Risk Of Smoking-related Cancer Research Articles

Estimating Additive Interaction in Two-Stage Individual Participant Data Meta-Analysis.

Individual participant data (IPD) meta-analysis provides important opportunities to study interaction and effect modification for which individual studies often lack power. While previous meta-analyses have commonly focused on multiplicative interaction, additive interaction holds greater relevance for public health and may in certain contexts better reflect biological interaction. Methodological literature on interaction in IPD meta-analysis does not cover additive interaction for models including binary or time-to-event outcomes. We aimed to describe how the Relative Excess Risk due to Interaction (RERI) and other measures of additive interaction or effect modification can be validly estimated within two-stage IPD meta-analysis. First, we explain why direct pooling of study-level RERI estimates may lead to invalid results. Next, we propose a three-step procedure to estimate additive interaction: 1) estimate effects of both exposures and their product term on the outcome within each individual study; 2) pool study-specific estimates using multivariate meta-analysis; 3) estimate an overall RERI and 95% confidence interval based on the pooled effect estimates. We illustrate this procedure by investigating interaction between depression and smoking and risk of smoking-related cancers using data from the PSYchosocial factors and Cancer (PSY-CA) consortium. We discuss implications of this procedure, including the application in meta-analysis based on published data.

Cancer risk and temporal trends in people with HIV during a quarter of a century – a nationwide population-based matched cohort study

Background It is important to understand current trends in cancer risk among people living with HIV (PLWH) to improve outcomes and to commission and delivery appropriate services. Methods Nationwide, population-based, matched cohort study on all adult PLWH treated at Danish HIV health care centres since 1 January 1995 and a comparison cohort, randomly selected from the background population and matched on sex and date of birth. Results We included 6327 PLWH and 63,270 individuals in the comparison cohort − 74% were men and median age was 37 (interquartile range: 30–46). For both smoking related cancers, virological cancers and other cancers, incidence was substantially higher in the first year of observation for PLWH than for the remaining observation period. The risk of smoking related cancer remained stably increased throughout the observation period, whereas the relative risk of virological cancers decreased, especially in the first year of follow up. Finally, the risk of other cancers for PLWH decreased to a level below that of the background population during the study period. Conclusion The fact that the risk of other cancers was probably not higher among PLWH than in the comparison cohort is encouraging, as the excess risk of virological and smoking related cancers is potentially preventable by timely treatment of HIV and smoking cessation.

Association of first primary cancer with risk of subsequent primary cancer among survivors of adult-onset cancers in Kentucky and Appalachian Kentucky.

Appalachia is a region with significant cancer disparities in incidence and mortality compared to Kentucky and the United States. However, the contribution of these cancer health disparities to subsequent primary cancers (SPCs) among survivors of adult-onset cancers is limited. This study aimed to quantify the overall and cancer type-specific risks of SPCs among adult-onset cancer survivors by first primary cancer (FPC) types, residence and sex. This retrospective cohort study from the Kentucky Cancer Registry included 148,509 individuals aged 20-84 years diagnosed with FPCs from 2000-2014 (followed until December 31, 2019) and survived at least 5 years. Expected numbers of SPC were derived from incidence rates in the Kentucky population; standardized incidence ratio (SIR) compared with those expected in the general Kentucky population. Among 148,509 survivors (50.2% women, 27.9% Appalachian), 17,970 SPC cases occurred during 829,530 person-years of follow-up (mean, 5.6 years). Among men, the overall risk of developing any SPCs was statistically significantly higher for 20 of the 30 FPC types, as compared with risks in the general population. Among women, the overall risk of developing any SPCs was statistically significantly higher for 20 of the 31 FPC types, as compared to the general population. The highest overall SIR were estimated among oral cancer survivors (SIR, 2.14 [95% CI, 1.97-2.33] among men, and among laryngeal cancer survivors (SIR, 3.62 [95% CI, 2.93-4.42], among women. Appalachian survivors had significantly increased risk of overall SPC and different site specific SPC when compared to non-Appalachian survivors. The highest overall SIR were estimated among laryngeal cancer survivors for both Appalachian and non-Appalachian residents (SIR, 2.50: 95%CI, 2.10-2.95; SIR, 2.02: 95% CI, 1.77-2.03, respectively). Among adult-onset cancer survivors in Kentucky, several FPC types were significantly associated with greater risk of developing an SPC, compared with the general population. Risk for Appalachian survivors was even higher when compared to non-Appalachian residents, but was not explained by higher risk of smoking related cancers. Cancers associated with smoking comprised substantial proportions of overall SPC incidence among all survivors and highlight the importance of ongoing surveillance and efforts to prevent new cancers among survivors.

Occupation-related cancer in urology-Current knowledge including environmental medical aspects

Occupation-related cancers are of considerable importance, which is not yet adequately recognized in the field of urology. The three numerically most significant entities are tumors of the urinary tract caused by carcinogenic aromatic amines or polycyclic aromatic hydrocarbons, renal cell cancer after high exposure to the solvent trichloroethylene, and mesotheliomas of the tunica vaginalis of the testis after exposure to asbestos; however, these can only be recognized as occupation-related if an occupational history regarding the hazard relevant to the organ bearing the tumor is documented from the beginning of employment, e.g. by aquestionnaire. This is because the relevant exposures generally date back several decades. With the exception of high exposure to trichloroethylene, the substances mentioned can also environmentally trigger the same tumors. In the context of environmental risk factors, it is of considerable importance that smoking is now considered to be atrigger for some 50% of all bladder cancers in men and women; however, smoking cessation results in areduction in smoking-related cancer risk of over 30% after only 3-4years. Work and commuting accidents, which are considered occupational risks, can lead to urological sequelae. For example, increased tumors of the bladder can occur after spinal cord injury lasting longer than 10years.

Abstract 2225: A composite smoking-related plasma protein score is associated with smoking-related cancer risk and mortality beyond self-reported smoking history in Atherosclerosis Risk in Communities Study (ARIC)

Abstract Background: Cigarette smoking is a leading causal risk factor for 13 cancers. Widely used self-reported smoking/packyears may not fully capture individualized risk of smoking-related cancer. Biomarkers (e.g., smoking-related proteins) may reflect biological effect of smoking and refine risk for personalized cancer screening recommendation. Methods: Protein levels were measured by SomaScan assay (log2 transformed) in Visit 3 plasma from ARIC. Participants were divided 50/50 into set-1 for protein selection and score building and set-2 for association analyses. In set-1, protein levels were evaluated in association with smoking status, packyears smoked, and time since quitting using linear regression. Proteins that passed the Bonferroni threshold were screened with elastic net regression to address correlation. For positively-related proteins, those with levels ≥median were assigned the weight of 1. For inversely-related proteins, those 3 yrs ago, former-quit<3 yrs ago, never) and packyears. Results: 9901 participants without a prior cancer history were included (46% male, mean age=60 yr, median follow-up=20.1 yr). In set-1, we selected 36, 46, 4 (65 unique) proteins related to current smoker, former-quit<3 yrs ago, packyears, respectively. In set-2, we ascertained 589 and 381 smoking-associated cancer cases and deaths, respectively. Median score was 31 (IQR: 12). The aHRs for smoking-related cancer incidence and mortality (Q4 vs Q1) were 2.35 (95% CI 1.83-3.02, p-trend<0.001) and 2.96 (2.12-4.14; p-trend<0.001) before adjusting for smoking, and 1.28 (0.96-1.70; p-trend=0.06) and 1.52 (1.04-2.22; p-trend=0.04) after adjusting for smoking. The aHRs for lung cancer were 6.81 (4.11-11.28), 6.84 (3.82-12.24), 2.02 (1.15-3.55) and 2.08 (1.09-3.95), respectively (all p-trend≤0.03). Conclusions: We showed that a preliminary, protein-derived composite score provides relative risk information beyond known cancer risk factors and self-reported smoking. Use of such a score may provide value for refining individualized risk for smoking-associated cancers and may guide precision screening. Funding: NHLBI, NCI, NPCR. Citation Format: Meng Ru, Christopher Douville, Christie M. Ballantyne, Kenneth R. Butler, Josef Coresh, David J. Couper, Ron C. Hoogeveen, Corinne E. Joshu, Jiayun Lu, Michael T. Marrone, Anna E. Prizment, Adrienne Tin, Elizabeth A. Platz. A composite smoking-related plasma protein score is associated with smoking-related cancer risk and mortality beyond self-reported smoking history in Atherosclerosis Risk in Communities Study (ARIC) [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2022; 2022 Apr 8-13. Philadelphia (PA): AACR; Cancer Res 2022;82(12_Suppl):Abstract nr 2225.

Effect of smoking reduction, cessation, and resumption on cancer risk: A nationwide cohort study.

The objective of this study was to investigate the effects of reduction, cessation, and resumption of smoking on cancer development. The authors identified 893,582 participants who currently smoked, had undergone a health screening in 2009, and had a follow-up screening in 2011. Among them, 682,996 participated in a third screening in 2013. Participants were categorized as quitters, reducers I (≥50% reduction), reducers II (<50% reduction), sustainers (referent), or increasers (≥20% increase). Outcome data were obtained through December 31, 2018. Reducers I exhibited a decreased risk of all cancers (adjusted hazard ratio [aHR], 0.96; 95% confidence interval [CI], 0.93-0.99), smoking-related cancers (aHR, 0.95; 95% CI, 0.92-0.99), and lung cancer (aHR, 0.83; 95% CI, 0.77-0.88). Quitters had the lowest risk of all cancers (aHR, 0.94; 95% CI, 0.92-0.96), smoking-related cancers (aHR, 0.91; 95% CI, 0.89-0.93), and lung cancer (aHR, 0.79; 95% CI, 0.76-0.83). In further analysis with 3 consecutive screenings, additional smoking reduction (from reducers II to reducers I) lowered the risk of lung cancer (aHR, 0.74; 95% CI, 0.58-0.94) in comparison with sustainers. Quitting among reducers I further decreased the risk of all cancers (aHR, 0.90; 95% CI, 0.80-1.00), smoking-related cancers (aHR, 0.81; 95% CI, 0.81-0.92), and lung cancer (aHR, 0.66; 95% CI, 0.52-0.84) in comparison with sustainers. Smoking resumption after quitting, even at a lower level, increased the risk of smoking-related cancers (aHR, 1.19; 95% CI, 1.06-1.33) and lung cancer (aHR, 1.48; 95% CI, 1.21-1.80) in comparison with sustained quitting. Smoking cessation and, to a lesser extent, smoking reduction decreased the risks of cancer. Smoking resumption increased cancer risks in comparison with sustained quitting. Worldwide, tobacco use is the single leading preventable risk factor for cancer and cancer death. This study examined the effects of reduction, cessation, and resumption of smoking on cancer development by measuring smoking behavior repetitively. Although smoking reduction has a substantial cancer prevention benefit for those who cannot quit, cessation should be encouraged whenever possible. Quitters should be monitored to ensure that they do not resume smoking.

778Risk of 27 cancer types in relation to tobacco smoking: cohort study involving 229,028 Australians

Abstract Background Tobacco smoke is a known carcinogen and the magnitude of smoking-related cancer risk varies according to time and population. Local, contemporary evidence can drive appropriate tobacco control. We provide comprehensive cancer risk estimates related to smoking in the population-based, New South Wales (NSW) 45 and Up Study. Methods We estimated smoking-related hazard ratios (HR) for cancer using Cox proportional hazards regression using linked questionnaire (2006-2009) and incident cancer data (n ≥ 50 cases per cancer type), from the NSW Cancer Registry (to December 2013) (via CHeReL). Results Of 18,475 cancers among 229,028 participants aged ≥45 years, current smokers had significantly increased risks of cancers of the lung, larynx, head and neck, oesophagus, liver, bladder, pancreas, stomach, colorectum, and cancers with unknown primary site, compared to never-smokers; lung cancer risk was markedly elevated, including for current-smokers of 1-5 cigarettes/day (HR = 9.25, 95%CI=5.2-16.6), increasing to 38.39 (26.2-56.2) for current-smokers of &amp;gt; 30 cigarettes/day. Quitting substantively decreased cancer risk compared to continued smoking, with lung cancer risk decreasing with decreasing age at quitting (p(trend)&amp;lt;0.05), however risks remained elevated for those quitting aged &amp;gt;25 compared to never-smokers (1.73, 1.1-2.6 for age 26-30 years). An estimated 20% of current-smokers in Australia will get lung cancer during their lifetime versus 1.6% of never-smokers. Conclusions Smoking-attributable cancer risks in Australia are significant, comparable to contemporary risks from other developed nations. Key messages Smokers – including “light” smokers – are at high cancer risk, with ∼one-fifth of Australian lifetime smokers developing lung cancer. Quitting is beneficial. Continued investment in tobacco control is essential.

The Inverse Association of Body Mass Index with Lung Cancer: Exploring Residual Confounding, Metabolic Aberrations and Within-Person Variability in Smoking

Abstract Background: The inverse observational association between body mass index (BMI) and lung cancer risk remains unclear. We assessed whether the association is explained by metabolic aberrations, residual confounding, and within-person variability in smoking, and compared against other smoking-related cancers. Methods: We investigated the association between BMI, and its combination with a metabolic score (MS) of mid-blood pressure, glucose, and triglycerides, with lung cancer and other smoking-related cancers in 778,828 individuals. We used Cox regression, adjusted and corrected for within-person variability in smoking (status/pack-years), calculated from 600,201 measurements in 221,958 participants. Results: Over a median follow-up of 20 years, 20,242 smoking-related cancers (6,735 lung cancers) were recorded. Despite adjustment and correction for substantial within-person variability in smoking, BMI remained inversely associated with lung cancer [HR per standard deviation increase, 0.87 (95% confidence interval 0.85–0.89)]. Individuals with BMI less than 25 kg/m2 and high MS had the highest risk [HR 1.52 (1.44–1.60) vs. BMI ≥25 with low MS]. These associations were weaker and nonsignificant among nonsmokers. Similar associations were observed for head and neck cancers and esophageal squamous cell carcinoma, whereas for other smoking-related cancers, we generally observed positive associations with BMI. Conclusions: The increased lung cancer risk with low BMI and high MS is unlikely due to residual confounding and within-person variability in smoking. However, similar results for other cancers strongly related to smoking suggest a remaining, unknown, effect of smoking. Impact: Extensive smoking-adjustments may not capture all the effects of smoking on the relationship between obesity-related factors and risk of smoking-related cancers.

Cancer incidence and cancer death in relation to tobacco smoking in a population-based Australian cohort study.

Tobacco smoke is a known carcinogen, but the magnitude of smoking-related cancer risk depends on country-specific, generational smoking patterns. We quantified cancer risk in relation to smoking in a population-based cohort, the 45 and Up Study (2006-2009) in New South Wales, Australia. Cox proportional hazards regressions estimated adjusted hazard ratios (HR) by self-reported smoking history at baseline (2006-2009) for incident, primary cancers via linkage to cancer registry data to 2013 and cancer death data to 2015. Among 229 028 participants aged ≥45 years, 18 475 cancers and 5382 cancer deaths occurred. Current-smokers had increased risks of all cancers combined (HR=1.42, 95% confidence interval [CI], 1.34-1.51), cancers of the lung (HR=17.66, 95%CI, 14.65-21.29), larynx (HR=11.29, 95%CI, 5.49-23.20), head-and-neck (HR=2.53, 95%CI, 1.87-3.41), oesophagus (HR=3.84, 95%CI, 2.33-6.35), liver (HR=4.07, 95%CI, 2.55-6.51), bladder (HR=3.08, 95%CI, 2.00-4.73), pancreas (HR=2.68, 95%CI, 1.93-3.71), colorectum (HR=1.31, 95%CI, 1.09-1.57) and unknown primary site (HR=3.26, 95%CI, 2.19-4.84) versus never-smokers. Hazards increased with increasing smoking intensity; compared to never-smokers, lung cancer HR=9.22 (95%CI, 5.14-16.55) for 1-5 cigarettes/day and 38.61 (95%CI, 25.65-58.13) for >35 cigarettes/day. Lung cancer risk was lower with quitting at any age but remained higher than never-smokers for quitters aged >25y. By age 80y, an estimated 48.3% of current-smokers (41.1% never-smokers) will develop cancer, and 14% will develop lung cancer, including 7.7% currently smoking 1-5 cigarettes/day and 26.4% for >35 cigarettes/day (1.0% never-smokers). Cancer risk for Australian smokers is significant, even for 'light' smokers. These contemporary estimates underpin the need for continued investment in strategies to prevent smoking uptake and facilitate cessation, which remain key to reducing cancer morbidity and mortality worldwide.

Lifestyle changes and risk of cancer: experience from the Swedish women's lifestyle and health cohort study

Background The impact of lifestyle changes on cancer risk is yet to be elucidated. We investigated this issue in the Swedish Women's Lifestyle and Health Cohort Study. Material and methods We measured changes by comparing two questionnaires, filled in 1991/92 and 2003. We followed women for cancer from 2003 until 2012. We used Cox regression models to assess the effect of changes in smoking, alcohol consumption, body mass index (BMI), physical activity and a lifestyle score on the risk of lifestyle-related cancer. One point was added to the lifestyle score for each of these: non-smoking, alcohol consumption ≤12 grams/day, BMI <25 kg/m2 and high level of physical activity. Results We included 29,930 women. From 1991/92 to 2003, median age changed from 40.0 to 51.7 years, alcohol consumption from 2.5 to 4.7 grams/day, BMI from 22.7 to 24.5 kg/m2, proportion of current smokers from 31.0 to 20.6% and women reporting high physical activity from 27.2 to 37.0%. Women who quit smoking had lower risk of smoking-related cancers compared to women who continued (hazard ratio (HR) 0.74, 95% confidence interval (CI) 0.55–1.00). Women who reduced their weight by more than 5%, compared to women with stable weight, had lower risk of breast cancer (HR 0.49, 95% CI 0.31–0.78). Among women with score of 0–2 in 1992/93, those who improved to 3-4 had lower risk of lifestyle-related cancers compared to women who did not (HR 0.81, 95% CI 0.66–0.99). Conclusions Healthy lifestyle changes, particularly smoking cessation and weight reduction, were associated with a decreased risk of cancer.

Risk of smoking-related cancers among women and men living with and without HIV.

We investigated whether the effect of smoking on the incidence of smoking-related cancers differs by HIV-infection status, if sex modifies the impact of risk factors for smoking-related cancers, and the sex-specific attributable risk of smoking on cancer incidence. Data from two large prospective studies in the United States were analyzed: 6789 men in the Multicenter AIDS Cohort Study from 1984 through 2018 and 4423 women in the Women's Interagency HIV Study from 1994 through 2018. Incidence rates, relative risks, and adjusted population attributable fractions (PAFs) were calculated for smoking-related cancers. During study follow-up, there were 214 incident smoking-related cancers in the men and 192 in the women. The age-adjusted incidence ratess for smoking-related cancers were higher in the women (392/100 000) than for the men (198/100 000; P < 0.01) and higher for people living with HIV (PLWH, 348/100 000) than for those without HIV (162/100 000; P < 0.01). Unadjusted incidence rates in PLWH were higher than in those without HIV when stratifying by cumulative pack-years of smoking (all P values <0.01). In adjusted interaction models, the effects of cumulative pack-years of smoking were significantly stronger in women. The adjusted PAFs for smoking-related cancers were nonsignificantly higher in the women than in the men (39 vs. 28%; P = 0.35). HIV looks to be an independent risk factor for smoking-related cancers and women appear to have a greater risk than men. These results highlight the need for interventions to help PLWH, especially women, quit smoking and sustain cessation to reduce their risk of smoking-related cancers.

Environmental tobacco smoke and cancer risk, a prospective cohort study in a Chinese population

Few prospective cohort studies have investigated associations between environmental tobacco smoke (ETS) and other cancer sites, in addition to lung cancer. We assessed these associations in a population-based prospective cohort study started from 2008 to 2011 with average of 9.1 years of follow-up, in Minhang district, Shanghai, China. The study included a total of 23,415 participants (8388 men, 15,027 women) and 205,515 person-years. Epidemiological data were collected by a standardized questionnaire including ETS exposure. Newly diagnosed patients with primary cancers and deaths were identified by record linkage system with the Shanghai Cancer Registry and Shanghai Vital Statistics. Hazard ratios (HRs) and their 95% confidence intervals (CIs) were estimated using Cox proportional hazards regression models, adjusting for potential confounders. During the study period, a total of 1462 patients with diagnoses of primary cancers were identified. Among all participants and non-smokers, ETS was associated with an increased risk of all smoking-related cancers (all: adjusted HR: 1.23, 95% CI: 1.05–1.43 and non-smokers: 1.24, 1.02–1.49), lung cancer (1.29, 0.98–1.71 and 1.27, 0.91–1.77), and stomach cancer (1.86, 1.21–2.85 and 1.75, 1.05–2.91), respectively. Furthermore, associations for lung and stomach cancers were the strongest among non-smoking females. The joint effects of both ETS and active smoking were strongest for all cancers, all smoking-related cancers, lung cancer, and stomach cancer. No clear interactions were observed. These results suggest that ETS exposure may increase the risk of smoking-related cancers in a Chinese population. Further studies on the relationship between ETS exposure and specific cancer sites are warranted to replicate our findings.

Extracolonic Cancer Risk After Total Colectomy for Inflammatory Bowel Disease: A Population-based Cohort Study.

Patients with inflammatory bowel disease are at increased risk of extracolonic cancers. Little is known regarding this risk following total colectomy [TC]. Patients who underwent TC for inflammatory bowel disease in Denmark during 1977-2013 were identified from the Danish National Patient Registry. Incidence rates of extracolonic cancers were determined through record linkage to the Danish Cancer Registry and compared with expected incidence rates in the general population. Standardized incidence ratios [SIRs] were calculated as the observed vs expected cancer incidence. In total, 4430 patients (3441 with ulcerative colitis [UC]; 989 with Crohn's disease [CD]) were followed for 54,183 person-years after TC. Following their surgery, 372 patients were diagnosed with extracolonic cancer compared to 331 expected [SIR = 1.1 (95% confidence interval {CI}: 1.0-1.2)]. The risk of extracolonic cancer overall was increased among patients with CD and TC (SIR = 1.5 [95% CI: 1.2-1.8]), but not among patients with UC and TC (SIR = 1.0 [95% CI: 0.9-1.2]). Patients with UC and TC had a higher risk of intestinal extracolonic cancer (SIR = 2.0 [95% CI: 1.4-2.7]). Patients with CD and TC had a higher risk of smoking-related cancers (SIR = 1.9 [95% CI: 1.2-2.9]), intestinal extracolonic cancer (SIR = 3.1 [95% CI: 1.6-5.5]) and immune-mediated cancers (SIR = 1.5 [95% CI: 1.0-2.1]). Patients with CD and TC had a higher risk of extracolonic cancer overall compared to the general population, while patients with UC and TC did not. Site-specific cancer risk varied according to inflammatory bowel disease type.

Effects of IL-4-590C/T (rs2243250) Polymorphism on the Susceptibility of Smoking-Related Cancer: A Meta-Analysis Involving 11,407 Subjects.

Background Several previous studies have assessed the relationship between IL-4-590C/T gene polymorphism and smoking-related cancer in recent years; however, the results remain controversial. Based on it, the study intends to clarify whether IL-4-590C/T variant increases the risk of smoking-related cancer through meta-analysis. Methods We searched PubMed, EMBASE, Web of Science, Cochrane Library database, China National Knowledge Infrastructure, and Wanfang data information service platform to collect qualified case-control studies in strict accordance with the inclusion and exclusion standards. The 95% confidence interval (95% CI) and its odds ratio (OR) were adopted to access the relation between IL-4-590C/T gene polymorphism and smoking-related cancer; sensitivity analysis and publication bias assessment were carried out after the studies' quality evaluation. Results 17 studies were included in total, with 5,061 patients and 6,346 control cases. A significant association between IL-4-590C/T variant and smoking-related cancer in total population was revealed in our meta-analysis results, and IL-4-590C/T variant might have a relatively protective effect on smoking-related cancer (CT vs. TT: P=0.026, OR = 0.900, 95% CI: 0.820–0.987). Subgroup analysis by ethnicity showed that the IL-4-590C/T polymorphism was associated with a decreased risk of smoking-related cancer in the Asian population (CT vs. TT: P=0.008, OR = 0.878, 95% CI: 0.798–0.967; CC + CT vs. TT: P=0.030, OR = 0.903, 95% CI: 0.824–0.990). Subgroup analysis based on types of cancer demonstrated the IL-4-590C/T variant achieved a lower risk in renal cell cancer (CC vs. TT: P=0.046, OR = 0.640, 95% CI: 0.412–0.993). Conclusion There is a conspicuous association between IL-4-590C/T polymorphism and decreased risk of smoking-related cancer, particularly in Asians. And IL-4-590C/T polymorphism may have a protective effect on renal cell cancer.

Lower risk of smoking-related cancer in individuals with familial hypercholesterolemia compared with controls: a prospective matched cohort study

According to guidelines, individuals with familial hypercholesterolemia (FH) shall receive lifestyle intervention and intensive lipid-lowering treatment from early in life to reduce the risk of coronary heart disease. Our aim was to study if treatment of FH also could affect risk of lifestyle-related cancer. We presented cumulative incidence of total cancer and lifestyle-related cancer sites in individuals with genetically verified FH (n = 5531) compared with age and sex matched controls (n = 108354). Individuals with FH had 20% lower risk of smoking-related cancer compared with the control population [HR 0.80 (95% CI, 0.65–0.98)], in particular men with FH at 40–69 years at age of diagnosis with HR 0.69 (95% CI, 0.49–0.97). The FH population and controls had similar rates of total cancer [HR 0.97 (95% CI, 0.86–1.09)], cancer related to poor diet [HR 0.82 (95% CI, 0.59–1.15)], cancer related to physical inactivity [HR 0.93 (95% CI, 0.73–1.18)], alcohol-related cancer [HR 0.98 (95% CI, 0.80–1.22)] and cancer related to obesity [HR 1.03 (95% CI, 0.89–1.21)]. In summary, we found reduced risk of smoking-related cancer in individuals with FH, most likely due to a lower prevalence of smoking. Implications of these findings can be increased motivation and thus compliance to treatment of hypercholesterolemia.

A Prospective Cohort Study of Cigarette Prices and Smoking Cessation in Older Smokers.

Background: Cigarette price increases effectively prevent smoking initiation and reduce cigarette consumption among young smokers. However, the impact of cigarette prices on smoking cessation among older smokers is less clear, particularly for those aged 65 years and older, a group that is at highest risk of smoking-related disease and will almost double in the United States between 2012 and 2050.Methods: Biennial questionnaires administered between 1997 and 2013 assessed smoking status for 9,446 Cancer Prevention Study-II Nutrition Cohort participants who were ≥50 years old and lived in Washington, DC, and 48 states. For each interval between biennial questionnaires, change in price per pack and average price level per pack were calculated. The separate associations between these price variables and smoking cessation during the same time interval were determined.Results: In multivariable-adjusted models, each $1.00 price increase was associated with a 9% higher rate of quitting [rate ratio (RR) = 1.09; 95% confidence interval (CI), 1.04-1.14). Each $1.00 increase in average price was associated with a 6% higher rate of quitting (RR = 1.06; 95% CI, 1.02-1.10). The association with average price was strongest among smokers aged 65 years and older (RR = 1.07; 95% CI, 1.04-1.11) and, for price change, for smokers with no major prevalent disease (RR = 1.13; 95% CI, 1.07-1.19).Conclusions: These results suggest that increasing cigarette prices will promote quitting even among smokers aged 65 years and older.Impact: Increasing cigarette prices through higher taxes could reduce smoking rates among older adults and decrease risk of smoking-related cancers and diseases in this high-risk group. Cancer Epidemiol Biomarkers Prev; 26(7); 1071-7. ©2017 AACR.

Tobacco Use and Cancer Risk in the Agricultural Health Study.

Background: Cigarettes are well known to cause cancer, but less is known about the risks of other tobacco products and use of more than one product.Methods: We examined cancer incidence in relation to exclusive use of six tobacco products [cigarettes, other combustibles (pipe, cigar, cigarillo), and smokeless tobacco (chewing tobacco, snuff)] in the Agricultural Health Study. We also examined the added cancer risks associated with use of cigarettes and other tobacco products.Results: In our study population of 84,015, ever use of smokeless tobacco was higher than the general United States population, whereas cigarette use was lower and other combustible product use was about the same. The strongest associations for exclusive ever use were for lung cancer [cigarettes HR = 15.48; 95% confidence interval (CI), 11.95-20.06; other combustible tobacco HR = 3.44; 95% CI, 1.53-7.71; smokeless tobacco HR = 2.21; 95% CI, 1.11-4.42]. Compared with exclusive cigarette smokers, cigarette smokers who additionally ever-used another combustible product had higher risks of smoking-related cancers (HR = 1.16; 95% CI, 1.04-1.30), especially among those who smoked cigarettes for more than 15 years.Conclusions and Impact: Cigarette smokers who additionally ever used smokeless tobacco had cancer risks similar to exclusive cigarette smokers. Users of cigarettes and other combustible tobacco may have higher risks of certain cancers than exclusive cigarette users. Cancer Epidemiol Biomarkers Prev; 26(5); 769-78. ©2016 AACR.

Smoking-related cancer in military veterans: retrospective cohort study of 57,000 veterans and 173,000 matched non-veterans.

BackgroundServing military personnel are more likely to smoke, and to smoke more heavily, than civilians. The aim of our study was to examine whether veterans have an increased risk of a range of smoking-related cancers compared with non-veterans, using a large, national cohort of veterans.MethodsWe conducted a retrospective cohort study of 57,000 veterans resident in Scotland and 173,000 age, sex and area of residence matched civilians. We used Cox proportional hazard models to compare the risk of any cancer, lung cancer and other smoking-related cancers overall, by sex and by birth cohort, adjusting for the potential confounding effect of socioeconomic deprivation.ResultsOver a mean of 29 years follow-up, 445 (0.79 %) veterans developed lung cancer compared with 1106 (0.64 %) non-veterans (adjusted hazard ratio 1.16, 95 % confidence intervals 1.04–1.30, p = 0.008). Other smoking-related cancers occurred in 737 (1.31 %) veterans compared with 1883 (1.09 %) non-veterans (adjusted hazard ratio 1.18, 95 % confidence intervals 1.08–1.29, p < 0.001). A significantly increased risk was observed among veterans born 1950–1954 for lung cancer and 1945–1954 for other smoking-related cancers. The risk of lung cancer was decreased among veterans born 1960 onwards. In comparison, there was no difference in the risk of any cancer overall (adjusted hazard ratio 0.98, 95 % confidence intervals 0.94–1.01, p = 0.171), whilst younger veterans were at reduced risk of any cancer (adjusted hazard ratio 0.88, 95 % confidence intervals 0.81–0.97, p = 0.006).ConclusionsMilitary veterans living in Scotland who were born before 1955 are at increased risk of smoking-related cancer compared with non-veterans, but younger veterans are not. The differences may reflect changing patterns of smoking behaviour over time in military personnel which may, in turn, be linked to developments in military health promotion policy and a changing military operational environment, as well as to wider societal factors.

Lack of Correlation between Stem-Cell Proliferation and Radiation- or Smoking-Associated Cancer Risk.

BackgroundA recent paper by Tomasetti and Vogelstein (Science 2015 347 78–81) suggested that the variation in natural cancer risk was largely explained by the total number of stem-cell divisions, and that most cancers arose by chance. They proposed an extra-risk score as way of distinguishing the effects of the stochastic, replicative component of cancer risk from other causative factors, specifically those due to the external environment and inherited mutations.ObjectivesWe tested the hypothesis raised by Tomasetti and Vogelstein by assessing the degree of correlation of stem cell divisions and their extra-risk score with radiation- and tobacco-associated cancer risk.MethodsWe fitted a variety of linear and log-linear models to data on stem cell divisions per year and cumulative stem cell divisions over lifetime and natural cancer risk, some taken from the paper of Tomasetti and Vogelstein, augmented using current US lifetime cancer risk data, and also radiation- and tobacco-associated cancer risk.ResultsThe data assembled by Tomasetti and Vogelstein, as augmented here, are inconsistent with the power-of-age relationship commonly observed for cancer incidence and the predictions of a multistage carcinogenesis model, if one makes the strong assumption of homogeneity of numbers of driver mutations across cancer sites. Analysis of the extra-risk score and various other measures (number of stem cell divisions per year, cumulative number of stem cell divisions over life) considered by Tomasetti and Vogelstein suggests that these are poorly predictive of currently available estimates of radiation- or smoking-associated cancer risk–for only one out of 37 measures or logarithmic transformations thereof is there a statistically significant correlation (p<0.05) with radiation- or smoking-associated risk.ConclusionsThe data used by Tomasetti and Vogelstein are in conflict with predictions of a multistage model of carcinogenesis, under the assumption of homogeneity of numbers of driver mutations across most cancer sites. Their hypothesis that if the extra-risk score for a tissue type is high then one would expect that environmental factors would play a relatively more important role in that cancer’s risk is in conflict with the lack of correlation between the extra-risk score and other stem-cell proliferation indices and radiation- or smoking-related cancer risk.

Cancer Screening Adherence of Asian Women According to Biochemically-verified Smoking Status: Korea National Health and Nutrition Examination Survey.

Men and women who smoke tend to show less compliance to screening guidelines than non- smokers. However, a recent study in Korea showed that self-reported female smokers constituted less than half of cotinine-verified smokers. Therefore, the aim of this study was to identify hidden smokers using cotinine- verified method and examine cancer screening behavior according to biochemically verified smoking status. Among 5,584 women aged 30 years and older who participated in the Fourth and Fifth Korea National Health and Nutrition Examination Survey (KNHANES), 372 (6.66%) hidden smokers were identified based on interview responses and verified by urinary cotinine levels. We compared cancer-screening behavior (cervical, breast, stomach, and colon cancer) of female hidden smokers to that of non-smokers and self- reported smokers by cross-sectional analysis. Hidden female smokers had significantly lower adherence to breast cancer screening compared to non-smokers (aOR (adjusted odds ratio) [95% CI] = 0.71 [0.51-0.98]). Adherence to stomach cancer (aOR [95% CI] = 0.75 [0.54-1.03]) and cervical cancer (aOR [95% CI] = 0.85 [0.66-1.10]) screening was also lower among hidden female smokers compared to non-smokers. Self-reported (current) smokers showed lowest adherence to cervical cancer (aOR: 0.64, 95% CI0.47-0.87), breast cancer (0.47 [0.32-0.68]), stomach cancer (0.66[0.46-0.95]), and colon cancer (0.62 [0.38-1.01]) screening compared to non-smokers, followed by female hidden smokers, then non-smokers. These lower adherence rates of current smokers were attenuated after we incorporated hidden smokers into the current smoker group. Cancer screening adherence of female hidden smokers was lower than cotinine-verified non-smokers but higher than current smokers. Considering the risk of smoking-related cancer among women, identifying hidden smokers is important to encourage appropriate cancer screening.