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Objectives This study compared the MR measurement of minimum uninvolved cervical stroma and maximum stromal invasion, and the detection of positive lymph nodes with the pathological results. In addition, tumour type and grade were correlated with nodal status and apparent diffusion coefficient (ADC) values. Methods Patients who underwent surgery and MR at our centre for early stage cervical cancer (FIGO IA1-IIB) were included. Data recorded included: age, date of MR, clinical FIGO (International Federation of Gynacology and Obstetrics) stage, histological type and grade, adjuvant therapy, pre-surgical conisation. MR evaluation included: measurement of the minimum uninvolved stroma, maximum thickness of stromal involvement, presence and site of positive pelvic lymph nodes, calculation of ADC values. Statistical analysis was performed to compare MR and pathological results. The agreement between MR and pathology in measuring depth of stromal invasion was analysed by Bland-Altman plot, calculating the limits of agreement (LoA). Results 113/217 patients underwent adjuvant therapies. Sensitivity, specificity, positive predictive value, negative predictive value and accuracy of MR in evaluation of minimum thickness of uninvolved cervical stroma were 88%, 75%, 70%, 90% and 80%; the same values in evaluation of pelvic positive lymph nodes were 64%, 85%, 65%, 84% and 78%. The mean difference between MR and pathological results in measuring maximum depth of stromal invasion was -0.65 mm (95% LoA: -9.37 mm; 8.07 mm). Depth of stromal invasion was strongly related to positive nodal status (p < 0.001). ADC values (available in 51/217 patients) were not associated with the features assessed. Conclusions Pre-surgical MR is accurate (80%) in evaluating the minimum thickness of uninvolved cervical stroma; MR measurements of maximum depth of stromal invasion differed ±9 mm from the pathological results in 95% of cases. Furthermore, a strong association was found between the depth

Background: Lifestyle-related health problems are an important health concern in the transport service industry. Web- and telephone-based interventions could be suitable for this target group requiring tailored approaches. Objective: To evaluate the effect of tailored Web-based health feedback and optional telephone coaching to improve lifestyle factors (body mass index\-BMI, dietary intake, physical activity, stress, sleep, tobacco and alcohol consumption, disease history, self-perceived health, and motivation to change health habits), in comparison to no health feedback or telephone coaching. Methods: Overall, 3,876 employees in the Swedish transport services were emailed a Web-based questionnaire. They were randomized into: control group (group A, 498 of 1238 answered, 40.23%), or intervention Web (group B, 482 of 1305 answered, 36.93%), or intervention Web + telephone (group C, 493 of 1333 answered, 36.98%). All groups received an identical questionnaire, only the interventions differed. Group B received tailored Web-based health feedback, and group C received tailored Web-based health feedback + optional telephone coaching if the participants' reported health habits did not meet the national guidelines, or if they expressed motivation to change health habits. The Web-based feedback was fully automated. Telephone coaching was performed by trained health counselors. Nine months later, all participants received a follow-up questionnaire and intervention Web + telephone. Descriptive statistics, the chi-square test, analysis of variance, and generalized estimating equation (GEE) models were used. Results: Overall, 981 of 1473 (66.60%) employees participated at baseline (men: 66.7%, mean age: 44 years, mean BMI: 26.4 kg/m2) and follow-up. No significant differences were found in reported health habits between the 3 groups over time. However, significant changes were found in motivation to change. The intervention groups reported higher motivation to improve dietary h

Background:Alcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.Methods:We investigated the effect of alcohol on 23 cancer types through a meta-analytic approach. We used dose-response meta-regression models and investigated potential sources of heterogeneity.Results:A total of 572 studies, including 486 538 cancer cases, were identified. Relative risks (RRs) for heavy drinkers compared with nondrinkers and occasional drinkers were 5.13 for oral and pharyngeal cancer, 4.95 for oesophageal squamous cell carcinoma, 1.44 for colorectal, 2.65 for laryngeal and 1.61 for breast cancer; for those neoplasms there was a clear dose-risk relationship. Heavy drinkers also had a significantly higher risk of cancer of the stomach (RR 1.21), liver (2.07), gallbladder (2.64), pancreas (1.19) and lung (1.15). There was indication of a positive association between alcohol consumption and risk of melanoma and prostate cancer. Alcohol consumption and risk of Hodgkin's and Non-Hodgkin's lymphomas were inversely associated.Conclusions:Alcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. There is accumulating evidence that alcohol drinking is associated with some other cancers such as pancreas and prostate cancer and melanoma.

The MC1R gene is a key regulator of skin pigmentation. We aimed to evaluate the association between MC1R variants and the risk of sporadic cutaneous melanoma (CM) within the M-SKIP project, an international pooled-analysis on MC1R, skin cancer and phenotypic characteristics. Data included 5,160 cases and 12,119 controls from 17 studies. We calculated a summary odds ratio (SOR) for the association of each of the nine most studied MC1R variants and of variants combined with CM by using random-effects models. Stratified analysis by phenotypic characteristics were also performed. Melanoma risk increased with presence of any of the main MC1R variants: the SOR for each variant ranged from 1.47 (95%CI: 1.17-1.84) for V60L to 2.74 (1.53-4.89) for D84E. Carriers of any MC1R variant had a 66% higher risk of developing melanoma compared with wildtype subjects (SOR; 95%CI: 1.66; 1.41-1.96) and the risk attributable to MC1R variants was 28%. When taking into account phenotypic characteristics, we found that MC1R-associated melanoma risk increased only for darker-pigmented Caucasians: SOR (95%CI) was 3.14 (2.06-4.80) for subjects with no freckles, no red hair and skin Type III/IV. Our study documents the important role of all the main MC1R variants in sporadic CM and suggests that they have a direct effect on melanoma risk, independently on the phenotypic characteristics of carriers. This is of particular importance for assessing preventive strategies, which may be directed to darker-pigmented Caucasians with MC1R variants as well as to lightly pigmented, fairskinned subjects.

It has been suggested that alcohol intake increases sunburn severity, a major risk factor for cutaneous melanoma (CM). Several epidemiological studies have investigated the relationship between alcohol consumption and CM, but the evidence is inconsistent. Therefore, we aimed to quantify this relationship better, using a meta-analytical approach. The dose-risk relationship was also modelled through a class of flexible nonlinear meta-regression random effects models. The present meta-analysis included 16 studies (14 case-control and two cohort investigations) with a total of 6251 cases of CM. The pooled relative risk (RR) for any alcohol drinking compared with no/occasional drinking was 1·20 [95% confidence interval (CI) 1·06-1·37]. The risk estimate was similar in case-control (RR 1·20, 95% CI 1·01-1·44) and cohort studies (RR 1·26, 95% CI 1·19-1·35). The pooled RR was 1·10 (95% CI 0·96-1·26) for light alcohol drinking (≤ 1 drink per day) and 1·18 (95% CI 1·01-1·40) for moderate-to-heavy drinking. The pooled RR from 10 studies adjusting for sun exposure was 1·15 (95% CI 0·94-1·41), while the RR from six unadjusted studies was 1·27 (95% CI 1·20-1·35). No evidence of publication bias was detected. This meta-analysis of published data reveals that alcohol consumption is positively associated with the risk of CM. However, caution in interpreting these results is required, as residual confounding by sun exposure cannot be ruled out. What's already known about this topic? Alcohol drinking increases sunburn severity, a major risk factor for cutaneous melanoma. Several epidemiological studies have investigated the relationship between alcohol consumption and cutaneous melanoma, but the evidence is inconsistent. What does this study add? We found a 20% increased risk of cutaneous melanoma with regular alcohol drinking. © 2014 British Association of Dermatologists.

Background. There is convincing evidence that alcohol consumption increases the risk of cancer of the colorectum, breast, larynx, liver, esophagus, oral cavity and pharynx. Most of the data derive from studies that focused on the effect of moderate/high alcohol intakes, while little is known about light alcohol drinking (up to 1 drink/day). Patients and methods. We evaluated the association between light drinking and cancer of the colorectum, breast, larynx, liver, esophagus, oral cavity and pharynx, through a meta-analytic approach. We searched epidemiological studies using PubMed, ISI Web of Science and EMBASE, published before December 2010. Results. We included 222 articles comprising ∼92 000 light drinkers and 60 000 non-drinkers with cancer. Light drinking was associated with the risk of oropharyngeal cancer [relative risk, RR = 1.17; 95% confidence interval (CI) 1.06-1.29], esophageal squamous cell carcinoma (SCC) (RR = 1.30; 95% CI 1.09-1.56) and female breast cancer (RR = 1.05; 95% CI 1.02-1.08). We estimated that ∼5000 deaths from oropharyngeal cancer, 24 000 from esophageal SCC and 5000 from breast cancer were attributable to light drinking in 2004 worldwide. No association was found for colorectum, liver and larynx tumors. Conclusions. Light drinking increases the risk of cancer of oral cavity and pharynx, esophagus and female breast.

Background:To know how moderate-to-vigorous physical activity (MVPA) and sedentary time change across lifespan periods is needed for designing successful lifestyle interventions. We aimed to study changes in objectively measured (accelerometry) MVPA and sedentary time from childhood to adolescence and from adolescence to young adulthood.Methods:Estonian and Swedish participants from the European Youth Heart Study aged 9 and 15 years at baseline (N = 2312) were asked to participate in a second examination 6 (Sweden) to 9/10 (Estonia) years later. 1800 participants with valid accelerometer data were analyzed.Results:MVPA decreased from childhood to adolescence (-1 to -2.5 min/d per year of follow-up, P = 0.01 and <0.001, for girls and boys respectively) and also from adolescence to young adulthood (-0.8 to -2.2 min/d per year, P = 0.02 and <0.001 for girls and boys, respectively). Sedentary time increased from childhood to adolescence (+15 and +20 min/d per year, for girls and boys respectively, P<0.001), with no substantial change from adolescence to young adulthood. Changes in both MVPA and sedentary time were greater in Swedish than in Estonian participants and in boys than in girls. The magnitude of the change observed in sedentary time was 3-6 time larger than the change observed in MVPA.Conclusions:The decline in MVPA (overall change = 30 min/d) and increase sedentary time (overall change = 2:45 h/d) observed from childhood to adolescence are of concern and might increase the risk of developing obesity and other chronic diseases later in life. These findings substantially contribute to understand how key health-related behaviors (physical activity and sedentary) change across important periods of life. © 2013 Ortega et al.

OBJECTIVE: In order to provide an updated quantification of the association between alcohol drinking and epithelial ovarian cancer risk, we conducted a meta-analysis of published observational studies. METHODS: Using PubMed, we performed a literature search of all case-control and cohort studies published as original articles in English up to September 2011. We included 27 observational studies, of which 23 were case-control studies, 3 cohort studies and one pooled analysis of prospective cohort studies, including a total of 16,554 epithelial ovarian cancer cases. We derived pooled meta-analytic estimates using random-effects models. RESULTS: The pooled relative risk (RR) for any alcohol drinking compared with non/occasional drinking was 1.00 [95% confidence interval (CI), 0.95-1.05]. The RRs were 0.97 (95% CI, 0.92-1.02), 1.03 (95% CI, 0.96-1.11) and 1.09 (95% CI, 0.80-1.50) for light (≤1drink/day), moderate (>1 to <3 drinks) and heavy drinking (≥3drinks/day), respectively. In particular, pooled RR for invasive epithelial ovarian cancers was 1.00 (95% CI, 0.95-1.06), while for borderline cancers was 0.96 (95% CI, 0.74-1.26). Stratified analyses across cancer histotypes revealed a modest protective effect of alcohol on endometrioid epithelial ovarian tumors (RR=0.82, 95% CI, 0.70-0.96), while no association was found for serous (RR=1.00, 95% CI, 0.84-1.19), mucinous (RR=0.91, 95% CI, 0.78-1.08) and clear cell (RR=0.93, 95% CI, 0.76-1.14) cancers. There was no evidence of publication bias. CONCLUSIONS: This comprehensive meta-analysis provided no evidence of a material association between alcohol drinking and epithelial ovarian cancer risk.

BACKGROUND: The role of alcohol consumption in relation with renal cell carcinoma is still unclear; a few studies have reported a beneficial effect of moderate levels of alcohol consumption, whereas it remains still under debate whether there is a dose-response association.Materials and methods:Twenty observational studies (4 cohort, 1 pooled and 15 case-control) reporting results on at least three levels of alcohol consumption were selected through a combined search with PubMed and EMBASE of articles published before November 2010. Overall relative risks (RRs) and 95% confidence intervals (CIs) were estimated using random-effects models, and both second-order fractional polynomials and random effect meta-regression models were implemented for the study of dose-risk relation. RESULTS: The estimated RRs were 0.85 (95% CI: 0.80-0.92) for any alcohol drinking, 0.90 (95% CI: 0.83-0.97) for light drinking (0.01-12.49 g/day), 0.79 (95% CI: 0.71-0.88) for moderate drinking (12.5-49.9 g/day) and 0.89 (95% CI: 0.58-1.39) for heavy drinking (≥50 g/day), respectively. CONCLUSION: Our meta-analysis supports the hypothesis of a negative effect of moderate alcohol consumption on the risk of renal cell cancer.