Tobacco use and cancer survival: A cohort study of 40,230 Swedish male construction workers with incident cancer

On theoretical grounds, nicotine has been implicated as a modifier of cancer progression. We investigated possible associations of smoking or use of Scandinavian moist snuff (snus) with survival after cancer among Swedish male construction workers. Snus use is associated with substantial exposure to nicotine but not to the combustion products in smoke. Among 336,381 workers with detailed information on tobacco use in 1971–1992, we observed 40,230 incident cancers. Complete follow‐up through 2007 was accomplished through linkage to population and health registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) for death from any cause, cancer‐specific death and death from other causes were derived from Cox proportional hazards regression models adjusted for age at diagnosis, body mass index at study entry and period of diagnosis. Never users of any tobacco served as reference. Increased risks of cancer‐specific death were observed both among exclusive smokers (HR_{all cancer} 1.15, 95% CI: 1.10–1.21) and never‐smoking snus users (1.15, 95% CI: 1.05–1.26). As regards deaths due to other causes, exclusive smokers had higher relative risks than exclusive snus users (p = 0.03). A history of tobacco use, even exclusive use of the seemingly benign snus, is associated with moderately increased cancer‐specific mortality. Although nicotine might play a role, the mechanisms warrant further investigation.     

Smoking,snus use and risk of right‐ and left‐sided colon,rectal and anal cancer: A 37‐year follow‐up study

Although some authorities consider smoking to be an established risk factor for colorectal cancer, the international literature is not entirely consistent. Further, only 1 study has addressed the association with smokeless tobacco and none with Scandinavian moist snuff (snus). This retrospective cohort study included 336,381 male Swedish construction workers with detailed information on tobacco use at cohort entry in 1971–1992. Complete follow‐up through 2007 was accomplished by means of linkage to population and health registers. Hazard ratios (HRs) and 95% confidence intervals (CIs) derived from Cox proportional hazards regression models estimated relative risks, adjusted for age and body mass index. Subjects who were never‐users of any tobacco served as reference. After up to 37 years of follow‐up, pure smoking was associated with a marginally increased risk of colon cancer (HR 1.08, 95% CI 0.99–1.19), a modestly elevated risk of rectal cancer (HR 1.16, 95% CI 1.04–1.30) and a substantial excess risk of anal cancer (HR 2.41, 95% CI 1.06–5.48). Snus use was not significantly associated with an increased risk of colorectal or anal cancer, although the point estimate for colon cancer was similar to that observed among smokers. Swedish data provide meager support for the association between tobacco use and colorectal cancer. A general tendency among Swedish men to quit smoking in recent decades might have attenuated true associations. A link between smoking and anal cancer was confirmed.     

Use of moist oral snuff (snus) and pancreatic cancer: Pooled analysis of nine prospective observational studies

While smoking is a well‐established risk factor for pancreatic cancer, the effect of smokeless tobacco is less well understood. We used pooled individual data from the Swedish Collaboration on Health Effects of Snus Use to assess the association between Swedish snus use and the risk of pancreatic cancer. A total of 424,152 male participants from nine cohort studies were followed up for risk of pancreatic cancer through linkage to health registers. We used shared frailty models with random effects at the study level, to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) adjusted for confounding factors. During 9,276,054 person‐years of observation, 1,447 men developed pancreatic cancer. Compared to never‐snus use, current snus use was not associated with risk of pancreatic cancer (HR 0.96, 95% CI 0.83–1.11) after adjustment for smoking. Swedish snus use does not appear to be implicated in the development of pancreatic cancer in men. Tobacco smoke constituents other than nicotine or its metabolites may account for the relationship between smoking and pancreatic cancer.     

The association of weight change in young adulthood and smoking status with risk of prostate cancer recurrence

The decades before prostate cancer diagnosis represent an etiologically relevant time period for prostate cancer carcinogenesis. However, the association of weight gain in young adulthood with subsequent biochemical recurrence among men with prostate cancer is not well studied, particularly among smokers. We conducted a prospective cohort study of 1,082 men with prostate cancer and treated with either radical prostatectomy or radiation between 2003 and 2010. The association of weight at age 20, weight at age 50 and weight change from age 20 to age 50 with biochemical recurrence was assessed using Cox Proportional Hazards with adjustment for confounders. Stratum‐specific hazard ratio (HR) estimates by smoking status were evaluated. In the overall cohort, weight at age 20 (HR per 30 kg: 1.56, 95% confidence interval (CI): 1.02, 2.38, p‐trend: 0.039), weight at age 50 (HR per 30 kg: 1.80, 95% CI: 1.32, 2.47, p‐trend: <0.001) and weight change from age 20 to age 50 (HR per 30 kg: 1.84, 95% CI: 1.24, 2.74, p‐trend: 0.003) were associated with biochemical recurrence. In stratified analyses, weight change from age 20 to age 50 was significantly associated with biochemical recurrence only in former smokers (HR per 30 kg: 3.87, 95% CI: 1.88, 8.00, p‐trend: <0.001) and ever smokers (HR per 30 kg: 2.38, 95% CI: 1.27, 4.45, p‐trend: 0.007). No significant association was observed between weight gain in young adulthood and biochemical recurrence in never smokers. Our study adds further evidence that weight gain during early adult years conveys long‐term risk for adverse cancer outcomes.     

Joint associations of smoking and television viewing time on cancer and cardiovascular disease mortality

Excessive sitting time and smoking are pro‐inflammatory lifestyle factors that are associated with both cancer and cardiovascular disease (CVD) mortality. However, their joint associations have not been investigated. We examined the associations of television (TV) viewing time with cancer and CVD mortality, according to smoking status, among 7,498 non‐smokers (34% ex‐smokers) and 1,409 current‐smokers in the Australian Diabetes, Obesity and Lifestyle Study. During 117,506 person‐years (median 13.6 years) of follow‐up, there were 346 cancer and 209 CVD‐related deaths. Including an interaction between TV time and smoking status in the model significantly improved the goodness of fit for cancer (p = 0.01) but not CVD mortality (p = 0.053). In the multivariate‐adjusted model, every additional hr/d of TV time was associated with increased risk of cancer‐related (HR 1.23; 95% CI 1.08–1.40), but not CVD‐related mortality (HR 1.16; 95% CI 0.97–1.38) in current‐smokers. Elevated multivariate‐adjusted cancer mortality HRs were observed for current‐smokers watching 2 to <4 hr/d (HR 1.45; 95% CI 0.78–2.71) and ≥4 hr/d (HR 2.26; 95% CI 1.10–4.64), compared to those watching <2 hr/d. Current‐smokers watching 2 to <4 hr/d (HR 1.07; 95% CI 0.45–2.53) and ≥4 hr/d (HR 1.92; 95% CI 0.76–4.84) did not have a significantly higher risk of CVD mortality, compared to <2 hr/d. No associations were observed for non‐smokers. These findings show an association of TV, a common sedentary behavior, with cancer mortality in current‐smokers. The association with CVD mortality was less clear. Further exploration in larger data sets is warranted. Limiting TV viewing time may be of benefit in reducing cancer mortality risk in current‐smokers.     

Prediagnosis and postdiagnosis smoking and survival following diagnosis with ovarian cancer

Little is known about the influence of prediagnosis and postdiagnosis smoking and smoking cessation on ovarian cancer survival. We investigated this relationship in two prospective cohort studies, the Nurses’ Health Study (NHS) and NHSII. Analyses included 1,279 women with confirmed invasive, Stage I–III epithelial ovarian cancer. We used Cox proportional hazards regression models to estimate hazard ratios (HR) and 95% confidence intervals (CI) for ovarian cancer-specific mortality by smoking status, adjusting for age and year of diagnosis, tumor stage, histologic subtype, body mass index and nonsteroidal anti-inflammatory use (postdiagnosis models only). When examining prediagnosis smoking status (assessed a median of 12 months before diagnosis), risk of death was significantly increased for former smokers (HR = 1.19, 95% CI: 1.02–1.39), and suggestively for current smokers (HR = 1.21, 95% CI: 0.96–1.51) vs. never smokers. Longer smoking duration (≥20 years vs. never, HR = 1.23, 95% CI: 1.05–1.45) and higher pack-years (≥20 pack-years vs. never, HR = 1.28, 95% CI: 1.07–1.52) were also associated with worse outcome. With respect to postdiagnosis exposure, women who smoked ≥15 cigarettes per day after diagnosis (assessed a median of 11 months after diagnosis) had increased mortality compared to never smokers (HR = 2.34, 95% CI: 1.63–3.37). Those who continued smoking after diagnosis had 40% higher mortality (HR = 1.40, 95% CI: 1.05–1.87) compared to never smokers. Overall, our results suggest both prediagnosis and postdiagnosis smoking are associated with worse ovarian cancer outcomes.     

Mortality risk in former smokers with breast cancer: Pack‐years vs. smoking status

It is unclear why successful quitting at time of breast cancer diagnosis should remove risk from a significant lifetime of smoking. Studies concluding this may be biased by how smoking is measured in many epidemiological cohorts. In the late 1990s, a randomized trial of diet and breast cancer outcomes enrolled early‐stage female breast cancer survivors diagnosed within the previous 4 years. Smoking history and key covariate measures were available at study entry for 2,953 participants. Participants were followed for an average of 7.3 years (96% response rate). There were 10.1% deaths (83% from breast cancer). At enrollment, 55.2% were never smokers, 41.2% former smokers and 4.6% current smokers. Using current smoking status in a Cox regression, there was no increased risk for former smokers for either all‐cause mortality [hazard ratio (HR) = 1.11; 95% confidence interval (CI) = 0.87–1.41; p‐value = 0.42) or breast cancer mortality. However, when we categorized on extensive lifetime exposure, former smokers with 20+ pack‐years of smoking (25.8%) had a significantly higher risk of both all‐cause (HR = 1.77; 95% CI = 1.17–2.48; p‐value = 0.0007) and breast cancer‐specific mortality (HR = 1.62; 95% CI = 1.11–2.37; p‐value = 0.01). Lifetime smoking exposure, not current status, should be used to assess mortality risk among former smokers.     

Impact of smoking on patients with stage III colon cancer

BACKGROUND:

Cigarette smoking has been shown to increase the risk of developing colorectal cancer, particularly smoking early in life. Little is known about the impact of tobacco use on colon cancer recurrence among colon cancer survivors.

METHODS:

The authors prospectively collected lifetime smoking history from stage III colon cancer patients enrolled in a phase 3 trial via self‐report questionnaires during and 6 months after completion of adjuvant chemotherapy. Smoking status was defined as never, current, or past. Lifetime pack‐years were defined as number of lifetime packs of cigarettes. Patients were followed for recurrence or death.

RESULTS:

Data on smoking history were captured on 1045 patients with stage III colon cancer receiving adjuvant therapy (46% never smokers; 44% past; 10% current). The adjusted hazard ratio (HR) for disease‐free survival (DFS) was 0.99 (95% confidence interval [CI], 0.70‐1.41), 1.17 (95% CI 0.89‐1.55), and 1.22 (95% CI 0.92‐1.61) for lifetime pack‐years 0‐10, 10‐20, and 20+, respectively, compared with never smoking (P = .16). In a preplanned exploratory analysis of smoking intensity early in life, the adjusted HR for 12+ pack‐years before age 30 years for DFS was 1.37 (95% CI, 1.02‐1.84) compared with never smoking (P = .04). The adjusted HR for DFS was 1.18 (95% CI, 0.92‐1.50) for past smokers and 1.10 (95% CI, 0.73‐1.64) for current smokers, compared with never smokers.

CONCLUSIONS:

Total tobacco usage early in life may be an important, independent prognostic factor of cancer recurrences and mortality in patients with stage III colon cancer. Cancer 2010. © 2010 American Cancer Society.     

Alcohol and smoking and subsequent risk of prostate cancer in Japanese men: The Japan Public Health Center‐based prospective study

Although alcohol and smoking have not been established as risk factors for prostate cancer, they are important risk factors for other human cancers and potentially major avoidable factors. Alcohol drinkers and smokers might be less likely to get screening, which might lead to attenuation of the positive association. Here, we investigated the association of alcohol drinking and smoking and prostate cancer according to stage, as well as prostate cancer detected by subjective symptoms, in a large prospective study among Japanese men. The Japan Public Health Center‐based prospective study (JPHC study) was established in 1990 for Cohort I and in 1993 for Cohort II. Subjects were 48,218 men aged 40–69 years who completed a questionnaire, which included their alcohol and smoking habits at baseline, and who were followed until the end of 2010. During 16 years of follow‐up, 913 men were newly diagnosed with prostate cancer; of whom 248 had advanced cases, 635 were organ‐localized and 30 were of an undetermined stage. Alcohol consumption was dose‐dependently associated with advanced prostate cancer [nondrinkers: reference, 0–150 g/week: hazard ratio (HR) = 1.23, 95% confidence interval (CI) = 0.83–1.82; 150–300 g/week: HR = 1.51, 95% CI = 1.04–2.19; ≥300 g/week: HR = 1.41, 95% CI = 0.97–2.05, p for trend = 0.02]. The positive association was not substantially changed among cancers detected by subjective symptoms. Smoking was inversely associated with prostate cancer among total subjects, but tended to increase the risk of advanced prostate cancer detected by subjective symptoms. In conclusion, abstinence from alcohol and prohibition of smoking might be important factors in the prevention of advanced prostate cancer.     

Dairy intake in relation to prostate cancer survival

Dairy intake has been associated with increased risk of advanced prostate cancer. Two US cohort studies reported increased prostate cancer‐specific mortality with increased high‐fat milk intake. We examined whether dairy and related nutrient intake were associated with prostate cancer progression in a Swedish patient population with high dairy consumption. We prospectively followed 525 men with newly diagnosed prostate cancer (diagnosed 1989–1994). We identified and confirmed deaths through February 2011 (n = 222 prostate cancer‐specific, n = 268 from other causes). Cox proportional hazards regression was used to calculate hazard ratios (HR) and 95% confidence intervals (CI) for the associations between food or nutrient intake and prostate cancer‐specific death. On average, patients consumed 5.0 servings/day of total dairy products at diagnosis. In the whole population, high‐fat milk intake was not associated with prostate cancer‐specific death (95% CI: 0.78, 2.10; p‐trend = 0.32; multivariate‐adjusted model). However, among patients diagnosed with localized prostate cancer, compared to men who consumed <1 servings/day of high‐fat milk, those who drank ≥3 servings/day had an increased hazard of prostate cancer mortality (HR = 6.10; 95% CI: 2.14, 17.37; p‐trend = 0.004; multivariate‐adjusted model). Low‐fat milk intake was associated with a borderline reduction in prostate cancer death among patients with localized prostate cancer. These associations were not observed among patients diagnosed with advanced stage prostate cancer. Our data suggest a positive association between high‐fat milk intake and prostate cancer progression among patients diagnosed with localized prostate cancer. Further studies are warranted to investigate this association and elucidate the mechanisms by which high‐fat milk intake may promote prostate cancer progression.     

Interaction between tobacco smoking and hepatitis B virus infection on the risk of liver cancer in a Chinese population

Although tobacco smoking has been reported as a risk factor for liver cancer, few studies have specifically explored the association among Chinese females and the potential interaction between smoking and other risk factors. A population‐based case–control study was conducted and 2,011 liver cancer cases and 7,933 healthy controls were enrolled in Jiangsu, China from 2003 to 2010. Epidemiological data were collected, and serum hepatitis B surface antigen (HBsAg) and anti‐HCV antibody were measured. Unconditional logistic regression was used to examine association and potential interaction, while semi‐Bayes (SB) method was employed to make estimates more conservative. The prevalence of serum HBsAg positivity was 43.2% among cases and 6.5% among controls. The adjusted odds ratios (OR) for ever smoking were 1.62 (95% confidence interval [CI]: 1.33–1.96) among male and 0.82 (95% CI: 0.53–1.26) among female. Age at first cigarette, duration of smoking and pack‐years of smoking were all significantly associated with liver cancer among men. Compared to HBsAg‐negative never smokers, the adjusted ORs were 1.25 (95% CI: 1.03–1.52) for HBsAg‐negative ever smokers, 7.66 (95% CI: 6.05–9.71) for HBsAg‐positive never smokers, and 15.68 (95% CI: 12.06–20.39) for HBsAg‐positive ever smokers. These different odds ratios indicated super‐additive (RERI: 7.77, 95% CI: 3.81–11.73) and super‐multiplicative interactions (ROR: 1.64, 95% CI: 1.17–2.30) between hepatitis B virus (HBV) infection and tobacco smoking. Most associations and interactions detected remained statistically significant after SB adjustments. Tobacco smoking and HBV infection positively interact in the development of liver cancer.     

Inverse associations of dietary fiber and menopausal hormone therapy with colorectal cancer risk in the Multiethnic Cohort Study

In the Multiethnic Cohort Study, we previously reported that dietary fiber intake was inversely associated with colorectal cancer risk in men only. In women, the inverse relationship was weaker and appeared to be confounded by menopausal hormone therapy (MHT). We re‐examined this observation with a greatly increased power. Using Cox proportional hazards models, we analyzed data from 187,674 participants with 4,692 cases identified during a mean follow‐up period of 16 years. In multivariable‐adjusted models, dietary fiber intake was inversely associated with colorectal cancer risk in both sexes: HR = 0.73, 95% CI: 0.61–0.89 for highest vs. lowest quintile, p_trend = 0.0020 in men and HR = 0.76, 95% CI: 0.62–0.91, p_trend = 0.0067 in women. Postmenopausal women who ever used MHT had a 19% lower risk of colorectal cancer (95% CI: 0.74–0.89) compared with MHT never users. In a joint analysis of dietary fiber and MHT, dietary fiber intake was associated with a lower colorectal cancer risk in MHT never users (HR = 0.75, 95% CI: 0.59–0.95, p_trend = 0.045), but did not appear to further decrease the colorectal cancer risk of MHT ever users (p_trend = 0.11). Our results support the overall protective roles of dietary fiber and MHT against colorectal cancer and suggest that dietary fiber may not lower risk further among women who ever used MHT. If confirmed, these results would suggest that MHT and dietary fiber may share overlapping mechanisms in protecting against colorectal cancer.     

Single nucleotide polymorphisms of 8 inflammation‐related genes and their associations with smoking‐related cancers

Tobacco smoke and its metabolites are carcinogens that increase tissue oxidative stress and induce target tissue inflammation. We hypothesized that genetic variation of inflammatory pathway genes plays a role in tobacco‐related carcinogenesis and is modified by tobacco smoking. We evaluated the association of 12 single nucleotide polymorphisms of 8 inflammation‐related genes with tobacco‐related cancers (lung, oropharynx, larynx, esophagus, stomach, liver, bladder, and kidney) using 3 case‐control studies from: Los Angeles (population‐based; 611 lung and 553 upper aero‐digestive tract cancer cases and 1,040 controls), Taixing, China (population‐based; 218 esophagus, 206 stomach, 204 liver cancer cases, and 415 controls), and Memorial Sloan‐Kettering Cancer Center (hospital‐based; 227 bladder cancer cases and 211 controls). After adjusting for age, education, ethnicity, gender, and tobacco smoking, IL10 rs1800871 was inversely associated with oropharyngeal cancer (CT+TT vs. CC adjusted odds ratio [aOR]: 0.69, 95% confidence interval [CI]: 0.50–0.95), and was positively associated with lung cancer among never smokers (TT vs. CT+CC aOR: 2.5, 95% CI: 1.3–5.1) and inversely with oropharyngeal cancer among ever smokers (CT+TT vs. CC aOR: 0.63, 95% CI: 0.41–0.95). Among all pooled never smokers (588 cases and 816 controls), TNF rs1799964 was inversely associated with smoking‐related cancer (CC vs. CT+TT aOR: 0.36, 95% CI: 0.17–0.77). Bayesian correction for multiple comparisons suggests that chance is unlikely to explain our findings (although epigenetic mechanisms may be in effect), which support our hypotheses, suggesting that IL10 rs1800871 is a susceptibility marker for oropharyngeal and lung cancers, and that TNF rs1799964 is associated with smoking‐related cancers among never smokers.     

Smokeless tobacco and risk of head and neck cancer: Evidence from a case–control study in New England

Current studies suggesting that smokeless tobacco use increases the risk of head and neck cancer are hampered by small numbers. Consequently, there remains uncertainty in the magnitude and significance of this risk. We examined the relationship between smokeless tobacco use and head and neck squamous cell carcinoma (HNSCC) in a population‐based case–control study with 1,046 cases and 1,239 frequency‐matched controls. Logistic regression models were used to estimate odds ratios (OR) and 95% confidence intervals (95% CI), adjusting for age, gender, race, education level, cigarette smoking, and alcohol consumption. A nonsignificant elevated association between having ever used smokeless tobacco and HNSCC risk (OR = 1.20, 95% CI: 0.67–2.16) was observed. Individuals who reported 10 or more years of smokeless tobacco use had a significantly elevated risk of HNSCC (OR = 4.06, 95% CI: 1.31–12.64), compared to never users. In an analysis restricted to never cigarette smokers, a statistically significant association was observed between ever use of smokeless tobacco and the risk of HNSCC (OR = 4.21, 95% CI: 1.01–17.57). These findings suggest that long‐term use of smokeless tobacco increases the risk of HNSCC.     

Dairy intake after prostate cancer diagnosis in relation to disease‐specific and total mortality

Information regarding postdiagnostic dairy intake and prostate cancer survival is limited. We evaluated intake of total, high‐fat and low‐fat dairy after prostate cancer diagnosis in relation to disease‐specific and total mortality. We included 926 men from the Physicians’ Health Study diagnosed with non‐metastatic prostate cancer between 1982 and 2000 who completed a diet questionnaire a median of 5 years after diagnosis and were followed thereafter for a median of 10 years to assess mortality. Cox proportional hazards regression was used to estimate associations between dairy intake and prostate cancer specific and all‐cause mortality. During 8,903 person‐years of follow‐up, 333 men died, 56 due to prostate cancer. Men consuming ≥3 servings/day of total dairy products had a 76% higher risk of total mortality and a 141% higher risk of prostate cancer‐specific mortality compared to men who consumed less than 1 dairy product/day (hazard ratio (HR) = 1.76, 95% confidence interval (CI): 1.21, 2.55, p_trend < 0.001 for total mortality; HR = 2.41, 95% CI: 0.96, 6.02, p_trend = 0.04 for prostate cancer‐specific mortality). The association between high‐fat dairy and mortality risk appeared to be stronger than that of low‐fat dairy, but the difference between them was not statistically significant (p for difference = 0.57 for prostate cancer‐specific mortality and 0.56 for total mortality). Among men without metastases when diagnosed, higher intake of dairy foods after prostate cancer diagnosis may be associated with increased prostate cancer‐specific and all‐cause mortality.     

Effects of α‐tocopherol and β‐carotene supplementation on cancer incidence and mortality: 18‐Year postintervention follow‐up of the Alpha‐Tocopherol,Beta‐Carotene Cancer Prevention Study

In the Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention Study among 29,133 Finnish male smokers aged 50–69 years, daily α‐tocopherol (50 mg) for a median of 6.1 years decreased the risk of prostate cancer, whereas β‐carotene (20 mg) increased risk of lung cancer and overall mortality. To determine the postintervention effects of α‐tocopherol and β‐carotene, 25,563 men were followed 18 years for cancer incidence and all causes of mortality through national registers. Neither supplement had significant effects on post‐trial cancer incidence. Relative risk (RR) for lung cancer (n = 2,881) was 1.04 (95% confidence interval [CI], 0.96–1.11) among β‐carotene recipients compared with nonrecipients. For prostate cancer (n = 2,321), RR was 0.97 (95% CI, 0.89–1.05) among α‐tocopherol recipients compared with nonrecipients with the preventive effect of α‐tocopherol continuing ～8 years postintervention. Body mass index significantly modified the effect of α‐tocopherol on prostate cancer (p for interaction = 0.01) RR 1.00 (95% CI, 0.88–1.14) in normal‐weight men, 0.87 (95% CI, 0.77–0.98) in overweight men, and 1.25 (95% CI, 1.01–1.55) in obese men. The post‐trial relative mortality (based on 16,686 deaths) was 1.02 (95% CI, 0.98–1.05) for α‐tocopherol recipients compared with nonrecipients and 1.02 (95% CI, 0.99–1.05) for β‐carotene recipients compared with nonrecipients. α‐Tocopherol decreased post‐trial prostate cancer mortality (RR, 0.84; 95% CI, 0.70–0.99), whereas β‐carotene increased it (RR, 1.20; 95% CI, 1.01–1.42). In conclusion, supplementation with α‐tocopherol and β‐carotene appeared to have no late effects on cancer incidence. The preventive effect of moderate‐dose α‐tocopherol on prostate cancer continued several years post‐trial and resulted in lower prostate cancer mortality.     

Associations of metabolic syndrome and C‐reactive protein with mortality from total cancer,obesity‐linked cancers and breast cancer among women in NHANES III

Although metabolic syndrome (MetS) is a prognostic factor for cancer occurrence, the association of MetS and cancer mortality remains unclear. The purpose of this study was to evaluate whether MetS, components of MetS and C‐reactive protein (CRP) are associated with cancer mortality in women. A total of 400 cancer deaths, with 140 deaths from obesity‐linked‐cancers (OLCas), [breast (BCa), colorectal, pancreatic and endometrial], linked through the National Death Index, were identified from 10,104 eligible subjects aged ≥18 years. Cox proportional hazards regression was used to estimate multivariable‐adjusted hazard ratios (HR) for cancer mortality. MetS was associated with increased deaths for total cancer [HR = 1.33, 95% confidence interval (CI) 1.04–1.70] and BCa [HR = 2.1, 95% CI, 1.09–4.11]. The risk of total cancer [HR = 1.7, 95% CI, 1.12–2.68], OLCas [HR = 2.1, 95% CI, 1.00–4.37] and BCa [HR = 3.8, 95% CI, 1.34–10.91] mortality was highest for women with all MetS components abnormal, compared to those without MetS. Linear associations of blood‐pressure [HR = 2.5, 1.02–6.12, Quartile (Q) 4 vs Q1, p trend = 0.004] and blood‐glucose [HR = 2.2, 1.04–4.60, Q4 vs. Q1, p trend = 0.04] with total‐OLCas mortality were observed. A threefold increased risk of BCa mortality was observed for women with enlarged waist circumference, ≥100.9 cm, [HR = 3.5, 1.14–10.51, p trend = 0.008] and in those with increased blood glucose, ≥101 mg/dL, [HR = 3.2, 1.11–9.20, p trend = 0.03] compared to those in Q1. None of the components of MetS were associated with total‐cancer mortality. CRP was not associated with cancer mortality. In conclusion, MetS is associated with total‐cancer and breast‐cancer mortality, with waist circumference, blood pressure and blood glucose as independent predictors of OLCas and BCa mortality.     

Higher carbohydrate intake is associated with increased risk of all‐cause and disease‐specific mortality in head and neck cancer patients: results from a prospective cohort study

No studies have evaluated associations between carbohydrate intake and head and neck squamous cell carcinoma (HNSCC) prognosis. We prospectively examined associations between pre‐ and post‐treatment carbohydrate intake and recurrence, all‐cause mortality, and HNSCC‐specific mortality in a cohort of 414 newly diagnosed HNSCC patients. All participants completed pre‐ and post‐treatment Food Frequency Questionnaires (FFQs) and epidemiologic surveys. Recurrence and mortality events were collected annually. Multivariable Cox Proportional Hazards models tested associations between carbohydrate intake (categorized into low, medium and high intake) and time to recurrence and mortality, adjusting for relevant covariates. During the study period, there were 70 deaths and 72 recurrences. In pretreatment analyses, high intakes of total carbohydrate (HR: 2.29; 95% CI: 1.23–4.25), total sugar (HR: 3.03; 95% CI: 1.12–3.68), glycemic load (HR: 2.10; 95% CI: 1.15–3.83) and simple carbohydrates (HR 2.26; 95% CI 1.19–4.32) were associated with significantly increased risk of all‐cause mortality compared to low intake. High intakes of carbohydrate (HR 2.45; 95% CI: 1.23–4.25) and total sugar (HR 3.03; 95% CI 1.12–3.68) were associated with increased risk of HNSCC‐specific mortality. In post‐treatment analyses, medium fat intake was significantly associated with reduced risk of recurrence (HR 0.08; 95% CI 0.01–0.69) and all‐cause mortality (HR 0.27; 95% CI 0.07–0.96). Stratification by tumor site and cancer stage in pretreatment analyses suggested effect modification by these factors. Our data suggest high pretreatment carbohydrate intake may be associated with adverse prognosis in HNSCC patients. Clinical intervention trials to further examine this hypothesis are warranted.     

The association between smoking and cancer incidence in BRCA1 and BRCA2 mutation carriers

Tobacco smoke is an established carcinogen, but the association between tobacco smoking and cancer risk in BRCA mutation carriers is not clear. The aim of this study was to evaluate prospectively the association between tobacco smoking and cancer incidence in a cohort of BRCA1 and BRCA2 mutation carriers. The study population consisted of unaffected BRCA mutation carriers. Information on lifestyle including smoking histories, reproductive factors, and past medical histories was obtained through questionnaires. Incident cancers were updated biennially via follow‐up questionnaires. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using time‐dependent Cox regression models. There were 700 incident cancers diagnosed over 26,711 person‐years of follow‐up. The most frequent cancers seen in BRCA mutation carriers were breast (n = 428; 61%) and ovarian (n = 109; 15%) cancer. Compared to nonsmokers, (ever) smoking was associated with a modest increased risk of all cancers combined (HR = 1.17; 95%CI 1.01–1.37). Women in the highest group of total pack‐years (4.3–9.8) had an increased risk of developing any cancer (HR = 1.27; 95%CI 1.04–1.56), breast cancer (HR = 1.33, 95%CI 1.02–1.75), and ovarian cancer (HR = 1.68; 95%CI 1.06–2.67) compared to never smokers. The associations between tobacco smoking and cancer did not differ by BRCA mutation type or by age at diagnosis. This prospective study suggests that tobacco smoking is associated with a modest increase in the risks of breast and ovarian cancer among women with BRCA1 or BRCA2 mutation.