Ramseymorrow5893

80 [95% confidence interval (CI) 0.75-0.85] after bias adjustments. The corresponding rate ratio for participating women was 0.73 (95% CI 0.66-0.81).

Continuing to screen women up to 74 years of age is effective compared with stopping screening at 69 years.

This large long-term study will add to the knowledge of the effect of mammography screening for women 70 to 74 years.

This large long-term study will add to the knowledge of the effect of mammography screening for women 70 to 74 years.

Studies of cancer risk among relatives of children with cancer beyond parents and siblings are limited. We have investigated the cancer risk up to the third degree of relation in families with pediatric cancer to reveal patterns of inheritance.

A single-center cohort of 757 patients with pediatric cancer was linked to the Swedish National Population Register, resulting in 16,137 relatives up to the third degree of relation. All relatives were matched to the Swedish Cancer Register, and standard incidence ratios (SIR) were calculated to define relatives at risk.

Children and adults up to the third degree of relation had increased cancer risk, with SIRs of 1.48 (

= 0.01) and 1.07 (

< 0.01), respectively. The SIRs for first- and third-degree adult relatives were 1.22 and 1.10, respectively, but no increased risk was observed in second-degree relatives. Male relatives had a higher risk than females, especially when related to a girl and when the child had leukemia. The risk was mainly increased for lung, prostate, and gastrointestinal cancer. When excluding 29 families of children with known pathogenic germline variants, the increased risk remained.

Relatives to children with cancer up to third degree of relation have an increased cancer risk. Known pathogenic germline variants do not explain this increased risk.

The overall increased cancer risk among relatives of children with cancer in this population-based cohort strengthens the importance of surveillance programs for families with pediatric cancer.

The overall increased cancer risk among relatives of children with cancer in this population-based cohort strengthens the importance of surveillance programs for families with pediatric cancer.

Global prostate cancer incidence rates are lower in Asian men than Caucasian men. Whether this is the result of less screening in Asian men remains to be determined. We examined whether Asian race was associated with prostate cancer diagnosis in the Reduction by Dutasteride of Cancer Events (REDUCE) study.

REDUCE was a 4-year, multicenter, randomized trial of dutasteride versus placebo for prostate cancer prevention among men who underwent prostate-specific antigen (PSA)-independent biopsies at 2 and 4 years. Eligible men were ages 50 to 75 years, had PSA between 2.5 and 10 ng/mL, and a negative prestudy prostate biopsy. We tested the association between Asian and Caucasian race and prostate cancer diagnosis using logistic regression.

Of 8,122 men in REDUCE, 5,755 (71%) were Caucasian and 105 (1.8%) were Asian. Asians had lower body mass index (24.8 vs. 26.9 kg/m

,

< 0.001), had smaller prostate volume (35.0 vs. 43.5 cc,

< 0.001), and were less likely to have abnormal digital rectal exams (

= 0.048), but were similar in baseline age, PSA, family history of prostate cancer, and smoking status compared with Caucasian men (all

≥ 0.164). Asian men were equally likely to receive any on-study biopsy compared with Caucasian men (

= 0.634). After adjusting for potential confounders, Asian men were less likely to be diagnosed with prostate cancer during the 4-year study (OR = 0.49; 95% confidence interval, 0.28-0.88;

= 0.016), compared with Caucasian men.

In REDUCE, where all men underwent biopsies largely independent of PSA, Asian race was associated with lower prostate cancer diagnosis.

These findings suggest that lower prostate cancer risk in Asian men may be due to biological, genetic, and/or lifestyle factors.

These findings suggest that lower prostate cancer risk in Asian men may be due to biological, genetic, and/or lifestyle factors.

Prevalence of

(

) infection, the main risk factor for gastric cancer, has been decreasing in the United States; however, there remains a substantial racial disparity. Moreover, the time-trends for prevalence of CagA-positive

infection, the most virulent form, are unknown in the U.S.

We sought to assess prevalence of CagA-positive

infection over time by race in the United States.

We utilized multiplex serology to quantify antibody responses to

antigens in 4,476 participants across five cohorts that sampled adults from 1985 to 2009. Using log-binomial regression models, we calculated prevalence ratios and 95% confidence intervals for the association between

-CagA sero-prevalence and birth year by race.

African Americans were three times more likely to be

-CagA sero-positive than Whites. After adjustment,

-CagA sero-prevalence was lower with increasing birth year among Whites (



= 0.001), but remained stable for African Americans. When stratified by sex and education separately, the decline in

-CagA sero-positivity among Whites remained only for females (



< 0.001) and was independent of educational attainment. Among African Americans, there was no difference by sex; furthermore, sero-prevalence increased with increasing birth year among those with a high school education or less (

= 0.006).

Among individuals in the United States born from the 1920s to 1960s,

-CagA sero-prevalence has declined among Whites, but not among African Americans.

Our findings suggest a widening racial disparity in the prevalence of the most virulent form of

, the main cause of gastric cancer.

Our findings suggest a widening racial disparity in the prevalence of the most virulent form of H. pylori, the main cause of gastric cancer.

Colorectal carcinogenesis is mechanistically linked to inflammation and is highly associated with diet and lifestyle factors that may affect chronic inflammation. We previously developed dietary (DIS) and lifestyle (LIS) inflammation scores, comprising inflammation biomarker-weighted components, to characterize the collective contributions of 19 food groups and four lifestyle exposures to systemic inflammation. Both scores were more strongly directly associated with circulating inflammation biomarkers in three validation populations, including a subset of the study population described below, than were the previously reported dietary inflammatory index and empirical dietary inflammatory pattern.

We calculated the DIS and LIS in three pooled case-control studies of incident, sporadic colorectal adenoma (

= 765 cases and 1,986 controls) with extensive dietary and lifestyle data, and investigated their associations with adenoma using multivariable unconditional logistic regression.

For those in the highest (more proinflammatory) relative to the lowest (more anti-inflammatory) quintiles of the DIS and LIS, the multivariable-adjusted ORs were 1.31 [95% confidence interval (CI), 0.98-1.75;



= 0.09] and 1.98 (95% CI, 1.48-2.66;



< 0.001), respectively. These associations were strongest for adenomas with high-risk characteristics and among men. Those in the highest relative to the lowest joint DIS/LIS quintile had a 2.65-fold higher odds (95% CI, 1.77-3.95) of colorectal adenoma.

These results support that diets and lifestyles with higher balances of pro- to anti-inflammatory exposures may be associated with higher risk for incident, sporadic colorectal adenoma.

Our findings support further investigation of the DIS and LIS in relation to colorectal neoplasms.

Our findings support further investigation of the DIS and LIS in relation to colorectal neoplasms.

Scalp and neck (SN) melanoma confers a worse prognosis than melanoma of other sites but little is known about its determinants. click here We aimed to identify associations between SN melanoma and known risk genes, phenotypic traits, and sun exposure patterns.

Participants were cases from the Western Australian Melanoma Health Study (

= 1,200) and the Genes, Environment, and Melanoma Study (

= 3,280). Associations between risk factors and SN melanoma, compared with truncal and arm/leg melanoma, were investigated using binomial logistic regression. Facial melanoma was also compared with the trunk and extremities, to evaluate whether associations were subregion specific, or reflective of the whole head/neck region.

Compared with other sites, increased odds of SN and facial melanoma were observed in older individuals [SN OR = 1.28, 95% confidence interval (CI) = 0.92-1.80,



= 0.016; Face OR = 4.57, 95% CI = 3.34-6.35,



< 0.001] and those carrying

-rs12203592*T (SN OR = 1.35, 95% CI = 1.12-1.63,



= 0.002; Face OR = 1.29, 95% CI = 1.10-1.50,



= 0.001). Decreased odds were observed for females (SN OR = 0.49, 95% CI = 0.37-0.64,

< 0.001; Face OR = 0.66, 95% CI = 0.53-0.82,

< 0.001) and the presence of nevi (SN OR = 0.66, 95% CI = 0.49-0.89,

= 0.006; Face OR = 0.65, 95% CI = 0.52-0.83,

< 0.001).

Differences observed between SN melanoma and other sites were also observed for facial melanoma. Factors previously associated with the broader head and neck region, notably older age, may be driven by the facial subregion. A novel finding was the association of

-rs12203592 with both SN and facial melanoma.

Understanding the epidemiology of site-specific melanoma will enable tailored strategies for risk factor reduction and site-specific screening campaigns.

Understanding the epidemiology of site-specific melanoma will enable tailored strategies for risk factor reduction and site-specific screening campaigns.

Work is needed to better understand how joint exposure to environmental and economic factors influence cancer. We hypothesize that environmental exposures vary with socioeconomic status (SES) and urban/rural locations, and areas with minority populations coincide with high economic disadvantage and pollution.

To model joint exposure to pollution and SES, we develop a latent class mixture model (LCMM) with three latent variables (SES Advantage, SES Disadvantage, and Air Pollution) and compare the LCMM fit with K-means clustering. We ran an ANOVA to test for high exposure levels in non-Hispanic black populations. The analysis is at the census tract level for the state of North Carolina.

The LCMM was a better and more nuanced fit to the data than K-means clustering. Our LCMM had two sublevels (low, high) within each latent class. The worst levels of exposure (high SES disadvantage, low SES advantage, high pollution) are found in 22% of census tracts, while the best levels (low SES disadvantage, high SES advantage, low pollution) are found in 5.7%. Overall, 34.1% of the census tracts exhibit high disadvantage, 66.3% have low advantage, and 59.2% have high mixtures of toxic pollutants. Areas with higher SES disadvantage had significantly higher non-Hispanic black population density (NHBPD;

< 0.001), and NHBPD was higher in areas with higher pollution (

< 0.001).

Joint exposure to air toxins and SES varies with rural/urban location and coincides with minority populations.

Our model can be extended to provide a holistic modeling framework for estimating disparities in cancer survival.



Our model can be extended to provide a holistic modeling framework for estimating disparities in cancer survival.See all articles in this CEBP Focus section, "Environmental Carcinogenesis Pathways to Prevention."