Association of C-peptide and leptin with prostate cancer incidence in the Health Professionals Follow-up Study

Purpose

Hyperinsulinemia is hypothesized to influence prostate cancer risk. Thus, we evaluated the association of circulating C-peptide, which is a marker of insulin secretion, and leptin, which is secreted in response to insulin and influences insulin sensitivity, with prostate cancer risk.

Methods

We identified prostate cancer cases (n = 1,314) diagnosed a mean of 5.4 years after blood draw and matched controls (n = 1,314) in the Health Professionals Follow-up Study. Plasma C-peptide and leptin concentrations were measured by ELISA. Odds ratios (ORs) and 95 % confidence intervals (CI) were estimated taking into account the matching factors age and history of a PSA test before blood draw and further adjusting for body mass index, diabetes, and other factors.

Results

Neither C-peptide (quartile [Q]4 vs. Q1: OR 1.05, 95 % CI 0.82–1.34, p-trend = 0.95) nor leptin (Q4 vs. Q1: OR 0.85, 95 % CI 0.65–1.12, p-trend = 0.14) was associated with prostate cancer risk. Further, neither was associated with risk of advanced or lethal disease (n = 156 cases; C-peptide: Q4 vs. Q1, OR 1.18, 95 % CI 0.69–2.03, p-trend = 0.78; leptin: Q4 vs. Q1, OR 0.74, 95 % CI 0.41–1.36, p-trend = 0.34).

Conclusions

In this large prospective study, circulating C-peptide and leptin concentrations were not clearly associated with risk of prostate cancer overall or aggressive disease. Well into the PSA era, our findings do not appear to be supportive of the hypothesis that hyperinsulinemia influences risk of total or aggressive prostate cancer.     

Gene–environment interactions between JAZF1 and occupational and household lead exposure in prostate cancer among African American men

Purpose

A single nucleotide polymorphism, rs10486567, in JAZF1 has consistently been associated with increased risk of prostate cancer. The physical interaction of zinc finger proteins, such as JAZF1, with heavy metals may play a role in carcinogenesis. This study assessed potential gene–environment statistical interactions (G×E) between rs10486567 and heavy metals in prostate cancer.

Methods

In a case-only study of 228 African American prostate cancer cases, G×E between rs10486567 and sources of cadmium and lead (Pb) were assessed. Unconditional logistic regression was used to estimate interaction odds ratios (IORs), and generalized estimating equations were used for models containing nested data. Case–control validation of IORs was performed, using 82 controls frequency matched to cases on age–race.

Results

Among cases, a potential G×E interaction was observed between rs10486567 CC genotype and living in a Census tract with a high proportion of housing built before 1950, a proxy for household Pb exposure, when compared to CT or TT carriers (OR 1.81; 95 % CI 1.04–3.16; p = 0.036). A stronger G×E interaction was observed when both housing and occupational Pb exposure were taken into account (OR 2.62; 95 % CI 1.03–6.68; p = 0.04). Case–control stratified analyses showed the odds of being a CC carrier were higher in cases compared to controls among men living in areas with older housing (OR 2.03; CI 0.99–4.19; p = 0.05) or having high occupational Pb exposure (OR 2.50; CI 1.01–6.18; p = 0.05).

Conclusions

In African American men, the association between JAZF1 rs10486567 and prostate cancer may be modified by exposure to heavy metals such as Pb.     

Components of the metabolic syndrome and risk of prostate cancer: the HUNT 2 cohort, Norway

Background

The metabolic syndrome has been suggested as a unifying link between a “western” lifestyle and an increased prostate cancer risk.

Methods

We assessed the associations of components of the metabolic syndrome with prostate cancer in a prospective cohort based on 29,364 Norwegian men followed up for prostate cancer incidence and mortality from 1995–1997 to the end of 2005 in the second Nord Trøndelag Health Study (HUNT 2).

Results

During a mean 9.3 years follow-up, 687 incident prostate cancers were diagnosed, and 110 men died from prostate cancer. There was little evidence that baseline BMI, waist circumference, waist–hip ratio, total or HDL-cholesterol, triglycerides, presence of the metabolic syndrome, diabetes, antihypertensive use, or cardiovascular disease were associated with incident or fatal prostate cancer. There was weak evidence that raised blood pressure was associated with an increased risk: for each SD (12 mm) increase in diastolic blood pressure, there was an 8% (95% CI = 1–17%; p = 0.04) increased risk of incident prostate cancer.

Conclusions

We found little evidence to support the hypothesis that the metabolic syndrome or its components explains higher prostate cancer mortality rates in countries with a “western” diet and lifestyle. The positive association of blood pressure with prostate cancer warrants further investigation.     

Circulating levels of obesity-related markers and risk of renal cell carcinoma in the PLCO cancer screening trial

Purpose

Obesity is an established risk factor for renal cell carcinoma (RCC). It is unclear what biologic mechanisms underlie this association, although recent evidence suggests that the effects of circulating hormones such as insulin-like growth factors (IGF) and adipokines may play a role.

Methods

To address this question, we conducted a nested case–control study of RCC (252 cases, 252 controls) within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial investigating associations with pre-diagnostic serum levels of total adiponectin, high-molecular-weight (HMW) adiponectin, IGF-1, IGF-binding protein-3 (IGFBP-3), and C-peptide. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were estimated using conditional logistic regression.

Results

After adjustment for potential confounders, non-significant associations with RCC were observed for total adiponectin (OR for highest vs. lowest quartile = 0.65, 95% CI 0.37–1.14; p _trend = 0.35), HMW adiponectin (0.67, 0.38–1.17; p _trend = 0.36), IGF-1 (1.35, 0.77–2.39; p _trend = 0.17), IGFBP-3 (1.47, 0.83–2.62; p _trend = 0.53), and C-peptide (1.52, 0.86–2.70; p _trend = 0.15). In a joint analysis with body mass index (BMI, kg/m²), obese individuals (BMI ≥30) with above-median levels of IGFBP-3 had a significantly higher risk versus those with BMI <25 and below-median IGFBP-3 (OR 2.42, 1.11–5.26), whereas obese individuals with low IGFBP-3 did not (1.18, 0.53–2.64) (p _interaction = 0.35).

Conclusions

The results of this study, while not clearly supporting associations with these obesity-related hormones, suggest that the association between obesity and RCC may be partially modified through mechanisms related to elevated IGFBP-3.

     

Coffee and risk of prostate cancer incidence and mortality in the Cancer of the Prostate in Sweden Study

Purpose

Coffee intake has recently been associated with significantly lower risk of lethal and advanced prostate cancer in a US population.

Methods

We studied the association between coffee and prostate cancer risk in the population-based case–control study Cancer of the Prostate in Sweden. Dietary data were available for 1,499 cases and 1,112 controls. We calculated odds ratios (ORs) for the risk of prostate cancer in high versus low categories of coffee intake using logistic regression. We studied overall prostate cancer risk as well as risk of fatal, advanced, localized, high-grade, grade 7, and low-grade disease.

Results

Mean coffee intake was 3.1 cups per day among both cases and controls. Coffee intake was not associated with overall prostate cancer risk. Risk of fatal prostate cancer was inversely, but not statistically significantly, associated with coffee intake, with an odds ratio of 0.64 [95 % confidence interval (CI) 0.34–1.19, p value for linear trend = 0.81] for men consuming greater than 5 cups per day compared to men drinking less than 1 cup per day. The highest intake of coffee was associated non-significantly with lower risk of advanced disease (OR = 0.73, 95 % CI 0.41–1.30, p trend = 0.98) and associated significantly with lower risk of high-grade cancer (Gleason 8–10; OR = 0.50, 95 % CI 0.26–0.98, p trend = 0.13). Risk of localized, grade 7, and low-grade cancers was not associated with coffee intake.

Conclusions

This study provides some support of an inverse association between coffee and lethal and high-grade prostate cancer.     

Lifetime body size and prostate cancer risk in a population-based case–control study in Sweden

Purpose

The role of body size in prostate cancer etiology is unclear and potentially varies by age and disease subtype. We investigated whether body size in childhood and adulthood, including adult weight change, is related to total, low–intermediate-risk, high-risk, and fatal prostate cancer.

Methods

We used data on 1,499 incident prostate cancer cases and 1,118 population controls in Sweden. Body figure at age 10 was assessed by silhouette drawings. Adult body mass index (BMI) and weight change were based on self-reported height and weight between ages 20 and 70. We estimated odds ratios (ORs) with 95 % confidence intervals (CIs) by unconditional logistic regression.

Results

Height was positively associated with prostate cancer. Overweight/obesity in childhood was associated with a 54 % increased risk of dying from prostate cancer compared to normal weight, whereas a 27 % lower risk was seen in men who were moderately thin (drawing 2) in childhood (P _trend = 0.01). Using BMI <22.5 as a reference, we observed inverse associations between BMI 22.5 to <25 at age 20 and all prostate cancer subtypes (ORs in the range 0.72–0.82), and between mean adult BMI 25 to <27.5 and low–intermediate-risk disease (OR 0.75, 95 % CI 0.55–1.02). Moderate adult weight gain increased the risk of disease in men with low BMI at start and in short men.

Conclusions

Our comprehensive life-course approach revealed no convincing associations between anthropometric measures and prostate cancer risk. However, we found some leads that deserve further investigation, particularly for early-life body size. Our study highlights the importance of the time window of exposure in prostate cancer development.     

Coffee consumption and the risk of overall and fatal prostate cancer in the NIH-AARP Diet and Health Study

Purpose

Evidence on the association between coffee consumption and prostate cancer risk is inconsistent; furthermore, few studies have examined the relationship between coffee consumption and fatal prostate cancer. The aim of this study was to investigate whether coffee intake is associated with the risk of overall and fatal prostate cancer.

Methods

We conducted a prospective analysis among 288,391 men in the National Institutes of Health AARP Diet and Health Study who were between 50 and 71 years old at baseline in 1995–1996. Coffee consumption was assessed at baseline. Cox proportional hazards models were used to calculate the age- and multivariable-adjusted hazard ratios (HR)s and 95 % confidence intervals (CIs).

Results

Over 11 years of follow-up, 23,335 cases of prostate cancer were ascertained, including 2,927 advanced and 917 fatal cases. Coffee consumption was not significantly associated with prostate cancer risk. The multivariable-adjusted HRs (95 % CI), comparing those who drank six or more cups per day to nondrinker, were as follows: 0.94 (0.86–1.02), p trend = 0.08 for overall prostate cancer, 1.13 (0.91–1.40), p trend = 0.62 for advanced prostate cancer, and 0.79 (0.53–1.17), p trend = 0.20 for fatal prostate cancer. The findings remained nonsignificant when we stratified by prostate-specific antigen testing history or restricted to nonsmokers.

Conclusions

We found no statistically significant association between coffee consumption and the risk of overall, advanced, or fatal prostate cancer in this cohort, though a modest reduction in risk could not be excluded.     

The APE1 Asp148Glu polymorphism and colorectal cancer susceptibility: a meta-analysis

Background

Published data regarding the association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility remained controversial. This meta-analysis of literatures was performed to draw a more precise estimation of the relationship.

Materials and methods

We systematically searched PubMed, Embase, and Web of Science with a time limit of August 19, 2013. Summary odds ratios (ORs) with 95 % CIs were used to assess the strength of association between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility using random-effects model.

Results

A total of eight case–control studies including 2,597 cases and 3,063 controls were included for analysis. Overall, no significant associations were found between the APE1 Asp148Glu polymorphism and colorectal cancer susceptibility for GG vs TT (OR?=?1.00, 95 % CI?=?0.73–1.36, p?=?0.00 for heterogeneity), TG vs TT (OR?=?1.17, 95 % CI?=?0.88–1.55, p?=?0.00 for heterogeneity), the dominant model GG + TG vs TT (OR?=?1.21, 95 % CI?=?0.91–1.60, p?=?0.00 for heterogeneity) nor the recessive model GG vs TG + TT(OR?=?0.95, 95 % CI?=?0.75–1.20, p?=?0.02 for heterogeneity). In subgroup analysis, no significant associations were found in the Asian or Caucasian populations.

Conclusion

This meta-analysis suggested that the APE1 Asp148Glu polymorphism was not associated with colorectal cancer susceptibility among Asians or Caucasians.     

Nutrient-based dietary patterns and prostate cancer risk: a case–control study from Italy

Purpose

The role of various foods and nutrients, and their combinations, on prostate cancer risk remains largely undefined. We addressed therefore the issue of complex dietary patterns.

Methods

We analyzed data from an Italian case–control study, including 1,294 men with prostate cancer and 1,451 hospital controls. We carried out an exploratory principal component factor analysis on 28 selected nutrients in order to identify dietary patterns. We estimated odds ratios (ORs) and corresponding confidence intervals (CIs) using logistic regression models on quintiles of factor scores, adjusting for major confounding variables.

Results

We identified five dietary patterns, labeled “Animal Products,” “Vitamins and Fiber,” “Starch-rich,” “Vegetable Unsaturated Fatty Acids (VUFA),” and “Animal Unsaturated Fatty Acids (AUFA).” We found positive associations between prostate cancer and “Animal Products” (OR for the highest vs. the lowest score quintile: 1.51, 95 % CI 1.16–1.96), “Starch-rich” (OR 1.50, 95 % CI 1.16 1.93), and “AUFA” (OR 1.32, 95 % CI 1.02–1.70) patterns. No significant associations emerged with “Vitamins and Fiber” (OR 0.93) and “VUFA” (OR 1.16) patterns.

Conclusions

Our findings suggest that a diet rich in animal products, including several types of meat and dairy products, as well as of (refined) cereals and sugars has an unfavorable role on prostate cancer.     

Coffee and tea consumption in relation to prostate cancer prognosis

Background

Bioactive compounds found in coffee and tea may delay the progression of prostate cancer.

Methods

We investigated associations of pre-diagnostic coffee and tea consumption with risk of prostate cancer recurrence/progression. Study participants were men diagnosed with prostate cancer in 2002–2005 in King County, Washington, USA. We assessed the usual pattern of coffee and tea consumption two years before diagnosis date. Prostate cancer-specific outcome events were identified using a detailed follow-up survey. Multivariable Cox proportional hazards regression models were used to estimate hazard ratios (HRs) and 95 % confidence intervals (CIs).

Results

The analysis of coffee intake in relation to prostate cancer recurrence/progression included 630 patients with a median follow-up of 6.4 years, during which 140 prostate cancer recurrence/progression events were recorded. Approximately 61 % of patients consumed at least one cup of coffee per day. Coffee consumption was associated with a reduced risk of prostate cancer recurrence/progression; the adjusted HR for ≥4 cups/day versus ≤1 cup/week was 0.41 (95 % CI: 0.20, 0.81; p for trend = 0.01). Approximately 14 % of patients consumed one or more cups of tea per day, and tea consumption was unrelated to prostate cancer recurrence/progression.

Conclusion

Results indicate that higher pre-diagnostic coffee consumption is associated with a lower risk of prostate cancer recurrence/progression. This finding will require replication in larger studies.     

Diabetes and prostate cancer screening in black and white men

Purpose

Prior studies conducted primarily among white men find a reduced risk of prostate cancer associated with time since developing diabetes. While biologic explanations are plausible, the association may in part arise from more frequent prostate cancer screening among those with a diabetes diagnosis. The purpose of the present study was to investigate the association between diabetes and prostate cancer screening.

Methods

We examined differences in prostate cancer screening (prostate-specific antigen and/or digital rectal examination) testing practices after a diabetes diagnosis among lower-income persons living in the southeastern United States and enrolled in the Southern Community Cohort Study between 2002 and 2009. Baseline in-person interviews collected information on history of diabetes and prostate cancer screening from 18,809 black and 6,404 white men aged 40–79 years.

Results

After adjustment for confounding, diabetic black [odds ratio (OR) 1.12, 95 % confidence interval (CI) 1.01–1.25] and white (OR 1.25, 95 % CI 1.03–1.51) men were more likely to undergo recent prostate cancer screening compared to non-diabetic men of the same race. The increased risk for prostate cancer screening, however, occurred primarily within the first 12 months after diabetes diagnosis.

Conclusions

Our results suggest that a diabetes diagnosis modestly increases the likelihood of having a prostate cancer screening test for both black and white men. The prevalence of screening was higher nearer to the time of diabetes diagnosis, which may contribute to an early increase in prostate cancer detection followed by lower prostate cancer detection after an extended time.     

Body mass index and weight change in men with prostate cancer: progression and mortality

Purpose

Body mass index (BMI) is a modifiable lifestyle factor that has been associated with an increased risk of fatal prostate cancer and biochemical recurrence. The main purpose of the present study was to investigate the association between the exposure BMI at the time of a prostate cancer diagnosis and weight change after diagnosis, and the outcomes of prostate cancer progression and mortality in a large cohort study.

Methods

Data from 4,376 men diagnosed with clinically localized prostate cancer between 1997 and 2002 were analyzed. BMI and weight change were self-reported in 2007. Hazard ratios (HRs) with 95 % confidence intervals (CIs) were estimated in complete-case analysis (n = 3,214) using Cox proportional hazards models.

Results

Progression was experienced among 639 (14.6 %) of the study participants, and in total, 450 (10.3 %) deaths of any cause and 134 (3.1 %) prostate cancer-specific deaths were recorded during follow-up. Obese men had a 47 % increased rate of overall mortality compared to normal weight men (HR 1.47, 95 % CI 1.03–2.10). No statistically significant associations were found for BMI and prostate cancer progression or prostate cancer-specific mortality. A weight loss >5 % after diagnosis almost doubled the rate of overall mortality compared to maintaining a stable weight (HR 1.94, 95 % CI 1.41–2.66), while a weight gain >5 % was associated with an almost doubled increased rate of prostate cancer-specific mortality (HR 1.93, 95 % CI 1.18–3.16).

Conclusions

Being obese was associated with an increased rate of overall mortality, and gaining weight after a prostate cancer diagnosis was associated with an increased rate of prostate cancer-specific mortality.     

Serum estrogen levels and prostate cancer risk in the prostate cancer prevention trial: a nested case�Ccontrol study

Objective

Finasteride reduces prostate cancer risk by blocking the conversion of testosterone to dihydrotestosterone. However, whether finasteride affects estrogens levels or change in estrogens affects prostate cancer risk is unknown.

Methods

These questions were investigated in a case?Ccontrol study nested within the prostate cancer prevention trial (PCPT) with 1,798 biopsy-proven prostate cancer cases and 1,798 matched controls.

Results

Among men on placebo, no relationship of serum estrogens with risk of prostate cancer was found. Among those on finasteride, those in the highest quartile of baseline estrogen levels had a moderately increased risk of Gleason score < 7 prostate cancer (for estrone, odds ratio [OR] = 1.51, 95% confidence interval [CI] = 1.06?C2.15; for estradiol, OR = 1.50, 95% CI = 1.03?C2.18). Finasteride treatment increased serum estrogen concentrations; however, these changes were not associated with prostate cancer risk.

Conclusion

Our findings confirm those from previous studies that there are no associations of serum estrogen with prostate cancer risk in untreated men. In addition, finasteride results in a modest increase in serum estrogen levels, which are not related to prostate cancer risk. Whether finasteride is less effective in men with high serum estrogens, or finasteride interacts with estrogen to increase cancer risk, is uncertain and warrants further investigation.     

Associations of tea and coffee consumption with prostate cancer risk

Purpose

Tea and coffee contain bioactive compounds and both beverages have recently been associated with a reduced risk of prostate cancer (PCa).

Methods

We studied associations of tea and coffee consumption with PCa risk in a population-based case–control study from King County, Washington, USA. Prostate cancer cases were diagnosed in 2002–2005 and matched to controls by 5-year age groups. Logistic regression was used to generate odds ratios (ORs) and 95 % confidence intervals (CIs).

Results

Among controls, 19 and 58 % consumed at least one cup per day of tea and coffee, respectively. The analysis of tea included 892 cases and 863 controls, and tea consumption was associated with a reduced overall PCa risk with an adjusted OR of 0.63 (95 % CI: 0.45, 0.90; P for trend = 0.02) for men in the highest compared to lowest category of tea intake (≥2 cups/day vs. ≤1 cup/week). Risk estimates did not vary substantially by Gleason grade or disease stage. Coffee consumption was not associated with risk of overall PCa or PCa in subgroups defined by tumor grade or stage.

Conclusions

Our results contribute further evidence that tea consumption may be a modifiable exposure that reduces PCa risk.     

Racial/ethnic differences in serum sex steroid hormone concentrations in US adolescent males

Objective

Contrary to the hypothesis that the racial/ethnic disparity in prostate cancer has a hormonal basis, we did not observe a difference in serum testosterone concentration between non-Hispanic black and white men in the Third National Health and Nutrition Examination Survey (NHANES III), although non-Hispanic black men had a higher estradiol level. Unexpectedly, Mexican–American men had the highest testosterone level. Next, we evaluated whether the same patterns are observed during adolescence, the time of prostate maturation.

Methods

We measured serum testosterone, estradiol, and sex hormone-binding globulin (SHBG) by immunoassay in 134 males aged 12–19 in NHANES III. Mean concentrations were compared by race/ethnicity adjusting for age, Tanner stage, percent body fat, waist, physical activity, tobacco smoke, and the other hormones.

Results

After multivariable adjustment, in the 12–15-year-old males, testosterone concentration was lower in non-Hispanic blacks than whites (p = 0.043), SHBG concentration did not significantly differ between the two groups. Mexican–Americans had the highest testosterone (versus non-Hispanic black: p = 0.002) and lowest SHBG (versus non-Hispanic white: p = 0.010; versus non-Hispanic black: p = 0.047) concentrations. Estradiol concentration was lower in non-Hispanic blacks (p = 0.11) and Mexican–Americans (p = 0.033) compared with non-Hispanic whites. After multivariable adjustment, in the 16–19-year-old males, testosterone, estradiol, and SHBG concentrations did not differ between non-Hispanic blacks and whites. Mexican–Americans had the highest testosterone concentration (versus non-Hispanic white: p = 0.08), but did not differ from the other groups on estradiol and SHBG concentrations. In both age groups, these patterns were generally present, but less pronounced after adjusting for age and Tanner stage only.

Conclusion

In adolescent males, non-Hispanic blacks did not have a higher testosterone concentration than non-Hispanic whites, and Mexican–Americans had the highest testosterone concentration, patterns similar to adult males.     

Associations of circulating retinol, vitamin E, and 1,25-dihydroxyvitamin D with prostate cancer diagnosis, stage, and grade

Purpose

Some epidemiological studies suggest that vitamin A (retinol), vitamin E, and vitamin D (total 25-hydroxyvitamin D, 25(OH)D; 1,25-dihydroxyvitamin, 1,25(OH)₂D) are protective against prostate cancer. However, the evidence is not conclusive, with positive and null associations reported for all three vitamins. Limitations of previous studies include small sample size, lack of population controls, and reliance on self-reported dietary intake. Few studies have explored the interactions of circulating 25(OH)D with 1,25(OH)₂D or retinol, which are biologically plausible interactions.

Methods

We investigated the associations of circulating retinol, vitamin E, and 1,25(OH)₂D with PSA-detected prostate cancer risk, stage, and grade in a case–control study nested within the Prostate Testing for Cancer and Treatment (ProtecT) trial. We investigated the possibility of an interaction between 25(OH)D and 1,25(OH)₂D and whether the previously observed association between 25(OH)D and prostate cancer may be modified by retinol levels.

Results

We included 1,433 prostate cancer cases and 1,433 healthy controls. There was no evidence of associations of circulating retinol, vitamin E, or 1,25(OH)₂D with overall prostate cancer risk, stage (advanced vs localized), or Gleason grade (high- (≥7) vs low (<7) grade). There was no evidence of an interaction of 1,25(OH)₂D and 25(OH)D with prostate cancer risk, stage, or grade (p interaction ≥ 0.24). The association between 25(OH)D and prostate cancer did not differ by retinol level (p interaction?=?0.34).

Conclusions

We found no evidence that retinol, vitamin E, or 1,25(OH)₂D concentrations were associated with overall prostate cancer risk or more aggressive prostate cancer phenotypes. There was no evidence of an interaction between 25(OH)D and 1,25(OH)₂D or retinol.     

Men with prostate cancer make positive dietary changes following diagnosis and treatment

Purpose

Few studies have measured dietary changes made among men diagnosed with prostate cancer (PC) without formal dietary interventions, yet they may offer insight into the needs of PC survivors. This study examined dietary changes in men before and after treatment for PC within the prostate testing for cancer and treatment randomized trial.

Methods

This was a prospective cohort study in community-based men aged 50–69 tested for PC in nine UK areas. 3,935 men completed food frequency questionnaires before diagnosis and 678 with localized PC repeated the questionnaire 1 year later (response 82.7 %).

Results

Men subsequently diagnosed with or without PC all consumed similar diets before diagnosis. Diagnosis of PC led to dietary changes, with 234 (34.7 %) men eating more fresh tomatoes (p < 0.0001) and 156 (23.5 %) more tomato products (p = 0.01). 271 (40.0 %) men consumed more protein (p < 0.0001) and 193 (28.6 %) more fruit/vegetable juice (p < 0.0001). Fewer macronutrients were obtained from dairy products (p < 0.01). Men undergoing active monitoring increased their fruit/vegetable juice intake after diagnosis (p = 0.0023) more than men who had surgery or radiotherapy.

Conclusions

Around one-third of men spontaneously adopted a healthier diet and also consumed more ‘prostate-healthy’ foods following a diagnosis of PC. Dietary choices also differed by radical or monitoring treatments, indicating that men undergoing active surveillance may be more likely to pursue dietary changes as an adjunct therapy. PC survivors can adopt healthier diets, thus providing clinicians with opportunities to support PC survivorship by providing targeted advice beneficial to general and potentially prostate-specific health.     

Epidemiological characteristics of a Spanish cohort of patients diagnosed with squamous cell carcinoma of head and neck: distribution of risk factors by tumor location

Purpose

Head and neck cancer is a highly heterogeneous disease comprising a large number of tumors located in the cervicofacial area. This study aimed to determine the epidemiological characteristics of squamous-cell carcinomas of the head and neck in the Spanish population, and the distribution of risk factors based on tumor locations.

Methods/patients

A cohort of 459 patients (75 oral cavity, 167 oro-/hypopharyngeal and 217 laryngeal cancers) recruited in 19 hospitals participating in the Spanish head and neck cancer cooperative group were included over 3 years (2012–2014). Epidemiological parameters and risk factors were obtained from a self-administered questionnaire, and tumor characteristics were obtained from clinical records. Multivariate multinomial logistic regression was used to assess factors associated with tumor location.

Results

Most patients were males (88.4 %), smokers (95 %) and drinkers (76.5 %). Relative to laryngeal cancer, pharyngeal cancer and oral cancer were more common in women than men (OR 3.58, p = 0.003 and 4.33, p = 0.001, respectively); pharyngeal cancer was more associated with rural environment (OR 1.81, p = 0.007) and weekly alcohol intake (10–140 g: OR 2.53, p = 0.012; 141–280 g: OR 2.47, p = 0.023; >280 g: OR 3.20, p = 0.001) and less associated with pack-years of smoking (21–40 packs: OR 0.46, p = 0.045; 41–70 packs: OR 0.43, p = 0.023; ≥71 packs: OR 3.20, p = 0.015).

Conclusions

The distribution of these tumors differs between the sexes, with a higher proportion of oral cavity and pharyngeal tumors in women than in men. Oro-/hypopharyngeal cancers were more strongly associated with rural areas and with alcohol consumption, although less strongly associated with smoking than laryngeal tumors.