: 0.89, 95% CI: 0.85-0.93, I2 = 65.7%, p < 0.001), lycopene intake (Pooled RR: 0.84, 95% CI: 0.81-0.86, I2 = 86.5%, p < 0.001) and lycopene levels (Pooled RR 0.76, 95% CI: 0.60-0.98, I2 = 70.9%, p = 0.031). Also, an inverse association was observed between blood lycopene levels and lung cancer mortality (Pooled RR: 0.65, 95% CI: 0.45-0.94, I2 = 0, p = 0.022).

Our findings show that dietary intake and blood levels of lycopene are associated with a lower risk of cancer and death due to cancer.

CRD42023432400.

Diet and nutrition are critical factors influencing cancer, the second leading cause of death worldwide. This study evaluated dietary risk factors and cancer mortality. 49,773 participants aged 40-75 years from the Golestan Cohort Study (GCS) were followed for a median of 15 years. Dietary intake was assessed using a validated food frequency questionnaire. Cox proportional hazard models estimated hazard ratios (HRs) and 95% confidence intervals (CIs), while population attributable fractions (PAFs) quantified the impact of reducing dietary risk factors. Low fruit intake accounted for 4.7% (95% CI: 0.5-8.7%) of all cancer deaths and 4.91% (95% CI: 0-9.85%) of male cancer deaths. It contributed to 23.5% (95% CI: 4.7-38.59%) of pancreatic cancer mortality in both sexes and 29.36% (95% CI: 5.15-47.38%) of male pancreatic cancer deaths. Low omega-3 intake increased esophageal and gastric cancer mortality risks, with PAFs of 21.65% (95% CI: 1.14-37.9%) and 21.46% (95% CI: 2.81-36.53%), respectively. In females, low omega-3 intake accounted for 38.68% (95% CI: 4.05-60.81%) of gastric cancer deaths. Low fruit and omega-3 consumption elevated cancer mortality risk. Community- and individual-level interventions are essential to enhance nutrient intake and reduce cancer mortality.

Cancer is a major global cause of death, and primary care is crucial for cancer prevention and early detection. However, there is conflicting information on the effectiveness, implementation, and sustainability of cancer control interventions in primary care.

This study aimed to summarize the evidence for cancer control in primary care, focussing on identifying relevant factors for implementation and sustainability.

We conducted a narrative, mixed-methods review of systematic reviews, guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). Four databases were screened, and two independent reviewers selected studies reporting on cancer prevention, screening, or early detection in primary or community settings. We analysed findings using the extended Reach-Effectiveness-Adopt-Implementation-Maintenance (RE-AIM) Framework.

From the 37 reviews that met the inclusion criteria, 6 focussed on primary prevention, 23 on screening, and 12 on early detection. Most reviews (78%) addressed intervention effectiveness, such as HPV vaccination, tobacco cessation, and cervical, breast, and colorectal screening. One-third of the reviews mentioned adoption and implementation factors, including barriers and facilitators to the implementation of cancer screening programs. Only one review addressed maintenance and sustainability factors, exploring continuous resources and funding strategies.

While numerous interventions are effective for cancer prevention and detection in primary care, literature on implementation and sustainability strategies is lacking. Focusing on continuous resources and funding for cancer strategies in primary care may aid sustainability. Future research should prioritize reporting on implementation and sustainability factors to enhance cancer prevention and control in primary care settings.

Our study examined the relationship between diet quality and the prevalence of metabolic syndrome (MetS) among 1779 U.S. cancer survivors using data from the National Health and Nutrition Examination Survey (NHANES, 2005-2016). Diet quality was assessed using the Healthy Eating Index 2015 (HEI-2015). Higher HEI-2015 scores were linked to significantly lower MetS prevalence (OR: 0.51, 95% CI: 0.32-0.80). Specifically, a higher intake of seafood and plant proteins, and fatty acids, coupled with a reduced intake of added sugars, was associated with decreased odds of MetS prevalence (OR: 0.93; 95% CI, 0.86-0.99) in cancer survivors. Additionally, a better diet quality was linked to lower prevalence of high waist circumference, elevated triglycerides, reduced high-density lipoprotein (HDL) cholesterol and high fasting glucose levels (OR, 0.44; 95% CI, 0.27-0.72). These results suggest that adopting healthy dietary habits may prevent MetS in cancer survivors.

We estimated the 5-year overall, age at diagnosis- and stage-specific colorectal cancer survival in patients treated through their coverage with Seguro Popular.

We conducted a retrospective study using a dataset that included 1418 colorectal cancer patients covered by Seguro Popular (Mexico's public health insurance system covering 60 % of the population) between 2013 and 2016. Deaths were identified using the Epidemiologic Death Statistics Subsystem registry, with a specialized algorithm for record linkage. The Kaplan-Meier method was used to estimate overall survival curves and the proportion of patients alive at various follow-up time points. We compared survival curves across subgroups using the log-rank test.

In this study the average age at diagnosis was 56 years with 31.9 % of patients diagnosed before the age of 50. Most cases (78.1 %) were diagnosed in advanced stages (i.e., III and IV), with nearly half of the cases originating in the rectum. The overall 5-year survival was 50 %, with higher survival (74 %) for patients with stage I-II and lower survival for those with stage III (58 %) and IV (33 %). While age at diagnosis was not associated with survival for early-stage colorectal cancer, younger patients with metastatic disease had a worse prognosis compared to older patients.

The 5-year overall colorectal cancer survival was 50 %, with variation by clinical stage. Almost 80 % of the population was diagnosed with advanced stages, underscoring the need for screening programs. Younger patients with metastatic disease exhibited a worse prognosis, highlighting the need for targeted interventions.

Previous studies reported higher lung cancer incidence in women than men among persons aged 35-54 years in the United States, a reversal of historically higher rates in men. We examined whether this pattern varies by state. Based on lung cancer incidence (2015-2019) data among adults aged 35-54 years from Cancer in North America database and historical cigarette smoking prevalence data (2004-2005) among adults 20-39 years from the Behavioral Risk Factor Surveillance System, incidence rates in women were equal to or higher than rates in their male counterparts in 40 of 51 states, with statistically significant differences in 20 states (two-sided, p < .05). In contrast, current and ever smoking prevalence in women compared to men was statistically significantly lower (33 and 34 states, respectively) or similar. Furthermore, there was no association between differences in historical smoking prevalence and lung cancer incidence by sex. Lung cancer incidence rate is higher in young women than young men in most states and is unexplained by differences in smoking prevalence.

Improving understanding of behaviors that increase or reduce cancer risk for different Hispanic groups is a public health priority; such knowledge is sparse in new gateway immigration locations such as Indiana. The aims of this study were to: 1) describe cancer beliefs and cancer preventive/risk reduction behaviors (physical activity, tobacco, and alcohol use) among Hispanic adults; 2) examine differences in cancer beliefs and preventive behaviors by country/territory of birth, socioeconomic status, and area of residence (urban vs. rural); and 3) determine predictors of engagement in cancer prevention and risk reduction behaviors in this population. A cross-sectional online survey targeted adult Indiana residents who identified as Latino, Hispanic, or Spanish recruited using Facebook-targeted advertising. Complete survey data from 1520 respondents were analyzed using descriptive, unadjusted, and adjusted models. The majority of respondents believed they were unlikely to get cancer but held many other fatalistic beliefs about cancer. Only 35.6% of respondents had received the HPV vaccine, 37.6% reported they were currently smoking cigarettes, and 64% reported occasional or frequent drinking of alcohol. Respondents spent an average of 3.55 days per week engaged in moderate exercise. Differences were observed by country/territory of birth, income, and education but not by rural residence status. Predictors of cancer risk/risk reduction behaviors were identified. The Hispanic population in Indiana is diverse and effective interventions for cancer prevention should be culturally targeted based on country/territory of birth and individually tailored based on cancer-related beliefs.

Western-style diets, characterized by higher fat and protein, and low micronutrient levels, promote the development of colorectal cancer (CRC). Here, we investigate the role of a Western diet on microbiome composition, sulfide production, and intestinal epithelial damage in pre-CRC mice, and validate taxonomic changes in a meta-analysis of human CRC patients.

NWD1 is a purified Western-style diet that produces sporadic intestinal and colon tumors in wild-type C57BL/6 mice in the absence of genetic or carcinogen exposure. To determine how this diet influences cancer risk by shaping microbial composition and sulfide chemistry, mice were fed NWD1 or a purified control diet for 24 weeks. Microbiome composition, sulfide production, and intestinal stem cell mRNA expression were assessed. Observed microbiome changes were validated in a human CRC meta-analysis.

Fecal sulfide levels were tripled in NWD1-fed mice ( P< 0.00001 ), concurrent with increased abundance of the sulfidogenic Erysipelotrichaceae family. NWD1-fed mice had increased expression of mitochondrial sulfide oxidation genes in Lgr5 hi intestinal stem cells, demonstrating an adaptive response to elevated sulfide. In a meta-analysis of human CRC studies, we observed that Erysipelotrichaceae were associated with CRC, validating both canonical CRC microbes such as Solobacterium moorei and highlighting the potential contribution of previously unrecognized, disease-associated microbes.

Our analyses connect the risk factors of Western diet, sulfide, and epithelial damage in a pre-cancer mouse model to microbiome changes observed in human CRC patients and suggest that microbial signatures of CRC and gut ecosystem alteration may manifest long before disease development.

Sleep health and other lifestyle behaviours are gaining increasing attention in public health, particularly for cancer prevention, but a comprehensive assessment is lacking.

The study included 380,042 UK Biobank participants. A healthy sleep score was constructed based on five sleep factors: chronotype, sleep duration, insomnia, snoring, and daytime dozing. A healthy lifestyle score was constructed based on four lifestyle factors: smoking, alcohol consumption, diet and physical activity. The effect of healthy sleep and lifestyle on cancer risk was examined by Cox proportional hazard models.

Both healthy sleep and lifestyle patterns were significantly associated with a reduced risk of overall cancer and specific cancer sites. Participants with healthy sleep and lifestyle patterns had a lower risk of overall cancer (HR = 0.72, 95% CI = 0.68-0.77), liver cancer (HR = 0.53, 95% CI = 0.31-0.90), bladder cancer (HR = 0.61, 95% CI = 0.47-0.79), lung cancer (HR = 0.22, 95% CI = 0.19-0.27), and colorectal cancer (HR = 0.80, 95% CI = 0.66-0.96) compared to those with unhealthy patterns.

Our findings highlight the importance of public health education and interventions to improve sleep and other lifestyle behaviours for cancer prevention.

Colorectal cancer (CRC) is the third most common cancer worldwide, with rising prevalence among younger adults. Several lifestyle factors, particularly disruptions in circadian rhythms by light-dark (LD) shifts, are known to increase CRC risk. Epidemiological studies previously showed LD-shifts are associated with increased risk of CRC. To explore the mechanisms and interactions between LD-shift and intestinal aging, we investigated how the combination of LD-shifts and aging impacts colon carcinogenesis development. Our data showed that LD-shifts and aging increased colon tumorigenesis. Notably, LD-shift accelerated intestinal aging by altering aging-related pathways, such as intestinal barrier damage, accompanied by dysbiotic changes in the intestinal microbiota that negatively impacts barrier stability. The increased carcinogenesis and intestinal aging were preceded by enrichment in host-microbiome features that are strongly regulated by the circadian clock. Overall, our results suggest that LD-shifts, increasingly prevalent among young adults, contribute to both intestinal aging and the development of colon carcinogenesis.

Lung cancer is a leading cause of cancer-related mortality, with disparities in incidence and outcomes observed across different racial and sex groups. Understanding the genetic factors of these disparities is critical for developing targeted treatment therapies. This study aims to identify both patient-specific and cohort-specific biomarker genes that contribute to lung cancer health disparities among African American males (AAMs), European American males (EAMs), African American females (AAFs), and European American females (EAFs). The real-world data is highly imbalanced with respect to race, and the lung cancer dataset is no exception. So, classification with race labels will generate highly biased results toward the larger cohort. We developed a computational framework by designing the classification problems with disease conditions instead of races and leveraging the local interpretability of explainable AI, SHAP (SHapley Additive exPlanations). This study used three disease conditions of lung cancer, including Lung Adenocarcinoma (LUAD), Lung Squamous Cell Carcinoma (LUSC), and Healthy samples (HEALTHY) to design four classification tasks: one 3-class problem (LUAD-LUSC-HEALTHY) and three 2-class problems (LUAD-LUSC, LUAD-HEALTHY, and LUSC-HEALTHY). This multiple-classification approach allows a LUAD patient to be interrogated via three classification problems, namely LUAD-LUSC-HEALTHY, LUAD-LUSC, and LUAD-HEALTHY, thus providing a robust approach of retrieving disparity information for individual patients through the local interpretation of SHAP. The proposed method successfully discovered the sets of genes and pathways related to health disparities in lung cancer between two cohorts, including AAMs vs. EAMs, AAFs vs. EAFs, AAMs vs. AAFs, and EAMs vs. EAFs. The discovered list of genes and pathways provide a short list for biological scientists to conduct wet lab experiment.

Findings from studies investigating the impacts of alcohol use and smoking on colorectal cancer outcomes are inconclusive. This study aimed to investigate associations between alcohol use and smoking status at the time of diagnosis on recurrence and overall mortality among patients with colorectal cancer.

The present study included 2,216 stage I-IV patients with colorectal cancer from the longitudinal multicenter ColoCare Study, with available data on recurrence and colorectal cancer-specific mortality. Cox proportional hazards models adjusted for age, sex, race, ethnicity, stage, tumor site, treatment, comorbidities, body mass index, and study site were fit, with imputations for missing data.

We observed 235 recurrences and 308 colorectal cancer-specific deaths over an average of 3 years of follow-up. After adjusting for confounders, current alcohol consumption and ever smoking, relative to not current consumption and never smoking, respectively, were not statistically significantly associated with colorectal cancer recurrence [alcohol-HR, 0.95. 95% confidence interval (CI), 0.71-1.29; ever smoking-HR, 0.98, 95% CI, 0.75-1.29] or colorectal cancer-specific mortality (alcohol-HR, 0.95. 95% CI, 0.74-1.22; ever smoking-HR, 0.98, 95% CI, 0.77-1.24).

No associations were observed between alcohol and smoking at diagnosis and clinical outcomes in this well-annotated longitudinal cohort.

Our cohort study reports no significant associations; however, limiting alcohol use and avoiding smoking are health behaviors recommended for colorectal cancer survivors for prevention of other cancers and chronic conditions.

Tobacco is the leading modifiable risk factor for cancer and other chronic diseases. The workplace provides an opportunity to advance tobacco cessation efforts. Combining tobacco cessation with complementary components addressing mental health, physical activity, and healthy eating has demonstrated effectiveness in non-workplace settings. This scoping review examines the literature on multicomponent workplace tobacco cessation interventions to identify core components and implementation facilitators and barriers to support uptake in the workplace setting.

A scoping review was conducted following PRISMA guidelines for Scoping Reviews and Arksey and O'Malley's five-step process. Peer-reviewed literature published in the past 20 years was searched across 9 databases. A search for relevant gray literature (i.e., conference papers/proceedings) was also completed. Articles were screened by two independent researchers for inclusion. Included studies evaluated workplace interventions recruiting individuals to participate in a tobacco cessation program alongside a complementary component (i.e., physical activity, mental health, healthy eating).

Most of the 12 included studies paired tobacco cessation with mental health or stress reduction interventions. Most complementary components targeted the individual versus organizational or policy levels. The synthesized facilitators indicated that multicomponent interventions should be incentivized and tailored to adequately meet the needs of different workplaces and employees.