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BACKGROUND: Insulin resistance is a hypothesised biological mechanism linking obesity with prostate cancer (PCa) death. Data in support of this hypothesis is limited. METHODS: We included 259,884 men from eight European cohorts, with 11,760 incident PCa's and 1784 PCa deaths during follow-up. We used the triglyceride-glucose (TyG) index as indicator of insulin resistance. We analysed PCa cases with follow-up from PCa diagnosis, and the full cohort with follow-up from the baseline cancer-free state, thus incorporating both PCa incidence and death. We calculated hazard ratios (HR) and the proportion of the total effect of body mass index (BMI) on PCa death mediated through TyG index. RESULTS: In the PCa-case-only analysis, baseline TyG index was positively associated with PCa death (HR per 1-standard deviation: 1.11, 95% confidence interval (CI); 1.01-1.22), and mediated a substantial proportion of the baseline BMI effect on PCa death (HRtotal effect per 5-kg/m2 BMI: 1.24; 1.14-1.35, of which 28%; 4%-52%, mediated). In contrast, in the full cohort, the TyG index was not associated with PCa death (HR: 1.03; 0.94-1.13), hence did not substantially mediate the effect of BMI on PCa death. CONCLUSIONS: Insulin resistance could be an important pathway through which obesity accelerates PCa progression to death.
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Resistência à Insulina , Neoplasias da Próstata , Masculino , Humanos , Índice de Massa Corporal , Análise de Mediação , Glucose , Obesidade/complicações , Obesidade/epidemiologia , Triglicerídeos , Glicemia , Fatores de Risco , BiomarcadoresRESUMO
PURPOSE: High consumption of fruits and vegetables decrease the risk of bladder cancer (BC). The evidence of specific fruits and vegetables and the BC risk is still limited. METHODS: Fruit and vegetable consumptions in relation to BC risk was examined by pooling individual participant data from case-control studies. Unconditional logistic regression was used to estimate study-specific odds ratio's (ORs) with 95% confidence intervals (CIs) and combined using a random-effects model for intakes of total fruits, total vegetables, and subgroups of fruits and vegetables. RESULTS: A total of 11 case-control studies were included, comprising 5637 BC cases and 10,504 controls. Overall, participants with the highest intakes versus the lowest intakes of fruits in total (OR 0.79; 95% CI 0.68-0.91), citrus fruits (OR 0.81; 95% CI 0.65-0.98), pome fruits (OR 0.76; 95% CI 0.65-0.87), and tropical fruits (OR 0.84; 95% CI 0.73-0.94) reduced the BC risk. Greater consumption of vegetables in total, and specifically shoot vegetables, was associated with decreased BC risk (OR 0.82; 95% CI 0.68-0.96 and OR 0.87; 95% CI 0.78-0.96, respectively). Substantial heterogeneity was observed for the associations between citrus fruits and total vegetables and BC risk. CONCLUSION: This comprehensive study provides compelling evidence that the consumption of fruits overall, citrus fruits, pome fruits and tropical fruits reduce the BC risk. Besides, evidence was found for an inverse association between total vegetables and shoot vegetables intake.
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Obesity is a risk factor for advanced, but not localised, prostate cancer (PCa), and for poor prognosis. However, the detection of localised PCa through asymptomatic screening might influence these associations. We investigated height and body mass index (BMI) among 431 902 men in five Swedish cohorts in relation to PCa risk, according to cancer risk category and detection mode, and PCa-specific mortality using Cox regression. Statistical tests were two-sided. Height was positively associated with localised intermediate-risk PCa (HR per 5 cm, 1.03, 95% CI 1.01-1.05), while overweight and obesity were negatively associated with localised low- and intermediate-risk PCa (HRs per 5 kg/m2 , 0.86, 95% CI 0.81-0.90, and 0.92, 95% CI 0.88-0.97). However, these associations were partially driven by PCa's detected by asymptomatic screening and, for height, also by symptoms unrelated to PCa. The HR of localised PCa's, per 5 kg/m2 , was 0.88, 95% CI 0.83 to 0.92 for screen-detected PCa's and 0.96, 95% CI 0.90 to 1.01 for PCa's detected through lower urinary tract symptoms. BMI was positively associated with PCa-specific mortality in the full population and in case-only analysis of each PCa risk category (HRs per 5 kg/m2 , 1.11-1.22, P for heterogeneity = .14). More active health-seeking behaviour among tall and normal-weight men may partially explain their higher risk of localised PCa. The higher PCa-specific mortality among obese men across all PCa risk categories in our study suggests obesity as a potential target to improve the prognosis of obese PCa patients.
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Obesidade/epidemiologia , Sobrepeso/epidemiologia , Neoplasias da Próstata/epidemiologia , Adulto , Idoso , Estatura , Índice de Massa Corporal , Estudos de Coortes , Humanos , Masculino , Pessoa de Meia-Idade , Obesidade/complicações , Sobrepeso/complicações , Prognóstico , Neoplasias da Próstata/mortalidade , Suécia/epidemiologiaRESUMO
While the association between fruit consumption and bladder cancer risk has been extensively reported, studies have had inadequate statistical power to investigate associations between types of fruit and bladder cancer risk satisfactorily. Fruit consumption in relation to bladder cancer risk was investigated by pooling individual data from 13 cohort studies. Cox regression models with attained age as time scale were used to estimate hazard ratios (HRs) for intakes of total fruit and citrus fruits, soft fruits, stone fruits, tropical fruits, pome fruits and fruit products. Analyses were stratified by sex, smoking status and bladder cancer subtype. During on average 11.2 years of follow-up, 2836 individuals developed incident bladder cancer. Increasing fruit consumption (by 100 g/day) was inversely associated with the risk of bladder cancer in women (HR = 0.92; 95% CI 0.85-0.99). Although in women the association with fruit consumption was most evident for higher-risk nonmuscle invasive bladder cancer (NMIBC; HR = 0.72; 95% CI 0.56-0.92), the test for heterogeneity by bladder cancer subtype was nonsignificant (P-heterogeneity = .14). Increasing fruit consumption (by 100 g/day) was not associated with bladder cancer risk in men (HR = 0.99; 95% CI 0.94-1.03), never smokers (HR = 0.96; 95% CI 0.88-1.05), former smokers (HR = 0.98; 95% CI 0.92-1.05) or current smokers (HR = 0.95; 95% CI 0.89-1.01). The consumption of any type of fruit was not found to be associated with bladder cancer risk (P values > .05). Our study supports no evidence that the consumption of specific types of fruit reduces the risk of bladder cancer. However, increasing total fruit consumption may reduce bladder cancer risk in women.
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Neoplasias da Bexiga Urinária/epidemiologia , Neoplasias da Bexiga Urinária/etiologia , Estudos de Coortes , Feminino , Seguimentos , Frutas , Humanos , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Fatores de Risco , Fumar/efeitos adversos , Bexiga Urinária/patologia , Neoplasias da Bexiga Urinária/patologiaRESUMO
BACKGROUND: Few studies have modeled smoking histories by combining smoking intensity and duration to show what profile of smoking behavior is associated with highest risk of bladder cancer. This study aims to provide insight into the association between smoking exposure history and bladder cancer risk by modeling both smoking intensity and duration in a pooled analysis. METHODS: We used data from 15 case-control studies included in the bladder cancer epidemiology and nutritional determinants study, including a total of 6,874 cases and 17,727 controls. To jointly interpret the effects of intensity and duration of smoking, we modeled excess odds ratios per pack-year by intensity continuously to estimate the risk difference between smokers with long duration/low intensity and short duration/high intensity. RESULTS: The pattern observed from the pooled excess odds ratios model indicated that for a fixed number of pack-years, smoking for a longer duration at lower intensity was more deleterious for bladder cancer risk than smoking more cigarettes/day for a shorter duration. We observed similar patterns within individual study samples. CONCLUSIONS: This pooled analysis shows that long duration/low intensity smoking is associated with a greater increase in bladder cancer risk than short duration/high intensity smoking within equal pack-year categories, thus confirming studies in other smoking-related cancers and demonstrating that reducing exposure history to a single metric such as pack-years was too restrictive.
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Modelos Biológicos , Fumar/epidemiologia , Fumar/psicologia , Neoplasias da Bexiga Urinária/epidemiologia , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Fatores de Risco , Fatores de TempoRESUMO
INTRODUCTION: There is some evidence that greater consumption of fruit and vegetables decreases the risk of bladder cancer. The role of fruit and vegetables in bladder cancer recurrence is still unknown. OBJECTIVE: The role of total fruit and vegetable intake in relation to the risk of developing bladder cancer recurrence in a prospective cohort study. METHODS: 728 patients with non-muscle invasive bladder cancer (NMIBC), who completed self-administrated questionnaires on fruit and vegetable intake at time of diagnosis (over the year before diagnosis) and 1 year after diagnosis, were included. Hazard ratios and 95% confidence intervals were calculated by multivariable Cox regression for developing recurrent bladder cancer in relation to fruit and vegetable intake. RESULTS: During 2,051 person-years of follow-up [mean (SD) follow-up 3.7 (1.5) years], 241 (33.1%) of the included 728 NMIBC patients developed a recurrence of bladder cancer. The sum of total fruit and vegetables before diagnosis was not related to a first bladder cancer recurrence (HR 1.07; 95% CI 0.78-1.47, p = 0.66). No association was found between greater consumption of fruit and vegetables over the year before diagnosis and the risk of developing multiple recurrences of bladder cancer (HR 1.02; 95% CI 0.90-1.15, p = 0.78). Among the remaining 389 NMIBC patients who reported on fruit and vegetable intake 1 year after diagnosis, no association was found between greater consumption of fruit and vegetables and a first recurrence of bladder cancer (HR 0.65; 95% CI 0.42-1.01, p = 0.06) nor with multiple recurrences of bladder cancer (HR 1.00, 95% CI 0.85-1.18, p = 1.00). Similar results were obtained when investigating the association between total intakes of fruit and vegetables separately and bladder cancer recurrence. CONCLUSION: Results from this study did not indicate a protective role for total fruit and vegetables in the development of a recurrence of NMIBC.
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Frutas , Neoplasias da Bexiga Urinária/epidemiologia , Verduras , Adulto , Idoso , Idoso de 80 Anos ou mais , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Modelos de Riscos Proporcionais , Estudos Prospectivos , Inquéritos e QuestionáriosRESUMO
BACKGROUND: Smoking is a major risk factor for bladder cancer, but the relationship between smoking cessation after initial treatment and bladder cancer recurrence has been investigated less frequently and not prospectively yet. METHODS: 722 non-muscle-invasive bladder cancer (NMIBC) patients (pTa, pT1, and CIS) from the prospective Bladder Cancer Prognosis Programme (BCPP) cohort, selected in the UK between 2005 and 2011, provided complete data on smoking behavior before and up to 5 years after diagnosis. The impact of smoking behavior on NMIBC recurrence was explored by multivariable Cox regression models investigating time-to-first NMIBC recurrence. RESULTS: Over a median follow-up period of 4.21 years, 403 pathologically confirmed NMIBC recurrences occurred in 210 patients. Only 25 current smokers at diagnosis quit smoking (14%) during follow-up and smoking cessation after diagnosis did not decrease risk of recurrence compared to continuing smokers (p = 0.352). CONCLUSIONS: Although quitting smoking after diagnosis might reduce the risk of recurrence based on retrospective evidence, this is not confirmed in this prospective study because the number of NMIBC patients quitting smoking before their first recurrence was too low. Nevertheless, this indicates an important role for urologists and other health care professionals in promoting smoking cessation in NMIBC.
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Abandono do Hábito de Fumar/métodos , Fumar/efeitos adversos , Neoplasias da Bexiga Urinária/etiologia , Idoso , Estudos de Coortes , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Recidiva Local de Neoplasia , Prognóstico , Modelos de Riscos Proporcionais , Estudos Prospectivos , Fatores de RiscoRESUMO
PURPOSE: Although cigarette smoking is a well established risk factor for urothelial cancer, its role in urothelial cancer prognosis is still undetermined. In this meta-analysis we quantify the role of lifetime smoking history in bladder cancer recurrence, progression and survival by pooling available data on nonmuscle invasive bladder cancer, muscle invasive bladder cancer and upper tract urothelial carcinoma. MATERIALS AND METHODS: A total of 24 studies, comprising data from 13,114 patients with bladder cancer and 2,259 patients with upper tract urothelial carcinoma, were included in this meta-analysis. Publication bias was addressed through Egger's test, and the heterogeneity among studies was assessed by the I(2) test statistic and subgroup analyses. RESULTS: Current smokers at diagnosis are at increased risk for local recurrence in nonmuscle invasive bladder cancer (HR 1.27, 95% CI 1.09-1.46) and smokers with muscle invasive bladder cancer have an increased risk of dying of bladder cancer (HR 1.23, 95% CI 1.02-1.44). In the upper tract urothelial carcinoma population smokers have an increased risk of recurrence in the operative bed (HR 1.57, 95% CI 1.19-1.95) and of death from upper tract urothelial carcinoma (HR 1.53, 95% CI 1.13-1.92). We did not identify significant heterogeneity among included studies. CONCLUSIONS: The body of evidence is limited due to the absence of prospective studies. However, the results from this meta-analysis unambiguously support the hypothesis that lifetime cigarette smokers are at increased risk for a more malignant type of urothelial carcinoma associated with a worse prognosis.
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Carcinoma de Células de Transição/etiologia , Neoplasias Renais/etiologia , Fumar/efeitos adversos , Neoplasias Ureterais/etiologia , Neoplasias da Bexiga Urinária/etiologia , Progressão da Doença , Humanos , Fatores de TempoRESUMO
BACKGROUND: Insulin resistance has been shown to be related to a higher risk of several cancers, but the association with prostate cancer (PCa) has been inconsistent. METHODS: We investigated prediagnostic markers of insulin resistance in men in four cohorts in Sweden, in relation to PCa risk (total, non-aggressive and aggressive) and PCa death using multivariable-adjusted Cox regression. The number of men, PCa cases and PCa deaths was up to 66,668, 3940 and 473 for plasma glucose and the triglyceride-glucose (TyG) index, and up to 3898, 586 and 102 for plasma insulin, glycated haemoglobin (HbA1c) and leptin. RESULTS: Higher HbA1c was related to a lower risk of non-aggressive PCa but no significant associations were found for insulin resistance markers with the risk of aggressive or total PCa. In PCa cases, higher glucose and TyG index were related to a higher risk of PCa death (hazard ratio [HR] per higher standard deviation, 1.22, 95% CI 1.00-1.49 and 1.24, 95% CI 1.00-1.55), which further increased when restricting the analyses to glucose and TyG index measures taken <10 years before the PCa diagnosis (HR, 1.70, 95% CI 1.09-2.70 and 1.66, 95% CI 1.12-2.51). No associations were observed for other markers in relation to PCa death. CONCLUSIONS: The results of this study showed no associations of insulin resistance markers with the risk of clinically relevant PCa, but higher glucose and TyG index were associated with poorer survival from PCa. The lack of association for other insulin resistance markers may be due to their smaller sample size.
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Resistência à Insulina , Neoplasias da Próstata , Masculino , Humanos , Glicemia , Hemoglobinas Glicadas , Fatores de Risco , Glucose , Neoplasias da Próstata/diagnóstico , Triglicerídeos , BiomarcadoresRESUMO
BACKGROUND: Prospective and detailed investigations of smoking and prostate cancer (PCa) risk and death are lacking. OBJECTIVE: To investigate prediagnosis smoking habit (status, intensity, duration, and cessation) as a risk factor, on its own and combined with body mass index (BMI), for PCa incidence and death. DESIGN, SETTING, AND PARTICIPANTS: We included 351448 men with smoking information from five Swedish cohorts. OUTCOME MEASUREMENTS AND STATISTICAL ANALYSIS: We used Cox regression to calculate hazard ratios (HRs) and confidence intervals (CIs) for PCa incidence (n = 24731) and death (n = 4322). RESULTS AND LIMITATIONS: Smoking was associated with a lower risk of any PCa (HR 0.89, 95% CI 0.86-0.92), which was most pronounced for low-risk PCa (HR 0.74, 95% CI 0.69-0.79) and was restricted to PCa cases diagnosed in the prostate-specific antigen (PSA) era. Smoking was associated with a higher risk of PCa death in the full cohort (HR 1.10, 95% CI 1.02-1.18) and in case-only analysis adjusted for clinical characteristics (HR 1.20, 95% CI 1.11-1.31), which was a consistent finding across case groups (p = 0.8 for heterogeneity). Associations by smoking intensity and, to lesser degree, smoking duration and cessation, supported the associations for smoking status. Smoking in combination with obesity (BMI ≥30 kg/m2) further decreased the risk of low-risk PCa incidence (HR 0.40, 95% CI 0.30-0.53 compared to never smokers with BMI <25 kg/m2) and further increased the risk of PCa death (HR 1.49, 95% CI 1.21-1.84). A limitation of the study is that only a subgroup of men had information on smoking habit around the time of their PCa diagnosis. CONCLUSIONS: The lower PCa risk for smokers in the PSA era, particularly for low-risk PCa, can probably be attributed to low uptake of PSA testing by smokers. Poor survival for smokers, particularly obese smokers, requires further study to clarify the underlying causes and the preventive potential of smoking intervention for PCa death. PATIENT SUMMARY: Smokers have a higher risk of dying from prostate cancer, which further increases with obesity.
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Antígeno Prostático Específico , Neoplasias da Próstata , Masculino , Humanos , Estudos Prospectivos , Fumar/efeitos adversos , Fumar/epidemiologia , Neoplasias da Próstata/epidemiologia , Fatores de Risco , Obesidade/complicações , Obesidade/epidemiologiaRESUMO
BACKGROUND: Smoking has shown interactions with bladder cancer (BC) genetic variants, especially N-acetyltransferase-2 (NAT2), a tobacco smoke metabolism gene, on BC risk. The interactions by disease aggressiveness are unknown. METHODS: We investigated the interaction between smoking and 18 single nucleotide polymorphisms (SNPs) for BC, individually and in a genetic risk score (GRS), on urothelial cancer (UC) risk including BC. We analysed data from 25,453 individuals with 520 incident UCs during follow-up, 339 non-aggressive (non-fatal, non-muscle invasive) and 163 aggressive (all other) UCs. Hazard ratios (HRs), absolute risks and additive and multiplicative interactions for two-by-two combinations of never/ever smoking with low/high genetic risk were calculated. RESULTS: Smoking and NAT2 rs1495741 interacted strongly, positively on aggressive UC on both the multiplicative (p = 0.004) and additive (p = 0.0002) scale, which was not observed for non-aggressive UC (pinteractions ≥ 0.6). This manifested in a higher HR of aggressive UC by ever smoking for the slow acetylation NAT2 genotype (HR, 5.00 [95% confidence interval, 2.67-9.38]) than for intermediate/fast acetylation NAT2 (HR, 1.50 [0.83-2.71]), and in differences in absolute risks by smoking and NAT2 genotype. Smoking also interacted additively and positively with the GRS on any UC (p = 0.01) and non-aggressive UC (p = 0.02), but not on aggressive UC (p = 0.1). Gene-smoking interactions of lesser magnitude than for NAT2 were found for SNPs in APOBEC3A, SLC14A1 and MYNN. CONCLUSIONS: This study suggests that smoking increases UC risk more than expected when combined with certain genetic risks. Individuals with the slow acetylation NAT2 variant might particularly benefit from smoking intervention to prevent lethal UC; however, replication in larger studies is needed.
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Arilamina N-Acetiltransferase , Carcinoma de Células de Transição , Neoplasias da Bexiga Urinária , Acetiltransferases/genética , Arilamina N-Acetiltransferase/genética , Arilamina N-Acetiltransferase/metabolismo , Carcinoma de Células de Transição/genética , Estudos de Casos e Controles , Citidina Desaminase , Genótipo , Humanos , Proteínas , Fatores de Risco , Fumar/efeitos adversos , Fumar/metabolismo , Neoplasias da Bexiga Urinária/genéticaRESUMO
BACKGROUND: The association of blood pressure (BP) with prostate cancer risk after accounting for asymptomatic prostate-specific antigen (PSA) testing, and with prostate cancer death, is unclear. METHODS: We investigated BP, measured at a mean age of 38 years among 430,472 men from five Swedish cohorts, in association with incident prostate cancer (n = 32,720) and prostate cancer death (n = 6718). HRs were calculated from multivariable Cox regression models. RESULTS: Increasing systolic and diastolic BP levels combined were associated with a slightly lower prostate cancer risk, with a HR of 0.98 (95% CI, 0.97-0.99) per standard deviation (SD) of mid-BP (average of systolic and diastolic BP). The association was restricted to the PSA era (1997 onwards, HR, 0.96; 95% CI, 0.95-0.98), to diagnoses initiated by a PSA test in asymptomatic men (HR, 0.95; 95% CI, 0.93-0.97), and to low-risk prostate cancer (HR, 0.95; 95% CI, 0.92-0.97). There was no clear association with more advanced disease at diagnosis. In cases, a slightly higher risk of prostate cancer death was observed for higher BP levels (HR, 1.05; 95% CI, 1.01-1.08) per SD of mid-BP; however, the association was restricted to distant metastatic disease (Pheterogeneity between case groups = 0.01), and there was no association for BP measured less than 10 years prior to diagnosis. CONCLUSIONS: Prediagnostic BP is unlikely an important risk factor for prostate cancer development and death. Less asymptomatic PSA testing among men with higher BP levels may explain their lower risk of prostate cancer. IMPACT: Elevated BP is unlikely to be an important risk factor for prostate cancer.
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Hipertensão , Neoplasias da Próstata , Adulto , Pressão Sanguínea/fisiologia , Estudos de Coortes , Humanos , Masculino , Antígeno Prostático Específico , Neoplasias da Próstata/patologia , Índice de Gravidade de DoençaRESUMO
BACKGROUND: The relation between obesity, blood pressure (BP) and bladder cancer (BC) risk and mortality remains unclear, partially due to potential confounding by smoking, the strongest risk factor for BC, and not accounting for tumor stage and grade in such studies. We investigated body mass index (BMI) and BP in relation to BC risk by stage and grade, and BC-specific mortality, including separately among never-smokers aimed at minimizing confounding by smoking. METHODS: We analyzed 338,910 men from three Swedish cohorts, with 4895 incident BC's (940 among never-smokers) during follow-up. Cox regression was used to calculate hazard ratios (HR) and 95% confidence intervals adjusted for smoking status. HRs for BMI and BP were corrected for their regression dilution ratios, calculated from 280,456 individuals with 758,641 observations. RESULTS: Body mass index was positively associated with non-muscle invasive BC (NMIBC, HR per 5 kg/m2 , 1.10 [1.02-1.19]) and NMIBC grade 3 (HR 1.17 [1.01-1.34]) in the full cohort, with similar effect sizes, albeit non-significant, among never-smokers. Systolic BP was positively associated with muscle-invasive BC (MIBC, HR per 10 mmHg, 1.25 [1.00-1.55]) and BC-specific mortality (HR 1.10 [1.01-1.20]) among never-smokers, with weaker and non-significant associations in the full cohort. CONCLUSIONS: In an analyses of BMI, BP and BC risk by stage and grade among men, we found modest positive associations between BMI and NMIBC and NMIBC grade 3. SBP was positively associated with MIBC and BC-specific mortality in an analysis of never-smokers, which may reflect the association, un-confounded by smoking, also in a broader population.
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Pressão Sanguínea , Índice de Massa Corporal , Neoplasias da Bexiga Urinária/epidemiologia , Neoplasias da Bexiga Urinária/mortalidade , Adulto , Estudos de Coortes , Seguimentos , Humanos , Masculino , Prognóstico , Fatores de Risco , Taxa de Sobrevida , Suécia/epidemiologia , Neoplasias da Bexiga Urinária/patologiaRESUMO
We recently found a negative association between body mass index (BMI) and the risk of localised prostate cancer (PCa), no association with advanced PCa, and a positive association with PCa-specific mortality. In a 15% subpopulation of that study, we here investigated the measures of abdominal adiposity including waist circumference (WC) and A Body Shape Index (ABSI) in relation to PCa risk and mortality. We used data from 58,457 men from four Swedish cohorts to assess WC and ABSI in relation to PCa risk according to cancer risk category, including localised asymptomatic and symptomatic PCa and advanced PCa, and PCa-specific mortality. Cox regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). During, on average, 10 years of follow-up, 3290 men were diagnosed with PCa and 387 died of PCa. WC was negatively associated with the risk of total PCa (HR per 10 cm, 0.95; 95% CI 0.92-0.99), localised PCa (HR per 10 cm, 0.93, 95% CI 0.88-0.96) and localised asymptomatic PCa cases detected through a prostate-specific antigen (PSA) test (HR per 10 cm, 0.87, 95% CI 0.81-0.94). WC was not associated with the risk of advanced PCa (HR per 10 cm, 1.02, 95% CI 0.93-1.14) or with PCa-specific mortality (HR per 10 cm, 1.04, 95% CI 0.92-1.19). ABSI showed no associations with the risk of PCa or PCa-specific mortality. While the negative association between WC and the risk of localised PCa was partially driven by PSA-detected PCa cases, no association was found between abdominal adiposity and clinically manifest PCa in our population.
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Neoplasias da Próstata/mortalidade , Somatotipos , Circunferência da Cintura , Idoso , Índice de Massa Corporal , Humanos , Masculino , Pessoa de Meia-Idade , Modelos de Riscos Proporcionais , Neoplasias da Próstata/diagnóstico , Neoplasias da Próstata/patologia , Neoplasias da Próstata/terapia , Fatores de Risco , SuéciaRESUMO
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.
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Índice de Massa Corporal , Neoplasias Pulmonares/epidemiologia , Fumar/efeitos adversos , Adulto , Áustria/epidemiologia , Fatores de Confusão Epidemiológicos , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Noruega/epidemiologia , Fatores de Risco , Suécia/epidemiologiaRESUMO
[This corrects the article DOI: 10.3233/BLC-180172.].
RESUMO
Cigarette smoking is a major risk factor for bladder cancer (BC); however, the impact of cigarette content remains unclear. This study aims to investigate tar, nicotine and carbon monoxide (TNCO) yields of different filtered cigarettes in relation to BC risk. From the Bladder Cancer Prognosis Programme 575 non-muscle-invasive bladder cancer (NMIBC) cases, 139 muscle-invasive bladder cancer (MIBC) cases and 130 BC-free controls with retrospective data on smoking behaviour and cigarette brand were identified. Independently measured TNCO yields of cigarettes sold in the UK were obtained through the UK Department of Health and merged with the Bladder Cancer Prognosis Programme dataset to estimate the daily intake of TNCO. BC risk increased by TNCO intake category for NMIBC cases (P <0.050 in all multivariate models), but only for the daily intake of tar for MIBC cases (P=0.046) in multivariate models. No difference in risk was observed between smokers of low-tar/low-nicotine and high-tar/high-nicotine cigarettes compared with never smokers, either for NMIBC (P=0.544) or MIBC (P=0.449). High daily intake of TNCO additionally increases the risk of both NMIBC and MIBC compared with low daily intake. However, as there is no difference in BC risk between low-tar/low-nicotine and high-tar/high-nicotine cigarette smokers, it remains unclear whether smoking behaviour or TNCO yield of cigarettes explains this association.
Assuntos
Monóxido de Carbono/efeitos adversos , Nicotina/efeitos adversos , Alcatrões/efeitos adversos , Produtos do Tabaco/efeitos adversos , Neoplasias da Bexiga Urinária/induzido quimicamente , Neoplasias da Bexiga Urinária/epidemiologia , Idoso , Monóxido de Carbono/análise , Estudos de Casos e Controles , Feminino , Humanos , Masculino , Pessoa de Meia-Idade , Invasividade Neoplásica/patologia , Nicotina/análise , Inquéritos e Questionários , Alcatrões/análise , Reino Unido/epidemiologia , Neoplasias da Bexiga Urinária/diagnósticoRESUMO
OBJECTIVE: To determine whether there is an association between dietary patterns/indices and foods from the main food groups (highest vs lowest intakes) prior to or after cancer diagnosis and mortality and cancer recurrence in cancer survivors. PARTICIPANTS: Survivors of common cancers with a 10-year survival rate of ≥50%: bladder, bowel, breast, cervical, kidney, laryngeal, prostate, testicular, uterine cancer, malignant melanoma and (non-)Hodgkin's lymphoma. OUTCOME MEASURES: Mortality (overall, cancer-specific, from other causes) and cancer recurrence. INFORMATION SOURCES: PubMed, Embase and the Cochrane Library were searched from inception to April 2017. Additional studies were identified by searching reference lists. Two authors independently screened titles and abstracts, assessed study quality and extracted the data. RESULTS: A total of 38 studies were included. The risk of bias was rated low for the included randomised controlled trials (RCTs) and moderate for the cohort studies. The quality of evidence was assessed with the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and was rated moderate (RCTs), and (very)low (cohort studies). Reducing the amount of fat after diagnosis appears to decrease the risk of breast cancer recurrence. Adherence to a high-quality diet and prudent diet after diagnosis appears to decrease the risk of death from other causes (and overall mortality for high-quality diet) in breast cancer survivors. Adherence to a Western diet, before and after diagnosis, appears to increase the risk of overall mortality and death from other causes among breast cancer survivors. Evidence from studies among other cancer survivors was too limited or could not be identified. CONCLUSION: For many cancer survivors, there is little evidence to date to indicate that particular dietary behaviours influence outcomes with regard to recurrence and mortality. Notwithstanding, limited evidence suggests that a low-fat diet, a high-quality diet and a prudent diet are beneficial for breast cancer survivors, while a Western diet is detrimental for breast cancer survivors.
Assuntos
Neoplasias da Mama/mortalidade , Dieta com Restrição de Gorduras , Dieta Ocidental/efeitos adversos , Recidiva Local de Neoplasia/mortalidade , Neoplasias da Mama/prevenção & controle , Sobreviventes de Câncer , Ingestão de Energia , Humanos , Ensaios Clínicos Controlados Aleatórios como Assunto , Taxa de Sobrevida , Fatores de TempoRESUMO
Background: Active smoking is a major risk factor for urothelial bladder cancer (UBC). However, the evidence that exposure to environmental tobacco smoke (ETS) either in childhood or adult life is also associated with UBC risk is ambiguous. With this meta-analysis, we aim to summarise how exposure to ETS is associated with UBC risk. Methods: In total, 11 studies (3 cohort studies, 8 case-control studies) were included in this meta-analysis and summary odds ratios (SORs) for UBC risk were calculated for never smokers who were exposed to ETS during childhood at home, during adulthood at home, or during adulthood in a work environment compared to never smokers who were never exposed to ETS. Sensitivity analyses were conducted to test the robustness of findings. Results: Never smokers exposed to ETS during childhood (SOR = 1.04, 95% confidence interval (CI) = 0.82-1.26), during adulthood at work (SOR = 0.98, 95% CI = 0.78-1.18) or at home (SOR = 0.99, 95% CI = 0.83-1.15) were at a similar risk of UBC compared to never smokers who were never exposed to ETS. Results for males and females were similar. Also, when pooling all estimates during both childhood and adulthood, no effect was observed (SOR = 1.00, 95% CI = 0.89-1.10). Conclusions: Although measurement of exposure to ETS was imprecise, there does not seem to be an association between UBC risk and exposure to ETS during childhood or adulthood. However, the current body of evidence mostly overlooks the duration and intensity of exposure to ETS.
Assuntos
Exposição Ambiental/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Neoplasias da Bexiga Urinária/epidemiologia , Adulto , Estudos de Casos e Controles , Criança , Exposição Ambiental/análise , Humanos , Razão de Chances , Fatores de Risco , Poluição por Fumaça de Tabaco/análise , Local de TrabalhoRESUMO
OBJECTIVES: To investigate the role of fluid intake from beverages before and after a diagnosis of bladder cancer in relation to the risk of developing bladder cancer recurrence. STUDY DESIGN: Prospective cohort study. METHODS: 716 patients with non-muscle invasive bladder cancer (NMIBC), who received transurethral resection of a primary bladder tumour (TURBT) and completed self-administrated questionnaires on usual fluid intake from beverages at time of diagnosis (over the year before diagnosis) and during follow-up (over the year after diagnosis), were included. Multivariable Cox regression was used to calculate hazard ratios and 95% confidence intervals of developing recurrent bladder cancer in relation to the intake of total fluid, total alcohol, and individual beverages. RESULTS: During 2,025 person-years of follow-up, 238 (33%) of the included 716 NMIBC patients developed one or more recurrences of bladder cancer. Total fluid intake before diagnosis was not associated with a first recurrence of bladder cancer when comparing the highest and lowest intake group (HR = 0.98, 95% C.I. 0.70-1.38, p = 0.91). Comparable results were obtained for total fluid intake pre-diagnosis and the risk of developing multiple recurrences of bladder cancer (HR = 1.01, 95% C.I. 0.87-1.19, p = 0.85). A total of 379 of the 716 patients reported on usual fluid intake within 1 year of diagnosis. No significant associations between total fluid intake 1 year after diagnosis and a first recurrence of bladder cancer were found when comparing the highest and lowest intake group (HR = 0.91; 95% C.I. 0.60-1.37, p = 0.65) or with multiple recurrences of bladder cancer (HR = 1.06; 95% C.I. 0.89-1.26, p = 0.54). In addition, total alcohol intake and individual beverages were not associated with bladder cancer recurrence. CONCLUSIONS: The results indicate that an individual's fluid intake from beverages is unlikely to have an important role in bladder cancer recurrence.