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A promoter polymorphism in the pro-inflammatory cytokine tumor necrosis factor (TNF) (TNF G-308A) is associated with increased non-Hodgkin lymphoma (NHL) risk. The protein product, TNF-alpha, activates the nuclear factor kappa beta (NF-kappaB) transcription factor, and is critical for inflammatory and apoptotic responses in cancer progression. We hypothesized that the TNF and NF-kappaB pathways are important for NHL and that gene variations across the pathways may alter NHL risk. We genotyped 500 tag single nucleotide polymorphisms (SNPs) from 48 candidate gene regions (defined as 20 kb 5', 10 kb 3') in the TNF and TNF receptor superfamilies and the NF-kappaB and related transcription factors, in 1946 NHL cases and 1808 controls pooled from three independent population-based case-control studies. We obtained a gene region-level summary of association by computing the minimum p-value (\"minP test\"). We used logistic regression to compute odds ratios and 95% confidence intervals for NHL and four major NHL subtypes in relation to SNP genotypes and haplotypes. For NHL, the tail strength statistic supported an overall relationship between the TNF/NF-kappaB pathway and NHL (p = 0.02). We confirmed the association between TNF/LTA on chromosome 6p21.3 with NHL and found the LTA rs2844484 SNP most significantly and specifically associated with the major subtype, diffuse large B-cell lymphoma (DLBCL) (p-trend = 0.001). We also implicated for the first time, variants in NFKBIL1 on chromosome 6p21.3, associated with NHL. Other gene regions identified as statistically significantly associated with NHL included FAS, IRF4, TNFSF13B, TANK, TNFSF7 and TNFRSF13C. Accordingly, the single most significant SNPs associated with NHL were FAS rs4934436 (p-trend = 0.0024), IRF4 rs12211228 (p-trend = 0.0026), TNFSF13B rs2582869 (p-trend = 0.0055), TANK rs1921310 (p-trend = 0.0025), TNFSF7 rs16994592 (p-trend = 0.0024), and TNFRSF13C rs6002551 (p-trend = 0.0074). All associations were consistent in each study with no apparent specificity for NHL subtype. Our results provide consistent evidence that variation in the TNF superfamily of genes and specifically within chromosome 6p21.3 impacts lymphomagenesis. Further characterization of these susceptibility loci and identification of functional variants are warranted.

Among patients with a history of skin cancer, nicotinamide treatment was associated with a 23% lower rate of new nonmelanoma (basal-cell and squamous-cell) skin cancers than placebo, resulted in 13% fewer actinic keratoses after 12 months, and had similar adverse effects. Nonmelanoma skin cancers, mainly basal-cell carcinomas and squamous-cell carcinomas, are the most common cancers in white populations. 1 In Australia, nonmelanoma skin cancers are four times as common as all other cancers combined, 2 , 3 and in the United States, the annual total cost of treating nonmelanoma skin cancers is estimated to be $4.8 billion. 4 Basal-cell carcinomas rarely metastasize but are locally invasive and can be disfiguring. 5 Squamous-cell carcinomas, especially less well-differentiated tumors on the head and neck, have metastatic potential and may originate from premalignant actinic keratoses. 6 Nonmelanoma skin cancers and actinic keratoses are caused primarily by exposure to ultraviolet (UV) . . .

Objective To determine the factors associated with symptom-detected breast cancers in a population offered screening. Methods We interviewed 1,459 Australian women aged 40-69, 946 with symptom-detected and 513 with mammogram-detected invasive breast cancers > 1.1 cm in diameter about their personal, mammogram, and breast histories before diagnosis and reviewed medical records for tumor characteristics and mammogram dates, calculating ORs and 95% confidence intervals (CIs) for symptomversus mammogram-detected cancers in logistic regression models. Results Lack of regular mammograms (< 2 mammograms in the 4.5 years before diagnosis) was the strongest correlate of symptom-detected breast cancer (OR = 3.04 for irregular or no mammograms). In women who had regular mammograms (> 2 mammograms in the 4.5 years before diagnosis), the independent correlates of symptom-detected cancers were low BMI (OR < 25 kg/m² vs. > 30 kg/m² = 2.18, 95% CI 1.23-3.84; p = 0.008), increased breast density (available in 498 women) (OR highest quarter vs. lowest = 3.50, 95% CI 1.76-6.97; p trend = 0.004), high-grade cancer, and a larger cancer (each p < 0.01). In women who did not have regular mammograms, the independent correlates were age < 50 years, a first cancer, and a > 2-cm cancer. Smoking appeared to modify the association of symptomdetected cancer with low BMI (higher ORs for low BMI in current smokers) and estrogen receptor (ER) status (higher ORs for low BMI in ER cancers). Conclusion Women with low BMI may benefit from a tailored approach to breast cancer detection, particularly if they smoke. of symptom-detected breast cancer (OR = 3.04 for irregular or no mammograms). In women who had regular mammograms (> 2 mammograms in the 4.5 years before diagnosis), the independent correlates of symptom-detected cancers were low BMI (OR < 25 kg/m² vs. > 30 kg/m² = 2.18, 95% CI 1.23-3.84; p = 0.008), increased breast density (available in 498 women) (OR highest quarter vs. lowest = 3.50, 95% CI 1.76-6.97; p trend = 0.004), high-grade cancer, and a larger cancer (each p < 0.01). In women who did not have regular mammograms, the independent correlates were age < 50 years, a first cancer, and a > 2-cm cancer. Smoking appeared to modify the association of symptomdetected cancer with low BMI (higher ORs for low BMI in current smokers) and estrogen receptor (ER) status (higher ORs for low BMI in ER cancers). Conclusion Women with low BMI may benefit from a tailored approach to breast cancer detection, particularly if they smoke.

Non-melanocytic skin cancer has long been regarded as one of the harmful effects of solar ultraviolet (UV) radiation on human health. In this review, we examine epidemiologic evidence linking sun exposure and skin cancer coming from both descriptive studies in populations and analytical studies involving estimates of exposure in individuals. Particular attention is given to the quality of the published data. The epidemiologic evidence that sun exposure causes skin cancer is mainly indirect. Incidence or mortality is inversely related to latitude in populations of mainly European origin (e.g., the United States, Australia), and is higher in people born in Australia (high ambient solar radiation) than in migrants to Australia from the United Kingdom (lower ambient radiation). Skin cancer occurs mainly at sun-exposed body sites and in people who are sensitive to the sun; a reduced capacity to repair UV-induced DNA damage appears to increase the risk. The direct evidence linking sun exposure and skin cancer is weaker with few well-conducted studies of sun exposure in individuals. Mostly, studies of total sun exposure have not found statistically significant positive associations; those that did, had not adjusted for potential confounding by age and gender and thus their interpretation is limited. Studies of occupational sun exposure had relative risks not greater than 2.0; recreational exposure has been little studied. Other measurements, less direct but potentially less prone to measurement error, are sunborn (not evidently associated with skin cancer risk) and indicators of benign cutaneous sun-damage (strongly associated but lacking empirical evidence that sun exposure is their main cause). Many questions remain about the relationship between sun exposure and skin cancer.

Objective To examine the contribution of life event and social support factors to diagnosis with a >=2 cm breast cancer. Methods We studied 1,459 Australian women aged 40-69 diagnosed in 2002-2003 with a first primary invasive breast cancer 1.1 cm or larger. We measured stressful life events, perceived stress levels, and social support in the year before diagnosis and collected information on other potential risk factors and confounders. Results The odds of a >=2 cm breast cancer relative to a 1.1-1.9 cm breast cancer were reduced in women who reported tension or change in an intimate relationship in the year before diagnosis (OR = 0.71 95% CI 0.54-0.92; p = 0.009); the reduction was greatest in women living with a partner (OR = 0.64 95% CI 0.47-0.88; p = 0.006) and was largely unaffected by adjustment for other variables independently associated with a >=2 cm breast cancer in our study. There was no evidence that the total number or severity of all studied life events influenced cancer size. Low partner support increased the odds of a >=2 cm cancer but only in women not living with a partner. Conclusion Intimate relationship stress may reduce risk of a >=2 cm breast cancer. Suppression by stress of estrogen synthesis and metabolism is a possible mechanism.

Vitamin D may reduce mortality from prostate cancer (PC). We examined the associations of post-treatment plasma 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D concentrations with PC mortality. Participants were PC cases from the New South Wales Prostate Cancer Care. All contactable and consenting participants, at 4.9 to 8.6 years after diagnosis, were interviewed and had plasma 25-hydroxyvitamin D (25(OH)D) and 1,25-dihydroxyvitamin D (1,25(OH) 2 D) measured in blood specimens. Cox regression allowing for left-truncation was used to calculate adjusted mortality hazards ratios (HR) and 95% confidence intervals (95% CI) for all-cause and PC-specific mortality in relation to vitamin D levels and other potentially-predictive variables. Of the participants (n = 111; 75·9% response rate), there were 198 deaths from any cause and 41 from PC in the study period. Plasma 25(OH)D was not associated with all-cause or PC-specific mortality (p-values > 0·10). Plasma 1,25(OH) 2 D was inversely associated with all-cause mortality (HR for highest relative to lowest quartile = 0·45; 95% CI: 0·29–0·69), and PC-specific mortality (HR = 0·40; 95% CI: 0·14–1·19). These associations were apparent only in men with aggressive PC: all-cause mortality HR = 0·28 (95% CI·0·15–0·52; p-interaction = 0·07) and PC-specific mortality HR = 0·26 (95% CI: 0·07–1.00). Time spent outdoors was also associated with lower all-cause (HR for 4 th relative to 1 st exposure quartile = 0·42; 95% CI: 0·24–0·75) and PC-specific (HR = 0·48; 95% CI: 0·14–1·64) mortality, although the 95% CI for the latter was wide. The inverse association between post-treatment plasma 1,25(OH) 2 D levels and all-cause and PC-specific mortality in men with aggressive PC, suggest a possible beneficial effect of vitamin D supplementation in these men.

Various occupations have been associated with an elevated risk of non-Hodgkin lymphoma (NHL), but results have been inconsistent across studies. We investigated occupational risk of NHL and of four common NHL subtypes with particular focus on occupations of a priori interest. We conducted a pooled analysis of 10,046 cases and 12,025 controls from 10 NHL studies participating in the InterLymph Consortium. We harmonized the occupational coding using the 1968 International Standard Classification of Occupations (ISCO-1968) and grouped occupations previously associated with NHL into 25 a priori groups. Odds ratios (ORs) adjusted for center, age, and sex were determined for NHL overall and for the following four subtypes: diffuse large B-cell lymphoma (DLBCL), follicular lymphoma (FL), chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), and peripheral T-cell lymphoma (PTCL). We confirmed previously reported positive associations between NHL and farming occupations [field crop/vegetable farm workers OR = 1.26; 95% confidence interval (CI): 1.05, 1.51; general farm workers OR = 1.19; 95% CI: 1.03, 1.37]; we also confirmed associations of NHL with specific occupations such as women's hairdressers (OR = 1.34; 95% CI: 1.02, 1.74), charworkers/cleaners (OR = 1.17; 95% CI: 1.01, 1.36), spray-painters (OR = 2.07; 95% CI: 1.30, 3.29), electrical wiremen (OR = 1.24; 95% CI: 1.00, 1.54), and carpenters (OR = 1.42; 95% CI: 1.04, 1.93). We observed subtype-specific associations for DLBCL and CLL/SLL in women's hairdressers and for DLBCL and PTCL in textile workers. Our pooled analysis of 10 international studies adds to evidence suggesting that farming, hairdressing, and textile industry-related exposures may contribute to NHL risk. Associations with women's hairdresser and textile occupations may be specific for certain NHL subtypes. 't Mannetje A, De Roos AJ, Boffetta P, Vermeulen R, Benke G, Fritschi L, Brennan P, Foretova L, Maynadié M, Becker N, Nieters A, Staines A, Campagna M, Chiu B, Clavel J, de Sanjose S, Hartge P, Holly EA, Bracci P, Linet MS, Monnereau A, Orsi L, Purdue MP, Rothman N, Lan Q, Kane E, Seniori Costantini A, Miligi L, Spinelli JJ, Zheng T, Cocco P, Kricker A. 2016. Occupation and risk of non-Hodgkin lymphoma and its subtypes: a pooled analysis from the InterLymph Consortium. Environ Health Perspect 124:396-405; http://dx.doi.org/10.1289/ehp.1409294.

Background: The melanocortin-1-receptor ( MC1R ) gene regulates human pigmentation and is highly polymorphic in populations of European origins. The aims of this study were to evaluate the association between MC1R variants and the risk of non-melanoma skin cancer (NMSC), and to investigate whether risk estimates differed by phenotypic characteristics. Methods: Data on 3527 NMSC cases and 9391 controls were gathered through the M-SKIP Project, an international pooled-analysis on MC1R , skin cancer and phenotypic characteristics. We calculated summary odds ratios (SOR) with random-effect models, and performed stratified analyses. Results: Subjects carrying at least one MC1R variant had an increased risk of NMSC overall, basal cell carcinoma (BCC) and squamous cell carcinoma (SCC): SOR (95%CI) were 1.48 (1.24–1.76), 1.39 (1.15–1.69) and 1.61 (1.35–1.91), respectively. All of the investigated variants showed positive associations with NMSC, with consistent significant results obtained for V60L, D84E, V92M, R151C, R160W, R163Q and D294H: SOR (95%CI) ranged from 1.42 (1.19–1.70) for V60L to 2.66 (1.06–6.65) for D84E variant. In stratified analysis, there was no consistent pattern of association between MC1R and NMSC by skin type, but we consistently observed higher SORs for subjects without red hair. Conclusions: Our pooled-analysis highlighted a role of MC1R variants in NMSC development and suggested an effect modification by red hair colour phenotype.

Background: and purpose Women who use illicit drugs (\"drug users\") are exposed to human papillomaviruses (HPVs) from lifestyle risks that include sex risk behaviors, human immunodeficiency virus infection, and high levels of tobacco smoking. Both HPVs and tobacco smoking are recognized causes of cervical cancer, but little is known about risk in drug users. We sought to examine risk of cervical neoplasia and to estimate cervical screening prevalence in drug users compared to non-drug-users in Australia. Methods: Our study linked hospital admission records of women aged 20–54 in 2000–2007 to Pap Test Register and Cancer Registry records for 19,699 with an illicit drug–related admission and 194,089 without. We designed a nested case–control study of risk of cervical intraepithelial neoplasia (CIN) 2/3 and cervical cancer and a cross-sectional study of screening prevalence in this cohort of women. Results: Drug users were less likely than non-users to be screened in the past 3 years (crude prevalence 47 vs 58 %; prevalence ratio 0.80; 95 % CI 0.78–0.81). Odds ratios (ORs) in drug users, adjusted for cervical screening history and smoking, were 1.13 (95 % CI 1.04–1.23) for CIN 2/3 and 1.43 (95 % CI 0.96–2.15) for cervical cancer. The adjusted ORs in each case were similar in cannabinoid users and users of other drugs. Conclusions: The increased risks of CIN 2/3 and cervical cancer we observed are probably due to sex risk behaviors and their associated high risk of HPV. Interventions in drug users, such as HPV vaccination and barrier contraception and more cervical screening, might reduce the risk of cervical neoplasia.

Sex differences in melanoma are prominent, with female having a significant survival advantage. However, it is unclear why we see this survival advantage. Here, we investigate the relationship between sex, clinicopathologic variables, and melanoma specific survival in 1753 single primary melanomas from patients in the GEM (Genes, Environment, and Melanoma) study. Using Cox proportional hazard models and formal mediation analysis, the effect of sex on survival is explained largely by differences in the clinicopathologic features of tumors at diagnosis. Specifically, we find evidence that 86.5% of the effect of sex on melanoma survival is mediated by differences in age at diagnosis, Breslow thickness, ulceration, mitoses, and site (hazard ratio [HR] = 1.85, P < .001). This analysis indicates that the female survival advantage in melanoma is not primarily due to a direct effect of sex (HR = 1.19, P = .42) but is largely a result of an indirect effect of sex mediated by clinicopathologic features.