Influence of pre-diagnostic cigarette smoking on colorectal cancer survival: overall and by tumour molecular phenotype.
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ABSTRACT:
SUBMITTER: Zhu Y
PROVIDER: S-EPMC3950884 | biostudies-other | 2014 Mar
REPOSITORIES: biostudies-other
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Project description:We examined whether smoking prior to non-Hodgkin lymphoma (NHL) diagnosis was associated with overall survival (OS) and conducted a meta-analysis to assess the evidence relating pre-diagnosis cigarette smoking with OS. Among 523 NHL patients, worse OS was suggested for greater pre-diagnostic smoking habits when compared to never smokers. In the meta-analysis (n = 5 patient populations), inferior OS was observed for greater number of cigarettes smoked per day, years of cigarette smoking, and pack-years of cigarette smoking. The inferior survival was more pronounced for follicular than for diffuse large B cell lymphoma. Pre-diagnosis cigarette smoking may adversely impact the survival of NHL patients.
| S-EPMC3797194 | biostudies-literature
Project description:BackgroundAn artificial intelligence method could accelerate the clinical implementation of tumour-stroma ratio (TSR), which has prognostic relevance in colorectal cancer (CRC). We, therefore, developed a deep learning model for the fully automated TSR quantification on routine haematoxylin and eosin (HE) stained whole-slide images (WSI) and further investigated its prognostic validity for patient stratification.MethodsWe trained a convolutional neural network (CNN) model using transfer learning, with its nine-class tissue classification performance evaluated in two independent test sets. Patch-level segmentation on WSI HE slides was performed using the model, with TSR subsequently derived. A discovery (N=499) and validation cohort (N=315) were used to evaluate the prognostic value of TSR for overall survival (OS).FindingsThe CNN-quantified TSR was a prognostic factor, independently of other clinicopathologic characteristics, with stroma-high associated with reduced OS in the discovery (HR 1.72, 95% CI 1.24-2.37, P=0.001) and validation cohort (2.08, 1.26-3.42, 0.004). Integrating TSR into a Cox model with other risk factors showed improved prognostic capability.InterpretationWe developed a deep learning model to quantify TSR based on histologic WSI of CRC and demonstrated its prognostic validity for patient stratification for OS in two independent CRC patient cohorts. This fully automatic approach allows for the objective and standardised application while reducing pathologists' workload. Thus, it can potentially be of significant aid in clinical prognosis prediction and decision-making.FundingNational Key Research and Development Program of China, National Science Fund for Distinguished Young Scholar, and National Science Foundation for Young Scientists of China.
| S-EPMC7648125 | biostudies-literature
Project description:The WHO study group on tobacco product regulation (TobReg) advised regulating and lowering toxicant levels in cigarette smoke. Aldehydes are one of the chemical classes on the TobReg smoke toxicants priority list. To provide insight in factors determining aldehyde yields, the levels of 12 aldehydes in mainstream cigarette smoke of 11 Dutch brands were quantified. Variations in smoking behavior and cigarette design affecting human exposure to aldehydes were studied by using four different machine testing protocols. Machine smoking was based on the International Standardization Organization (ISO) and Health Canada Intense (HCI) regime, both with and without taping the filter vents. The 11 cigarette brands differed in (i) design and blend characteristics; (ii) tar, nicotine, and carbon monoxide (TNCO) levels; (iii) popularity; and (iv) manufacturer. Cigarette smoke was trapped on a Cambridge filter pad and carboxen cartridge. After being dissolved in methanol/CS2 and derivatization with DNPH, the aldehyde yields were determined using HPLC-DAD. Using an intense smoking regime (increased puff volume, shorter puff interval) significantly increased aldehyde yields, following the pattern: ISO < ISO-taped < HCI-untaped < HCI. For all of the regimes, acetaldehyde and acrolein yields were strongly correlated ( r = 0.804). The difference in TNCO and aldehyde levels between regular and highly ventilated low-TNCO cigarettes (as measured using ISO) diminished when smoking intensely; this effect is stronger when combined with taping filter vents. The highly ventilated low-TNCO brands showed six times more aldehyde production per mg nicotine for the intense smoking regimes. In conclusion, acetaldehyde and acrolein can be used as representatives for the class of volatile aldehydes for the different brands and smoking regimes. The aldehyde-to-nicotine ratio increased when highly ventilated cigarettes were smoked intensely, similar to real smokers. Thus, a smoker of highly ventilated low-TNCO cigarettes has an increased potential for higher aldehyde exposures compared to a smoker of regular cigarettes.
| S-EPMC6008735 | biostudies-literature
Project description:BackgroundIt is uncertain whether smoking is related to colorectal cancer risk. Cytochrome P-450 CYP1A1, glutathione-S-transferase (GST) and NAD(P)H:quinone oxidoreductase 1 (NQO1) are important enzymes in the metabolism of tobacco carcinogens, and functional genetic polymorphisms are known for these enzymes. We investigated the relation of cigarette smoking and related genetic polymorphisms to colorectal cancer risk, with special reference to the interaction between smoking and genetic polymorphism.MethodsWe used data from the Fukuoka Colorectal Cancer Study, a population-based case-control study, including 685 cases and 778 controls who gave informed consent to genetic analysis. Interview was conducted to assess lifestyle factors, and DNA was extracted from buffy coat.ResultsIn comparison with lifelong nonsmokers, the odds ratios (OR) of colorectal cancer for <400, 400-799 and > or = 800 cigarette-years were 0.65 (95% confidence interval [CI], 0.45-0.89), 1.16 (0.83-1.62) and 1.14 (0.73-1.77), respectively. A decreased risk associated with light smoking was observed only for colon cancer, and rectal cancer showed an increased risk among those with > or = 400 cigarette-years (OR 1.60, 95% CI 1.04-2.45). None of the polymorphisms under study was singly associated with colorectal cancer risk. Of the gene-gene interactions studied, the composite genotype of CYP1A1*2A or CYP1A1*2C and GSTT1 polymorphisms was associated with a decreased risk of colorectal cancer, showing a nearly statistically significant (Pinteraction = 0.06) or significant interaction (Pinteraction = 0.02). The composite genotypes of these two polymorphisms, however, showed no measurable interaction with cigarette smoking in relation to colorectal cancer risk.ConclusionsCigarette smoking may be associated with increased risk of rectal cancer, but not of colon cancer. The observed interactions between CYP1A1 and GSTT1 polymorphisms warrant further confirmation.
| S-EPMC2906477 | biostudies-literature
Project description:Tobacco smoking might be impacted by various influences, including psychological, socio-cultural, and economic factors. A community-based cross-sectional survey was conducted in Syrian Arab Republic from March to April 2019 using a web-based questionnaire. The survey aimed at assessing tobacco use (shisha and cigarettes) as well as examining the association between current tobacco use and various sociodemographic and war-related factors. The sample comprised 978 participants (251 males: 727 females) and had a mean age of 24.7 years (SD: 7.60). Most participants were single (n = 825, 84.4%), reside in Damascus and Rif-Dimashq (n = 579, 59.2%), and had a college/university education (n = 911, 93.1%). Concerning smoking, a total of 371 participants (37.9%) were identified to be current tobacco smokers, of whom 211, 84, 76 were exclusive shisha smokers, exclusive cigarette smokers, and dual smokers, respectively. The prevalence of cigarette smoking (exclusive and dual) among males and females was found to be 34.7%, and 10.0%, respectively. On the other hand, the prevalence of shisha smoking (exclusive and dual) among males and females was around 34.3% and 27.6%, respectively. Additionally, various factors have predicted a higher likelihood of cigarette smoking including male gender (AOR = 4.152; 95% CI: 2.842-6.064; p<0.001), and losing someone due to the war (AOR = 1.487; 95% CI: 1.028-2.151; p = 0.035), while unemployed individuals were found to have lower odds of being cigarette smokers (AOR = 0.634; 95% CI: 0.429-0.937; p = 0.022). Concerning shisha smoking, married (AOR = 0.622; 95% CI: 0.402-0.963; p = 0.033), and unemployed individuals (AOR = 0.679; 95% CI: 0.503-0.916; p = 0.011) were found to have lower odds of shisha smoking. Amid the tobacco epidemic in the region, rates of tobacco use in Syria are still worrying. The Syrian armed conflicts may possess a double-edged effect on smoking, and tobacco users who adopt smoking to cope with various stressors should be targeted with well-structured health education, along with appropriate psychological services.
| S-EPMC8412248 | biostudies-literature
Project description:BackgroundCigarette smoking is an established risk factor for colorectal cancer. Because colorectal carcinogenesis is a heterogeneous process, we investigated whether cigarette smoking is differentially associated with molecularly defined subtypes of colorectal cancer.MethodsWe evaluated associations between smoking and incident colorectal cancer, overall and by microsatellite instability (MSI) phenotype (MSI-high vs MSI-low or microsatellite stable), CpG island methylator phenotype (CIMP positive or CIMP negative), and BRAF mutation status (BRAF mutation positive or BRAF mutation negative), among 37 399 participants in a population-based cohort study (the Iowa Women's Health Study). Cigarette smoking (and other exposures) was assessed by self-report at baseline in 1986, including smoking status (never and ever [former or current]), age at initiation, total duration, average number of cigarettes smoked per day, cumulative pack-years, and induction period. Vital status and state of residence were determined by mailed follow-up questionnaires in 1987, 1989, 1992, and 1997 and by linkage to Iowa death certificate records. Nonrespondents were checked via the National Death Index to identify descendants. Participants with newly diagnosed (ie, incident) colorectal cancer were identified through annual linkage with the Iowa Cancer Registry. Archived paraffin-embedded tumor tissue specimens were obtained for 555 patients with colorectal cancer who were diagnosed from January 1, 1986, through December 31, 2002, and MSI status, CIMP status, and BRAF status were determined. Multivariable Cox regression models were fit to estimate relative risks (RRs) and 95% confidence intervals (CIs).ResultsEver-smokers were at moderately increased risk for incident colorectal cancer (RR = 1.19, 95% CI = 1.05 to 1.35) compared with never-smokers. Higher risk estimates were observed for current smokers with MSI-high tumors (RR = 1.99, 95% CI = 1.26 to 3.14), CIMP-positive tumors (RR = 1.88, 95% CI = 1.22 to 2.90), and BRAF mutation-positive tumors (RR = 1.92, 95% CI = 1.22 to 3.02). Other smoking-related variables (ie, age at initiation, total duration, average number of cigarettes smoked per day, cumulative pack-years, and induction period) were also associated with MSI-high, CIMP-positive, and BRAF mutation-positive tumor subtypes. Conversely, cigarette smoking status (ever vs never) was not associated with the MSI-low or microsatellite stable (RR = 1.00, 95% CI = 0.79 to 1.25), CIMP-negative (RR = 1.02, 95% CI = 0.81 to 1.30), or BRAF mutation-negative subtypes (RR = 1.00, 95% CI = 0.65 to 1.27).ConclusionsIn this prospective study of older women, cigarette smoking was associated with the MSI-high, CIMP-positive, and BRAF mutation-positive colorectal cancer subtypes, which indicates that epigenetic modification may be functionally involved in smoking-related colorectal carcinogenesis.
| S-EPMC2915616 | biostudies-literature
Project description:BackgroundMitochondrial DNA copy number (mtDNAcn) is considered a biomarker for mitochondrial function and oxidative stress. Although previous studies have suggested a potential relationship between mtDNAcn at the time of colorectal cancer (CRC) diagnosis and CRC prognosis, findings have been inconsistent, and no study has specifically investigated the association of pre-diagnostic mtDNAcn with CRC survival.MethodsWe examined the association of pre-diagnostic leukocyte mtDNAcn (measured by qPCR) with overall and CRC-specific survival among 587 patients in Nurses' Health Study and Health Professionals Follow-Up Study. Cox models were constructed to estimate hazard ratios (HRs) and 95 % confidence intervals (95 % CIs).ResultsDuring a mean follow-up of 10.5 years, 395 deaths were identified; 180 were due to CRC. Overall, we did not observe significant associations between mtDNAcn and either overall or CRC-specific survival among all cases or by cancer location, grade, or stage. In an exploratory stratified analysis, a suggestive inverse association of mtDNAcn and overall death risk appeared among current smokers [HR (95 % CI) for 1 SD decrease in mtDNAcn = 1.50 (0.98, 2.32), P-trend = 0.06]. Reduced mtDNAcn and lower CRC-specific death risk was observed among patients aged ≤ 70.5 at diagnosis [HR (95 % CI) for 1 SD decrease of mtDNAcn = 0.71 (0.52, 0.97), P-trend = 0.03], ≤ 5 years from blood collection to diagnosis [HR (95 % CI) for 1 SD decrease in mtDNAcn = 0.65 (0.44, 0.96), P-trend = 0.03] and those consuming a low-inflammatory diet [HR (95 % CI) for 1 SD decrease in mtDNAcn = 0.61 (0.42, 0.88), P-trend = 0.009].Conclusionno significant associations between pre-diagnostic leukocyte mtDNAcn and either overall or CRC-specific survival appeared but exploratory analysis identified potential sub-group associations.
| S-EPMC8981089 | biostudies-literature
Project description:The purpose of this study was to examine whether at-diagnosis smoking and postdiagnosis changes in smoking within five years after breast cancer were associated with long-term all-cause and breast cancer-specific mortality. A population-based cohort of 1508 women diagnosed with first primary in situ or invasive breast cancer in 1996 to 1997 were interviewed shortly after diagnosis and again approximately five years later to assess smoking history. Participants were followed for vital status through December 31, 2014. After 18+ years of follow-up, 597 deaths were identified, 237 of which were breast cancer related. Multivariable Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Compared with never smokers, risk of all-cause mortality was elevated among the 19% of at-diagnosis smokers (HR=1.69, 95% CI=1.36 to 2.11), those who smoked 20 or more cigarettes per day (HR=1.85, 95% CI=1.42 to 2.40), women who had smoked for 30 or more years (HR=1.62, 95% CI=1.28 to 2.05), and women who had smoked 30 or more pack-years (HR=1.82, 95% CI=1.39 to 2.37). Risk of all-cause mortality was further increased among the 8% of women who were at-/post-diagnosis smokers (HR=2.30, 95% CI=1.56 to 3.39) but was attenuated among the 11% women who quit smoking after diagnosis (HR=1.83, 95% CI=1.32 to 2.52). Compared with never smokers, breast cancer-specific mortality risk was elevated 60% (HR=1.60, 95% CI=0.79 to 3.23) among at-/postdiagnosis current smokers, but the confidence interval included the null value and elevated 175% (HR=2.75, 95% CI=1.26 to 5.99) when we considered postdiagnosis cumulative pack-years. Conclusions: Smoking negatively impacts long-term survival after breast cancer. Postdiagnosis cessation of smoking may reduce the risk of all-cause mortality. Breast cancer survivors may benefit from aggressive smoking cessation programs starting as early as the time of diagnosis.
| S-EPMC5875926 | biostudies-literature
Project description:BACKGROUND:Cigarette smoking is a known risk factor in a number of gastrointestinal (GI) diseases in which the microbiota is implicated, including duodenal ulcer and Crohn's disease. Smoking has the potential to alter the microbiota; however, to date, the impact of smoking on the mucosa-associated microbiota (MAM), and particularly that of the upper GI tract, remains very poorly characterised. Thus, we investigated the impact of smoking on the upper small intestinal MAM. A total of 102 patients undergoing upper GI endoscopy for the assessment of GI symptoms, iron deficiency, or Crohn's disease, but without identifiable lesions in the duodenum, were recruited. Smoking status was determined during clinical assessment and patients classified as current (n?=?21), previous smokers (n?=?40), or having never smoked (n?=?41). The duodenal (D2) MAM was profiled via 16S rRNA gene amplicon sequencing. RESULTS:Smoking, both current and previous, is associated with significantly reduced bacterial diversity in the upper small intestinal mucosa, as compared to patients who had never smoked. This was accompanied by higher relative abundance of Firmicutes, specifically Streptococcus and Veillonella spp. The relative abundance of the genus Rothia was also observed to be greater in current smokers; while in contrast, levels of Prevotella and Neisseria were lower. The MAM profiles and diversity of previous smokers were observed to be intermediate between current and never smokers. Smoking did not impact the total density of bacteria present on the mucosa. CONCLUSIONS:These data indicate the duodenal MAM of current smokers is characterised by reduced bacterial diversity, which is partially but not completely restored in previous smokers. While the precise mechanisms remain to be elucidated, these microbiota changes may in some part explain the adverse effects of smoking on mucosa-associated diseases of the GI tract. Smoking status requires consideration when interpreting MAM data.
| S-EPMC6116507 | biostudies-literature
Project description:The prevalence of electronic cigarette (e-cigarette) use has rapidly increased among young people, while conventional cigarette use has decreased in this age group. However, some evidence suggests that e-cigarette use is likely to induce conventional cigarette smoking. The present study explored the social influence of the prevalence of e-cigarette use in the peer network and in the general population as a potential mechanism by which e-cigarette use affects adolescents' overall smoking behaviours. For this purpose, we developed an agent-based model in which young agents repeatedly choose to smoke conventional cigarettes and/or e-cigarettes, or to remain non-smokers. The choice is based on the agent's evaluation of the utility derived from smoking and attitude towards smoking ('openness'), which is influenced by smoking prevalence in the agent's peer network and in the broader society. We also assumed a 'crossover' effect between the different types of smoking. The model was calibrated with United States National Youth Tobacco Survey data to reflect real-world numbers. We further simulated the prevalence of different types of smoking under counterfactual scenarios with different levels of openness and crossover effects. The models developed successfully reproduced actual prevalence trends in different types of smoking from 2011 to 2014. Openness to smoking is associated with a dramatic increase in e-cigarette smoking and especially in dual smoking, which cancels out the decline in sole conventional smoking. Larger crossover effects are associated with a higher prevalence of conventional smoking. The simulation results indicate that the social influence of the prevalence of e-cigarette use may influence young people to initiate or continue conventional cigarette smoking. Assessing the impact of e-cigarettes in the general population as a 'healthier' alternative to conventional smoking may require carefully monitoring trends in young people's smoking behaviours.
| S-EPMC6715222 | biostudies-other