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Aims: To determine the relationship of diabetes with pancreatic cancer incidence among African American and Whites of similar socio‐economic status. Methods: Using the Southern Community Cohort Study, we conducted a follow‐up during 2002–2015 of pancreatic cancer incidence of 73,378 mostly low‐income participants aged 40–79 years; 15,913 reported diabetes at baseline. Multivariable Cox analysis controlling for sex, family history of pancreatic cancer, BMI, smoking status, alcohol consumption, education, income and other important covariates, and with age as the timescale was used. Results: Totally, 265 incident pancreatic cancer cases were observed. Pancreatic cancer risk was increased among those with diabetes (HR 1.54, CI 1.16–2.05), with similar increases among African Americans (HR 1.51, CI 1.08–2.11) and Whites (HR 1.78, CI 1.00–3.16). No trend in risk was observed for diabetes duration among those with diabetes, with HRs of 1.39 (0.91–2.11), 2.31 (1.51–3.54) and 1.23 (0.80–1.89) for <5, 5–9 and 10+ years duration, respectively. African Americans were at increased risk of pancreatic cancer (HR = 1.40, 95% CI 1.05–1.87), which persisted after adjusting for diabetes (HR 1.36, CI 1.02–1.81). The effect sizes for other pancreatic cancer risk factors with pancreatic cancer were similar by diabetes status, although a stronger association with low BMI was evident among those with diabetes. Conclusions: Diabetes increases pancreatic cancer risk similarly among African Americans and Whites in this Southern U.S. cohort. [ABSTRACT FROM AUTHOR]

Background: The feasibility of precision smoking treatment in socioeconomically disadvantaged communities has not been studied. Methods: Participants in the Southern Community Cohort Study who smoked daily were invited to join a pilot randomized controlled trial of three smoking cessation interventions: guideline-based care (GBC), GBC plus nicotine metabolism-informed care (MIC), and GBC plus counseling guided by a polygenic risk score (PRS) for lung cancer. Feasibility was assessed by rates of study enrollment, engagement, and retention, targeting > 70% for each. Using logistic regression, we also assessed whether feasibility varied by age, sex, race, income, education, and attitudes toward precision smoking treatment. Results: Of 92 eligible individuals (79.3% Black; 68.2% with household income < $15,000), 67 (72.8%; 95% CI 63.0–80.9%) enrolled and were randomized. Of these, 58 (86.6%; 95% CI 76.4–92.8%) engaged with the intervention, and of these engaged participants, 43 (74.1%; 95% CI 61.6–83.7%) were retained at 6-month follow-up. Conditional on enrollment, older age was associated with lower engagement (OR 0.83, 95% CI 0.73–0.95, p = 0.008). Conditional on engagement, retention was significantly lower in the PRS arm than in the GBC arm (OR 0.18, 95% CI 0.03–1.00, p = 0.050). No other selection effects were observed. Conclusions: Genetically informed precision smoking cessation interventions are feasible in socioeconomically disadvantaged communities, exhibiting high enrollment, engagement, and retention irrespective of race, sex, income, education, or attitudes toward precision smoking treatment. Future smoking cessation interventions in this population should take steps to engage older people and to sustain participation in interventions that include genetic risk counseling. Trial registration: ClinicalTrials.gov No. NCT03521141, Registered 27 April 2018, https://www.clinicaltrials.gov/study/NCT03521141 [ABSTRACT FROM AUTHOR]

Background: Although tobacco smoking is the leading cause of lung cancer, interest in the relationship of diet quality on risk has been growing. Methods: We examined the association between Healthy Eating Index-2010 (HEI-10) at enrollment and lung cancer incidence among 70,802 participants in a predominantly African American and low-income prospective cohort in the southern United States. Outcomes were ascertained through linkages with state cancer registries and the National Death Index (NDI). Hazard ratios by HEI-10 quartiles were assessed using Cox proportional hazard models adjusted for potential confounders. Results: During ≤16 years of follow-up, 1454 incident lung cancers were identified. The lowest HEI-10 quartile compared to the highest was adversely associated with lung cancer risk (HR: 1.89, 95% CI 1.16–3.07) among male former smokers and female never smokers (HR: 2.58, 95% CI 1.06–6.28). Conclusions: Low-quality diet was associated with increased lung cancer risk among male former smokers and female never smokers but cautious interpretation of the findings should be taken due to the small number of lung cancers among never smokers and the possibility of residual confounding by smoking in ever smokers. [ABSTRACT FROM AUTHOR]

To investigate how differences in income and education levels may contribute to disparities in incidence of Alzheimer's disease and related dementia (ADRD), we compared ADRD incidence in traditional Medicare claims for 11,132 Black and 7703 White participants aged 65 and over from a predominantly low-income cohort. We examined whether the relationship between ADRD incidence and race varied by income or education. Based on 2015 incident ADRD diagnoses, Black and White participants had unadjusted incidence rates of 26.5 and 23.2 cases per 1000 person-years, respectively (rate ratio 1.14, 95% CI 1.05–1.25). In multivariable Cox proportional hazard models, the relationship between race and incident ADRD diagnosis did not vary by education level (p-interaction = 0.748) but was modified by income level (p-interaction = 0.007), with higher ADRD incidence among Black participants observed only among higher income groups. These results highlight the importance of understanding how race and economic factors influence ADRD incidence and diagnosis rates. [ABSTRACT FROM AUTHOR]

Purpose: Physical activity (PA) is associated with many health benefits. While PA has been associated with reduced mortality after breast cancer diagnosis in many studies, few studies have examined the role of PA in breast cancer survival among underserved and minority populations, including Black women. We investigated PA in association with mortality among Black predominantly low-income breast cancer survivors in the Southern Community Cohort Study (SCCS). Methods: Study participants were women diagnosed with incident breast cancer (n = 949) in the SCCS, which is a prospective cohort study of predominantly low-income adults aged 40–79 years recruited from 12 Southeastern states between 2002 and 2009. Participants completed a detailed baseline questionnaire, with annual follow-up for mortality via registry linkages. Cox regression models were used to estimate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations of pre-diagnosis PA (measured via a validated questionnaire) with all-cause and breast cancer-specific mortality. Results: Breast cancer survivors had a mean age of 61.1 years and most (79.3%) had a household income of < $25,000. In adjusted models, higher levels of total PA (MET-hours/day) were inversely associated with all-cause mortality with HRs (95% CIs): 0.79 (0.59–1.06), 0.66 (0.49–0.90), and 0.60 (0.43–0.84), for Q2, Q3, and Q4 (reference: Q1), respectively, ptrend ≤ 0.01. A similar inverse association was found for breast cancer-specific mortality. Conclusion: Higher levels of pre-diagnosis PA were associated with improved survival among low-income Black breast cancer survivors. Resources to reduce barriers to PA participation and increase support for education and intervention efforts to promote PA among Black women are needed. [ABSTRACT FROM AUTHOR]

Simple Summary: Lung cancer is the second most common cancer and the leading cause of cancer death in the U.S. It is critical to identify the risk factors for lung cancer. However, previous results on the associations of dietary carotenoids and vitamin A intakes with lung cancer risk were inconclusive, and the study populations were mainly European descendants and Asians. This study aimed to prospectively investigate the associations among low-income African Americans and European Americans using resources from the Southern Community Cohort Study. Our findings suggested positive associations between dietary vitamin A intake and lung cancer risk among current smokers and racial-specific associations between dietary vitamin A intake and adenocarcinoma risk. Our study may contribute to understanding the role of nutrient intakes and lung cancer associations among the underrepresented study populations and improving the risk assessment of lung cancer risk. Observational studies found inverse associations of dietary carotenoids and vitamin A intakes with lung cancer risk. However, interventional trials among high-risk individuals showed that β-carotene supplements increased lung cancer risk. Most of the previous studies were conducted among European descendants or Asians. We prospectively examined the associations of lung cancer risk with dietary intakes of carotenoids and vitamin A in the Southern Community Cohort Study, including 65,550 participants with 1204 incident lung cancer cases. Multivariate Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Lung cancer cases had lower energy-adjusted dietary intakes of all carotenoids and vitamin A than non-cases. However, dietary intakes of carotenoids and vitamin A were not associated with overall lung cancer risk. A significant positive association of dietary vitamin A intake with lung cancer risk was observed among current smokers (HRQ4 vs. Q1 = 1.23; 95% CI: 1.02–1.49; Ptrend = 0.01). In addition, vitamin A intake was associated with an increased risk of adenocarcinoma among African Americans (HRQ4 vs. Q1 = 1.55; 95%CI: 1.08–2.21; Ptrend = 0.03). Dietary lycopene intake was associated with an increased risk of lung cancer among former smokers (HRQ4 vs. Q1 = 1.50; 95% CI: 1.04–2.17; Ptrend = 0.03). There are positive associations of dietary β-cryptoxanthin intake with squamous carcinoma risk (HRQ4 vs. Q1 = 1.49; 95% CI: 1.03–2.15; Ptrend = 0.03). Further studies are warranted to confirm our findings. [ABSTRACT FROM AUTHOR]

Background: A ban on the sale of menthol cigarettes in the United States is currently under consideration. A justification is that menthol cigarettes are harder to quit, particularly for African American smokers who use menthols much more frequently than White smokers, but epidemiologic data are limited.Methods: In a cohort of 16 425 mostly low-income African American and White current cigarette smokers enrolled during 2002-2009, we computed smoking quit and reuptake rates at 3 follow-ups conducted means of 4.6, 7.7, and 11 years after entry. Generalized estimation equations were used to compute odds ratios (ORs) and 95% confidence intervals (CIs) for quitting and resuming smoking for menthol vs nonmenthol smokers adjusted for race, age, education, income, and smoking pack-years.Results: Crude annual quit rates among current smokers were 4.3% for menthol and 4.5% for nonmenthol smokers, with adjusted odds ratios of quitting for menthol vs nonmenthol smokers of 1.01 (95% CI = 0.91 to 1.11) overall, 0.99 (95% CI = 0.87 to 1.12) among African American smokers, and 1.02 (95% CI = 0.88 to 1.20) among White smokers. Crude annual smoking reuptake rates were somewhat higher among menthol smokers (8.4%) than nonmenthol smokers (7.1%), with an adjusted odds ratio of 1.19 (95% CI = 0.97 to 1.47), but net quit rates remained similar (OR = 1.01, 95% CI = 0.90 to 1.13 overall; OR = 1.00, 95% CI = 0.86 to 1.15 among African American participants; and OR = 1.04, 95% CI = 0.87 to 1.24 among White participants).Conclusions: This large-scale prospective survey revealed similar quit rates among menthol and nonmenthol smokers. Results contribute to policy discussions, especially if, as a meta-analysis suggests, lung cancer risk is higher for nonmenthol smokers and a ban leads menthol smokers to switch to nonmenthol cigarettes. [ABSTRACT FROM AUTHOR]

Background: Previous studies conducted among European and Asian decedents reported inverse associations of serum total bilirubin and albumin with lung cancer risk. Yet, no study has been conducted among African Americans or low-income European Americans. Methods: This study included 522 incident lung cancer cases and 979 matched controls nested in the Southern Community Cohort Study, a cohort of predominantly low-income African and European Americans. Serum levels of total bilirubin and albumin, collected up to 11 years prior to case diagnoses, were measured by a clinical chemistry analyzer. Conditional logistic regression models were applied to evaluate the associations of total bilirubin and albumin with lung cancer risk. Results: Overall, serum levels of total bilirubin (ORT3 vs. T1 = 0.96, 95% CI: 0.66-1.39) were not significantly associated with lung cancer risk. However, higher levels of serum total bilirubin were significantly associated with decreased risk of lung cancer among participants who were diagnosed within two years following sample collection (ORT3 vs. T1 = 0.36, 95% CI: 0.15-0.87) and among former/never smokers (ORT3 vs. T1 = 0.54, 95% CI: 0.32-0.93). Serum levels of albumin were significantly associated with decreased risk of lung cancer overall (ORT3 vs. T1 = 0.70, 95% CI: 0.50-0.98) and among African Americans (ORT3 vs. T1 = 0.62, 95% CI: 0.41-0.96), but not among European Americans. Conclusion: Our results indicate that in a low-income African American and European American population, serum levels of total bilirubin may be related to lung cancer progression and differ by smoking status. Meanwhile, the association of serum albumin levels with lung cancer risk may differ by race. Further studies are warranted to confirm these results. [ABSTRACT FROM AUTHOR]

Helicobacter pylori infection has been suggested to be associated with lung cancer risk. However, information is lacking on whether the association differs by H. pylori antigen. We conducted a nested case-control study within the Southern Community Cohort Study, including 295 incident lung cancer cases and 295 controls. Helicobacter pylori multiplex serology assay was performed to detect antibodies to 15 H. pylori proteins. Conditional logistic regression was used to estimate odds ratios (ORs) and confidence intervals (95% CIs) after adjustment for covariates. Overall H. pylori + was associated with a non-statistically significant increased risk of lung cancer (OR: 1.29; 95% CI: 0.85–1.95). Significant associations, however, were observed for H. pylori + VacA+ (OR: 1.64; 95% CI: 1.02–2.62) and H. pylori + Catalase+ (OR: 1.75; 95% CI: 1.11–2.77). The positive association of H. pylori + Catalase+ with lung cancer risk was predominantly seen among African Americans (OR: 2.09; 95% CI: 1.11–3.95) but not European Americans (OR: 1.20; 95% CI: 0.56–2.54). Among participants who smoked ≥ 30 pack-years, overall H. pylori + (OR: 1.85; 95% CI: 1.02–3.35), H. pylori + CagA+ (OR: 2.77; 95% CI: 1.35–5.70), H. pylori + VacA+ (OR: 2.53; 95% CI: 1.25–5.13) and H. pylori + HP1564+ (OR: 2.01; 95% CI: 1.07–3.77) were associated with increased risk of lung cancer. Our study provides novel evidence that associations of H. pylori infection with lung cancer risk differ by H. pylori biomarker, may be more evident among African Americans and may be modified by smoking habits. Furthermore, studies are warranted to confirm our findings. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the association between obesity and the relative prevalence of tumor subtypes among Black women with breast cancer (BC). Methods: We conducted a pooled case-only analysis of 1,793 Black women with invasive BC recruited through three existing studies in the southeastern US. Multivariable case-only polytomous logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between obesity, measured by pre-diagnostic body mass index (BMI), and human epidermal growth factor receptor 2 + (HER2 +) and triple negative BC (TNBC) subtype relative to hormone receptor (HR) + /HER2- status (referent). Results: Among 359 premenopausal women, 55.4% of cases were HR + /HER2 −, 20.1% were HER2 + , and 24.5% were TNBC; corresponding percentages among 1,434 postmenopausal women were 59.3%, 17.0%, and 23.6%. Approximately, 50–60% of both pre- and postmenopausal women were obese (BMI > 30 kg/m2), regardless of BC subtype. We did not observe a significant association between obesity and BC subtype. Among postmenopausal women, class I obesity (BMI 35 + kg/m2) was not associated with the development of HER2 + BC (OR 0.69; 95% CI 0.42–1.14) or TNBC (OR 0.93; 95% CI 0.60–1.45) relative to HR + /HER2- tumors. Corresponding estimates among premenopausal women were 1.03 (95% CI 0.43–2.48) and 1.13 (95% CI 0.48–2.64). Conclusion: In this large study of Black women with BC, there was no evidence of heterogeneity of BMI by BC subtype. [ABSTRACT FROM AUTHOR]

The risk of mesothelioma, including cancers of the pleura and peritoneum, was examined within two large cohorts of workers monitored for exposure to ionizing radiation. Mortality was assessed among 253,632 workers routinely monitored for external radiation, including 30,724 industrial radiographers (IR) at shipyards, 142,583 workers at nuclear power plants (NPP), and 83,441 IR who had not worked at an NPP or shipyard. Follow-up was from 1969 through 2011. Standardized mortality ratios (SMRs) and 95% confidence intervals (CIs) were computed; observed numbers of deaths from mesothelioma (including cancers of the pleura and peritoneum) and asbestosis were compared with numbers expected based on age-, sex-, and calendar year-specific national mortality rates. Job history and quantitative asbestos exposure data were unavailable, but work at a shipyard was taken as a surrogate for the likelihood of exposure. Cox proportional hazards models were used to estimate hazard ratios (HRs) for mesothelioma in relation to estimated cumulative radiation exposure to the lung. The mean duration of follow-up was 25.3 years (max 42 years). The mean cumulative lung dose was 28.6 mGy (7.3% > 250 mGy). Nearly 20% of the workers had died by 2011. A total of 421 mesothelioma deaths were found (75% occurring after 1999) with increased SMRs among workers monitored in shipyards (SMR 9.97; 95% CI 8.50–11.63) and for NPP workers (SMR 5.55; 95% CI 4.88–6.29), but not for IR who had not worked in shipyards (SMR 1.15; 95% CI 0.53–2.19). Likewise, deaths from asbestosis (n = 189) were also increased for shipyard and NPP workers (SMR = 18.1 and 9.2, respectively), but not among workers who never worked at a shipyard or NPP (SMR = 0.70; n = 1). Radiation dose to the lung was not associated with a statistically meaningful dose-response trend for mesothelioma in the combined cohorts (HR at 100 mGy = 1.10; 95% CI 0.96–1.27; p =.18), nor was mesothelioma risk associated with radiation exposure among IR who had not worked in a shipyard and assumed minimally exposed to asbestos. An elevated rate of death from mesothelioma was observed in two radiation-exposed occupational groups with potential for asbestos exposure. The increased risk of death from asbestosis, combined with little evidence of a rising trend in mesothelioma mortality with increasing radiation exposure, suggests that the mesothelioma (and asbestosis) excess in these workers was due to asbestos exposure in shipyards and power plants and not to occupational low-dose radiation. [ABSTRACT FROM AUTHOR]

Colonization of specific bacteria in the human mouth was reported to be associated with gastric cancer risk. However, previous studies were limited by retrospective study designs and low taxonomic resolutions. We performed a prospective case‐control study nested within three cohorts to investigate the relationship between oral microbiome and gastric cancer risk. Shotgun metagenomic sequencing was employed to characterize the microbiome in prediagnostic buccal samples from 165 cases and 323 matched controls. Associations of overall microbial richness and abundance of microbial taxa, gene families and metabolic pathways with gastric cancer risk were evaluated via conditional logistic regression. Analyses were performed within each cohort, and results were combined by meta‐analyses. We found that overall microbial richness was associated with decreased gastric cancer risk, with an odds ratio (OR) per standard deviation (SD) increase in Simpson's reciprocal index of 0.77 (95% confidence interval [CI] = 0.61‐0.99). Nine taxa, 38 gene families and six pathways also showed associations with gastric cancer risk at P <.05. Neisseria mucosa and Prevotella pleuritidis were enriched, while Mycoplasma orale and Eubacterium yurii were depleted among cases with ORs and 95% CIs per SD increase in centered log‐ratio transformed taxa abundance of 1.31 (1.03‐1.67), 1.26 (1.00‐1.57), 0.74 (0.59‐0.94) and 0.80 (0.65‐0.98), respectively. The top two gene families (P = 3.75 × 10−4 and 3.91 × 10−4) and pathways (P = 1.75 × 10−3 and 1.53 × 10−3) associated with gastric cancer were related to the decreased risk and are involved in hexitol metabolism. Our study supports the hypothesis that oral microbiota may play a role in gastric cancer etiology. What's new? Previous studies of oral microbiome and gastric cancer risk were mainly conducted in Asians and were limited by retrospective designs and low taxonomic resolutions. This study is the first multi‐racial study to prospectively investigate the relationship between oral microbiome and gastric cancer risk, utilizing shotgun metagenomic sequencing to assess the microbiome in pre‐diagnostic buccal samples. Decreased overall microbial richness, altered abundance of several microbial taxa, and multiple microbial functional markers were found to be associated with gastric cancer risk. The study supports the hypothesis that oral microbiota may play a role in gastric cancer etiology. [ABSTRACT FROM AUTHOR]

Purpose: Oral microbiome plays an important role in oral health and systemic diseases, including cancer. We aimed to prospectively investigate the association of oral microbiome with lung cancer risk. Methods: We analyzed 156 incident lung cancer cases (73 European Americans and 83 African Americans) and 156 individually matched controls nested within the Southern Community Cohort Study. Oral microbiota were assessed using 16S rRNA gene sequencing in pre-diagnostic mouth rinse samples. Paired t test and the permutational multivariate analysis of variance test were used to evaluate lung cancer risk association with alpha diversity or beta diversity, respectively. Conditional logistic regression models were used to evaluate the association of individual bacterial abundance or prevalence with lung cancer risk. Results: No significant differences were observed for alpha or beta diversity between lung cancer cases and controls. Abundance of families Lachnospiraceae_[XIV], Peptostreptococcaceae_[XI], and Erysipelotrichaceae and species Parvimonas micra was associated with decreased lung cancer risk, with odds ratios (ORs) and 95% confidence intervals (CIs) of 0.76 (0.59–0.98), 0.80 (0.66–0.97), 0.81 (0.67–0.99), and 0.83 (0.71–0.98), respectively (all p < 0.05). Prevalence of five pre-defined oral pathogens were not significantly associated with overall lung cancer risk. Prevalence of genus Bacteroidetes_[G-5] and species Alloprevotella sp._oral_taxon_912, Capnocytophaga sputigena, Lactococcus lactis, Peptoniphilaceae_[G-1] sp._oral_taxon_113, Leptotrichia sp._oral_taxon_225, and Fretibacterium fastidiosum was associated with decreased lung cancer risk, with ORs and 95% CIs of 0.55 (0.30–1.00), 0.36 (0.17–0.73), 0.53 (0.31–0.92), 0.43 (0.21–0.88), 0.43 (0.19–0.94), 0.57 (0.34–0.99), and 0.54 (0.31–0.94), respectively (all p < 0.05). Species L. sp._oral_taxon_225 was significantly associated with decreased lung cancer risk in African Americans (OR [95% CIs] 0.28 [0.12–0.66]; p = 0.00012). Conclusion: Results from this study suggest that oral microbiota may play a role in the development of lung cancer. [ABSTRACT FROM AUTHOR]

Background: The history of gestational diabetes mellitus (GDM) has been associated with breast cancer risk in some studies, particularly in young women, but results of cohort studies are conflicting.Methods: We pooled data from 257 290 young (age <55 years) women from five cohorts. We used multivariable Cox proportional-hazards regression to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between GDM history and risk of breast cancer, overall and by oestrogen receptor (ER) status, before age 55 years, adjusted for established breast cancer risk factors.Results: Five percent of women reported a history of GDM and 6842 women reported an incident breast-cancer diagnosis (median follow-up = 16 years; maximum = 24 years). Compared with parous women without GDM, women with a history of GDM were not at increased risk of young-onset breast cancer overall (HR = 0.90; 95% CI: 0.78, 1.03) or by ER status (HR = 0.96; 95% CI: 0.79, 1.16 for ER-positive; HR = 1.07; 95% CI: 0.78, 1.47 for ER-negative). Compared with nulliparous women, parous women with a history of GDM had a lower risk of breast cancer overall (HR = 0.79; 95% CI: 0.68, 0.91) and of ER-positive (HR = 0.82; 95% CI: 0.66, 1.02) but not ER-negative (HR = 1.09; 95% CI: 0.76, 1.54) invasive breast cancer. These results were consistent with the HRs comparing parous women without GDM to nulliparous women.Conclusions: Results of this analysis do not support the hypothesis that GDM is a risk factor for breast cancer in young women. Our findings suggest that the well-established protective effect of parity on risk of ER-positive breast cancer persists even for pregnancies complicated by GDM. [ABSTRACT FROM AUTHOR]

There is limited evidence on the association between red meat consumption and pancreatic cancer among ethnic minorities. We assessed this relationship in two large prospective cohorts: the Multiethnic Cohort Study (MEC) and the Southern Community Cohort Study (SCCS). Demographic, dietary and other risk factor data were collected at cohort entry. Red meat intake was assessed using cohort‐specific validated food frequency questionnaires. Incident pancreatic cancer cases were identified via linkages to state cancer registries. Cox regression was used to calculate relative risks (RRs) and 95% confidence intervals (CIs) for the association of red meat intake with pancreatic cancer risk in each cohort. We performed additional analyses to evaluate cooking methods, mutagens and effect modification by NAT1/2 genotypes. From a total of 184 542 (MEC) and 66 793 (SCCS) at‐risk participants, we identified 1618 (MEC) and 266 (SCCS) incident pancreatic cancer cases. Red meat consumption was associated with pancreatic cancer risk in the MEC (RRQ4vsQ1 1.18, 95% CI 1.02‐1.37) and with borderline statistical significance in the SCCS (RRQ4vsQ1 1.31, 95% CI 0.93‐1.86). This association was significant in African Americans (RRQ4vsQ1 1.49, 95% CI 1.06‐2.11) and Latinos (RRQ4vsQ1 1.44, 95% CI 1.02‐2.04) in the MEC, and among African Americans (RRQ4vsQ1 1.55, 95% CI 1.03‐2.33) in the SCCS. NAT2 genotypes appeared to modify the relationship between red meat and pancreatic cancer in the MEC (pinteraction = 0.03). Our findings suggest that the associations for red meat may be strongest in African Americans and Latinos. The mechanisms underlying the increased risk for these populations should be further investigated. What's new? Studies in white populations indicate that eating red meat may boost pancreatic cancer risk. These authors investigated this association in ethnic minorities in the US. They also looked at cooking methods, mutagens such as heterocyclic aromatic amines (HAAs), and genetic variants in the enzymes N‐acetyltransferase 1/2 (NAT1/2), which impact a person's ability to neutralize these mutagens. By analyzing data from two large ethnically diverse cohorts, they found a significant association between red meat consumption and pancreatic cancer in African Americans and Latinos. They also found that NAT2 genotypes may play a role in this association. [ABSTRACT FROM AUTHOR]

Associations of coffee and tea consumption with lung cancer risk have been inconsistent, and most lung cancer cases investigated were smokers. Included in this study were over 1.1 million participants from 17 prospective cohorts. Cox regression analyses were conducted to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Potential effect modifications by sex, smoking, race, cancer subtype and coffee type were assessed. After a median 8.6 years of follow-up, 20 280 incident lung cancer cases were identified. Compared with noncoffee and nontea consumption, HRs (95% CIs) associated with exclusive coffee drinkers (≥2 cups/d) among current, former and never smokers were 1.30 (1.15-1.47), 1.49 (1.27-1.74) and 1.35 (1.15-1.58), respectively. Corresponding HRs for exclusive tea drinkers (≥2 cups/d) were 1.16 (1.02-1.32), 1.10 (0.92-1.32) and 1.37 (1.17-1.61). In general, the coffee and tea associations did not differ significantly by sex, race or histologic subtype. Our findings suggest that higher consumption of coffee or tea is associated with increased lung cancer risk. However, these findings should not be assumed to be causal because of the likelihood of residual confounding by smoking, including passive smoking, and change of coffee and tea consumption after study enrolment [ABSTRACT FROM AUTHOR]

Purpose: Long intergenic non-coding RNAs (lincRNAs) are increasingly recognized as important regulators for pathogenesis and/or prognosis of breast cancer, including triple-negative breast cancer (TNBC) subtype. However, few previous studies used RNA-sequencing (RNA-Seq) technology, and none included an independent replication. Methods: To systematically evaluate the association between expression of lincRNAs and TNBC survival, we examined lincRNA expression profiles in TNBC tissues using RNA-Seq data for 200 TNBC patients from the Shanghai Breast Cancer Survival Study (SBCSS) and Southern Community Cohort Study (SCCS). Results: Twenty-five lincRNAs were found to be associated with overall survival (P < 0.05 and no significant heterogeneity across studies at Q statistic P > 0.1), and 61 lincRNAs were associated with disease-free survival (DFS). Among these, two lincRNAs (LINC01270 and LINC00449) were significantly associated with both worse overall survival and DFS and were expressed at significantly higher levels in tumor tissues compared with adjacent normal breast tissues (log2[Fold Change] > 0.5 and FDR < 0.05). We further evaluated the potential functions of LINC01270 and LINC00449 using in vitro functional experiments and found that siRNA-mediated knockdown of LINC01270 and LINC00449 expression significantly decreased cell viability, colony formation and cell migration ability in TNBC cells (P < 0.05). Conclusions: Evidence from observational studies and in vitro experiments indicates that LINC00449 and LINC01270 may be prognostic biomarkers for TNBC. [ABSTRACT FROM AUTHOR]

Background: Coenzyme Q10 (CoQ10) is a ubiquitous molecule in living organisms serving as a cofactor in energy production. Epidemiological studies have reported low CoQ10 levels being associated with an increased risk of various cancers. We conducted the first study to evaluate the association of CoQ10 concentrations with lung cancer risk. Methods: A nested case‐control study including 201 lung cancer cases and 395 matched controls from the Southern Community Cohort Study was conducted. Plasma CoQ10 levels were measured using high‐performance liquid chromatography with photo‐diode array detection. Conditional logistic regression models were applied to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between plasma CoQ10 levels and lung cancer risk. Results: Plasma CoQ10 concentration was inversely associated with the risk of lung cancer. After adjusting for age, sex, race, and socioeconomic status, the OR (95% CI) comparing the third to first tertile was 0.57 (0.36–0.91, P for trend = 0.02). Further adjustments for smoking, alcohol, chronic obstructive pulmonary disease, and body mass index attenuated the point estimate slightly (OR = 0.60, 95% CI = 0.34–1.08, P for trend = 0.11), comparing third to first tertiles. Stratified analyses identified a significant inverse association between plasma CoQ10 levels and lung cancer risk in current smokers, but not in former/never smokers. The association was more evident in cases who were diagnosed within 1 year of blood draw than in cases diagnosed after 1 year. Conclusions: Low plasma CoQ10 was significantly associated with increased lung cancer risk, particularly among current smokers. The stronger association seen shortly following the blood draw suggests that CoQ10 may be related to disease progression. [ABSTRACT FROM AUTHOR]

Polygenic hazard score (PHS) models are associated with age at diagnosis of prostate cancer. Our model developed in Europeans (PHS46) showed reduced performance in men with African genetic ancestry. We used a cross‐validated search to identify single nucleotide polymorphisms (SNPs) that might improve performance in this population. Anonymized genotypic data were obtained from the PRACTICAL consortium for 6253 men with African genetic ancestry. Ten iterations of a 10‐fold cross‐validation search were conducted to select SNPs that would be included in the final PHS46+African model. The coefficients of PHS46+African were estimated in a Cox proportional hazards framework using age at diagnosis as the dependent variable and PHS46, and selected SNPs as predictors. The performance of PHS46 and PHS46+African was compared using the same cross‐validated approach. Three SNPs (rs76229939, rs74421890 and rs5013678) were selected for inclusion in PHS46+African. All three SNPs are located on chromosome 8q24. PHS46+African showed substantial improvements in all performance metrics measured, including a 75% increase in the relative hazard of those in the upper 20% compared to the bottom 20% (2.47‐4.34) and a 20% reduction in the relative hazard of those in the bottom 20% compared to the middle 40% (0.65‐0.53). In conclusion, we identified three SNPs that substantially improved the association of PHS46 with age at diagnosis of prostate cancer in men with African genetic ancestry to levels comparable to Europeans. What's new? Polygenic models can provide personalized estimates of cancer risk. However, Africans are a population generally under‐served in genome‐wide studies. In this report, the authors used machine learning to identify three SNPs that significantly improved the performance of an established polygenic‐hazard model of prostate‐cancer risk vs age at diagnosis, specifically tailored to men of African genetic ancestry. Inclusion of these SNPs improved the performance of this novel 'PHS46+African' score by as much as 79% compared to the original model, to levels comparable with Europeans. [ABSTRACT FROM AUTHOR]

Purpose: Diets with a high glycemic load (GL) or glycemic index (GI) may increase cancer risk. Findings from prior studies on the relationship between GL, GI, and lung cancer risk are inconsistent. We investigated this relationship in a large prospective cohort. Methods: We analyzed data from the Southern Community Cohort Study, a prospective cohort that includes diverse racial groups predominantly low-income adults aged 40–79 in 12 southeastern states of the USA. We estimated dietary GL and GI values using data collected from food frequency questionnaires at baseline. Dietary GL and GI were energy adjusted by residual method and categorized into sex-specific quintiles. Cox proportional hazard regression was used to assess the associations between dietary GL, GI, and lung cancer risk. We further performed stratified analyses by various factors. Results: Intakes of individual food items or food groups that commonly contribute to GL were similar between blacks and whites in the cohort. After excluding the first two years of follow-up, 947 incident lung cancers were ascertained among 55,068 participants. Neither dietary GL nor GI was significantly associated with incident lung cancer risk in the overall population (GL: Q5 vs. Q1, HR = 0.88, 95% CI 0.72–1.07, ptrend = 0.29; GI: Q5 vs. Q1, HR = 1.06, 95% CI 0.86–1.30, ptrend = 0.71), nor in subgroups of populations (ptrend > 0.05), in multivariable-adjusted analyses. Conclusion: Dietary GL and GI were not independently associated with incident lung cancer risk in a large understudied population. [ABSTRACT FROM AUTHOR]

Previously, we found that risk of colorectal cancer (CRC) is increased in individuals with serum antibody response to both Helicobacter pylori (HP) Vacuolating Cytotoxin (VacA) toxin or Streptococcus gallolyticus (SGG) pilus protein Gallo2178. In the present analysis, we tested the hypothesis that combined seropositivity to both antigens is a better indicator of CRC risk than seropositivity to single antigens. We used multiplex serologic assays to analyze pre-diagnostic serum for antibody responses from 4063 incident CRC cases and 4063 matched controls from 10 US cohorts. To examine whether combined SGG Gallo2178 and HP VacA sero-status was associated with CRC risk, we used conditional logistic regression models to estimate odds ratios (ORs) and 95% confidence intervals (CIs). Compared to dual sero-negative individuals, there was no increased risk for individuals sero-positive to SGG Gallo2178 only (OR: 0.93; 95% CI: 0.66–1.31) or to HP VacA only (OR: 1.08; 95% CI: 0.98–1.19). However, dual sero-positive individuals had a >50% increased odds of developing CRC (OR: 1.54; 95% CI: 1.16–2.04), suggesting an interaction between antibody responses to these two pathogens and CRC risk (pinteraction = 0.06). In conclusion, this study suggests that dual sero-positivity to HP VacA and SGG Gallo2178 is an indicator of increased risk of CRC. [ABSTRACT FROM AUTHOR]

Purpose: Helicobacter pylori (H. pylori) is the leading cause of gastric cancer. High antibody levels to H. pylori virulence factors Vacuolating cytotoxin A (VacA) and Cytotoxin-associated gene A (CagA) have been suggested as gastric cancer risk markers. In the USA, H. pylori sero-prevalence is twofold higher in African Americans compared to whites. We sought to assess whether African Americans also exhibit higher antibody levels to VacA and CagA.Methods: Antibody responses to H. pylori proteins were measured by multiplex serology in 686 African Americans and whites of the Southern Community Cohort Study. Among VacA- and CagA-seropositives, we analyzed the association of race with antibody level using logistic regression models to produce odds ratios (OR) and 95% confidence intervals (CI).Results: Sero-positive African Americans had significantly higher mean antibody levels to both VacA and CagA, which resulted in increased odds for the highest quartile of antibody levels compared to sero-positive whites (VacA, OR: 6.08; 95% CI 3.41, 10.86; CagA, OR: 3.77; 95% CI 1.61, 8.84).Conclusion: Our findings support future studies to assess the association of differential antibody responses by race with risk of gastric cancer in the USA, which could then aid in developing targeted H. pylori eradication strategies. [ABSTRACT FROM AUTHOR]

Cell‐mediated immune suppression may play an important role in lung carcinogenesis. We investigated the associations for circulating levels of tryptophan, kynurenine, kynurenine:tryptophan ratio (KTR), quinolinic acid (QA) and neopterin as markers of immune regulation and inflammation with lung cancer risk in 5,364 smoking‐matched case–control pairs from 20 prospective cohorts included in the international Lung Cancer Cohort Consortium. All biomarkers were quantified by mass spectrometry‐based methods in serum/plasma samples collected on average 6 years before lung cancer diagnosis. Odds ratios (ORs) and 95% confidence intervals (CIs) for lung cancer associated with individual biomarkers were calculated using conditional logistic regression with adjustment for circulating cotinine. Compared to the lowest quintile, the highest quintiles of kynurenine, KTR, QA and neopterin were associated with a 20–30% higher risk, and tryptophan with a 15% lower risk of lung cancer (all ptrend < 0.05). The strongest associations were seen for current smokers, where the adjusted ORs (95% CIs) of lung cancer for the highest quintile of KTR, QA and neopterin were 1.42 (1.15–1.75), 1.42 (1.14–1.76) and 1.45 (1.13–1.86), respectively. A stronger association was also seen for KTR and QA with risk of lung squamous cell carcinoma followed by adenocarcinoma, and for lung cancer diagnosed within the first 2 years after blood draw. This study demonstrated that components of the tryptophan–kynurenine pathway with immunomodulatory effects are associated with risk of lung cancer overall, especially for current smokers. Further research is needed to evaluate the role of these biomarkers in lung carcinogenesis and progression. What's new? The kynurenine pathway, by which tryptophan is degraded and NAD+ is synthesized, plays a role in inflammation and immune response. It may also be involved in cancer development and progression. Here, the authors investigated the relationship between the metabolites of the kynurenine pathway and risk of lung cancer. They found that lower levels of tryptophan and higher levels of kynurenine and quinolinic acid were associated with increased risk of lung cancer, especially in smokers. These biomarkers may be signs that immune suppression in the tumor microenvironment may boost cancer progression. [ABSTRACT FROM AUTHOR]

Purpose: We prospectively examined associations of lung cancer risk with food intake of B vitamins involved in one-carbon metabolism and the use of folic acid-containing supplements among a low-income population of black and white adults in the Southeastern US. Methods: Within the Southern Community Cohort Study, we included 1064 incident lung cancer cases among 68,236 participants aged 40–79 years at study enrollment. Food intake and the use of folic acid-containing supplements were assessed using a validated food frequency questionnaire at study enrollment. Multivariate Cox regression was used to estimate hazards ratios (HRs) and the 95% confidence intervals (CIs). Results: Folate and/or folic acid intake from food were not associated with lung cancer risk; HRs (95% CI) for highest compared with lowest quartile were 1.08 (0.91–1.29) for total dietary folate, 1.00 (0.84–1.19) for food folate, and 1.09 (0.91–1.30) for food folic acid, respectively. Similarly, no associations were observed after stratifying by sex, race and smoking status, except for a positive association with total dietary folate intake among black women (HR 1.46, 95% CI 1.04–2.05 for the highest quartile compared with the lowest quartile, P trend = 0.02). Neither the use of folic acid-containing supplements nor food intake of vitamin B6, vitamin B12 and riboflavin were associated with lung cancer risk. Conclusions: Our findings do not support a protective effect of folate or folic acid for lung cancer prevention in a low-income population of black and white adults in the Southeastern US. Our finding of a positive association with total dietary folate intake among black women needs to be interpreted with caution and replicated in other studies. [ABSTRACT FROM AUTHOR]

Background Breast cancer–related lymphedema (BCRL) is a well-known side effect of cancer and its treatment with wide-ranging prevalence estimates. Objective This study describes associations between breast cancer–related lymphedema (BCRL) signs, symptoms, and diagnosis for women who were African American, white, or had a low income and survived breast cancer. Design This is a cross-sectional, observational study that used a computer-assisted telephone interview. Methods Women who had survived breast cancer were queried on the presence of 5 lymphedema signs and symptoms (edema in the breast, axilla, arm, and/or hand; tissue fibrosis; pitting; hemosiderin staining; heaviness) and whether they had a diagnosis of BCRL. Relationships between signs/symptoms and diagnosis for each group were evaluated with kappa and chi-square statistics. Results The study sample included 528 women who had survived breast cancer (266 white and 262 African American), with 514 reporting complete data on household income; 45% of the latter reported an annual household income of ≤$20,000. Women who were African American or had a low income were nearly twice as likely as women who were white to have any of 8 signs/symptoms of BCRL. Regardless of race and income, >50% of women with all BCRL signs and symptoms reported that they were not diagnosed with BCRL. Limitations The main limitations of our study are the lack of medical chart data and longitudinal design. Conclusions Women who were African American or had a low income and had survived breast cancer had a greater burden of BCRL signs and symptoms than women who were white. The lack of a strong association between BCRL signs, symptoms, and diagnosis suggests that BCRL may be underdiagnosed. These findings suggest that more rigorous screening and detection of BCRL—especially for women who are African American or have a low income—may be warranted. Cancer rehabilitation programs may be able to fill this gap. [ABSTRACT FROM AUTHOR]

Background Choline-related nutrients are dietary precursors of a gut microbial metabolite, trimethylamine-N-oxide, which has been linked to cardiometabolic diseases and related death. However, epidemiologic evidence on dietary choline and mortality remains limited, particularly among nonwhite populations. Objectives This study aimed to investigate the associations of choline-related nutrients with cardiometabolic and all-cause mortality among black and white Americans and Chinese adults. Methods Included were 49,858 blacks, 23,766 whites, and 134,001 Chinese, aged 40–79 y, who participated in 3 prospective cohorts and lived ≥1 y after enrollment. Cox regression models were used to estimate HRs and 95% CIs for cardiometabolic [e.g., ischemic heart disease (IHD), stroke, and diabetes] and all-cause deaths. To account for multiple testing, P values < 0.003 were considered significant. Results Mean choline intake among blacks, whites, and Chinese was 404.1 mg/d, 362.0 mg/d, and 296.8 mg/d, respectively. During a median follow-up of 11.7 y, 28,673 deaths were identified, including 11,141 cardiometabolic deaths. After comprehensive adjustments, including for overall diet quality and disease history, total choline intake was associated with increased cardiometabolic mortality among blacks and Chinese (HR for highest compared with lowest quintile: 1.26; 95% CI: 1.13, 1.40 and HR: 1.23; 95% CI: 1.11, 1.38, respectively; both P -trend < 0.001); among whites, the association was weaker (HR: 1.12; 95% CI: 0.95, 1.33; P -trend = 0.02). Total choline intake was also associated with diabetes and all-cause mortality in blacks (HR: 1.66; 95% CI: 1.26, 2.19 and HR: 1.20; 95% CI: 1.12, 1.29, respectively), with diabetes mortality in Chinese (HR: 2.24; 95% CI: 1.68, 2.97), and with IHD mortality in whites (HR: 1.31; 95% CI: 1.02, 1.69) (all P -trend < 0.001). The choline–mortality association was modified by alcohol consumption and appeared stronger among individuals with existing cardiometabolic disease. Betaine intake was associated with increased cardiometabolic mortality in Chinese only (HR: 1.16; 95% CI: 1.08, 1.25; P -trend < 0.001). Conclusions High choline intake was associated with increased cardiometabolic mortality in racially diverse populations. [ABSTRACT FROM AUTHOR]

Few studies have evaluated the relationship of oral microbiome with obesity. We investigated the oral microbiome among 647 obese and 969 non-obese individuals from the Southern Community Cohort Study, through 16S rRNA gene sequencing in mouth rinse samples. We first investigated 16 taxa in two probiotic genera, Bifidobacterium and Lactobacillus. Among them, eight showed nominal associations with obesity (P < 0.05). Especially, Bifidobacterium (odds ratio [OR] = 0.67, 95% confidence interval [CI]:0.54, 0.83) and Bifidobacterium longum (OR = 0.57, 95% CI: 0.45, 0.73) were significantly associated with decreased obesity prevalence with false-discovery rate (FDR)-corrected P of 0.01 and 5.41 × 10−4, respectively. Multiple other bacterial taxa were also significantly associated with obesity prevalence at FDR-corrected P < 0.05. Among them, five in Firmicutes and two respectively in Actinobacteria and Proteobacteria were significantly associated with increased obesity prevalence. Significant associations with decreased obesity prevalence were observed for two taxa respectively in Actinobacteria and Firmicutes. Most of these taxa were associated with body mass index at study enrollment and weight gain during adulthood. Also, most of these associations were observed in both European- and African-Americans. Our findings indicate that multiple oral bacterial taxa, including several probiotic taxa, were significantly associated with obesity. [ABSTRACT FROM AUTHOR]

Background: Low physical activity (PA) is linked to cancer and other diseases prevalent in racial/ethnic minorities and low-income populations. This study evaluated the PA questionnaire (PAQ) used in the Southern Cohort Community Study, a prospective investigation of health disparities between African-American and white adults. Methods: The PAQ was administered upon entry into the cohort (PAQ 1) and after 12-15 months (PAQ2) in 118 participants (40-60 year-old, 48% male, 74% African-American). Test-retest reliability (PAQ 1 versus PAQ2) was assessed using Spearman correlations and the Wilcoxon signed rank test. Criterion validity of the PAQ was assessed via comparison with a PA monitor and a last-month PA survey (LMPAS), administered up to 4 times in the study period. Results: The PAQ test-retest reliability ranged from 0.25-0.54 for sedentary behaviors and 0.22-0.47 for active behaviors. The criterion validity for the PAQ compared with PA monitor ranged from 0.21-0.24 for sedentary behaviors and from 0.17-0.31 for active behaviors. There was general consistency in the magnitude of correlations between the PAQ and PA-monitor between African-Americans and whites. Conclusions: The SCCS-PAQ has fair to moderate test-retest reliability and demonstrated some evidence of criterion validity for ranking participants by their level of sedentary and active behaviors. [ABSTRACT FROM AUTHOR]

In the article, the authors present their cohort study on the relationship between light at night (LAN) and incident breast cancer in African American and White women in the U.S. Topics include how LAN inhibits nighttime production of melatonin, the use of Cox proportional hazards models in estimating hazard ratios (HR) and 95% confidence intervals (CI), and the strong correlation between LAN and urbanization.

Vitamin B supplementation can have side effects for human health, including cancer risk. We aimed to elucidate the role of vitamin B12 in lung cancer etiology via direct measurements of pre‐diagnostic circulating vitamin B12 concentrations in a nested case–control study, complemented with a Mendelian randomization (MR) approach in an independent case–control sample. We used pre‐diagnostic biomarker data from 5183 case–control pairs nested within 20 prospective cohorts, and genetic data from 29,266 cases and 56,450 controls. Exposures included directly measured circulating vitamin B12 in pre‐diagnostic blood samples from the nested case–control study, and 8 single nucleotide polymorphisms associated with vitamin B12 concentrations in the MR study. Our main outcome of interest was increased risk for lung cancer, overall and by histological subtype, per increase in circulating vitamin B12 concentrations. We found circulating vitamin B12 to be positively associated with overall lung cancer risk in a dose response fashion (odds ratio for a doubling in B12 [ORlog2B12] = 1.15, 95% confidence interval (95%CI) = 1.06–1.25). The MR analysis based on 8 genetic variants also indicated that genetically determined higher vitamin B12 concentrations were positively associated with overall lung cancer risk (OR per 150 pmol/L standard deviation increase in B12 [ORSD] = 1.08, 95%CI = 1.00–1.16). Considering the consistency of these two independent and complementary analyses, these findings support the hypothesis that high vitamin B12 status increases the risk of lung cancer. What's new? Several B‐complex vitamins have been linked to cancer risk. In this study, high serum levels of vitamin B12 were associated with an increased risk of lung cancer. The authors first ran a nested case‐control study, then confirmed their findings using a Mendelian randomization approach based on genetic data from a much larger database including both lung‐cancer patients and controls. The authors conclude that these findings support the hypothesis that high circulating vitamin B12 concentrations increase the risk of lung cancer. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to evaluate the impacts of various forms of religious involvement, beyond individual socioeconomic status, lifestyle factors, emotional wellbeing and social support, on all-cause and cause-specific mortality in socioeconomic disadvantaged neighbourhoods. Design: This is a prospective cohort study conducted from 2002 through 2015. Settings: This study included underserved populations in the Southeastern USA. Participants: A total of nearly 85 000 participants, primarily low-income American adults, were enrolled. Eligible participants were aged 40-79 years at enrolment, spoke English and were not under treatment for cancer within the prior year. Results: We found that those who attended religious service attendance >1/week had 8% reduction in allcause death and 15% reduction in cancer death relative to those who never attended. This association was substantially attenuated by depression score, social support, and socioeconomic and lifestyle covariates, and further attenuated by other forms of religious involvement. This association with all-cause mortality was found being stronger among those with higher socioeconomic status or healthier lifestyle behaviours. Conclusion: Our results indicate that the association between religious services attendance >1/week and lower mortality was moderate but robust, and could be attenuated and modified by socioeconomic or lifestyle factors in this large prospective cohort study of underserved populations in the Southeastern USA. [ABSTRACT FROM AUTHOR]

Oral microbiome may play an important role in cancer pathogenesis. However, no study has prospectively investigated the association of the oral microbiome with subsequent risk of developing colorectal cancer (CRC). We conducted a nested case–control study including 231 incident CRC cases and 462 controls within the Southern Community Cohort Study with 75% of the subjects being African‐Americans. The controls were individually matched to cases based on age, ethnic group, smoking, season‐of‐study enrollment and recruitment method. Oral microbiota were assessed using 16S rRNA gene sequencing in pre‐diagnostic mouth rinse samples. Multiple bacterial taxa showed an association with CRC risk at p <0.05. Oral pathogens Treponema denticola and Prevotella intermedia were associated with an increased risk of CRC, with odds ratios (ORs) and 95% confidence intervals (CIs) of 1.76(1.19–2.60) and 1.55(1.08–2.22), respectively, for the individuals carrying these bacteria compared to non‐carriers. In the phylum Actinobacteria, Bifidobacteriaceae was more abundant among CRC patients than among controls. In the phylum Bacteroidetes, Prevotella denticola and Prevotella sp. oral taxon 300 were associated with an increased CRC risk, while Prevotella melaninogenica was associated with a decreased risk of CRC. In the phylum Firmicutes, Carnobacteriaceae, Streptococcaceae, Erysipelotrichaceae, Streptococcus, Solobacterium, Streptococcus sp. oral taxon 058 and Solobacterium moorei showed associations with a decreased risk of CRC. Most of these associations were observed among both African‐ and European‐Americans. Most of the associations were not significant after Bonferroni correction for multiple testing, which may be conservative. Our study suggests that the oral microbiome may play a significant role in CRC etiology. What's new? Oral microbiome composition is of special interest in research on colorectal cancer risk, owing in part to evidence that certain oral microbes cause chronic inflammation. In this prospective investigation of participants in the Southern Community Cohort Study in the United States, multiple oral bacterial taxa were associated with risk of developing colorectal cancer. Among the taxa, two species, Treponema denticola and Prevotella intermedia, previously were described as pathogenic in the oral cavity. The findings suggest that oral microbiome composition influences colorectal cancer risk, warranting further investigation for the possible use of oral microbiota in colorectal cancer detection and prevention. [ABSTRACT FROM AUTHOR]

Abstract Objective. To determine associations of adverse childhood experiences (ACE) with adult health care utilization in an underserved, low-income population. Methods. Questionnaires on ACE were completed by 38,200 adults (mean age 54), two-thirds African American, recruited from community health centers (CHCs) across 12 Southeastern states. Odds ratios (ORs) and accompanying 95% confidence intervals (CIs) were computed. Results. The percentages reporting emergency room visits and doctor's office visits, with high chronic disease index scores, rose monotonically (ptrend<.001) with rising ACE score. Odds ratios (CIs) for those with four or more vs. zero ACEs were 1.37 (95% CI 1.27–1.47) for 1–10 times and 1.80 (95% CI 1.29–2.52) for more than 10 times ER visits, 1.37 (95% CI 1.18–1.59) for over 10 doctor's visits, and 2.29 (95% CI 2.06–2.54) for three or more chronic diseases. Conclusions. High ACE levels were associated with greater chronic disease burden and greater health care utilization in adulthood. Long-lasting effects from ACE on the health care of underserved populations are indicated. There is an urgent need to train health care providers, patients, and their families on ACE effects and treatments for better health care outcomes. [ABSTRACT FROM AUTHOR]

Purpose: Meta-analyses have reported a small but positive association between diabetes and postmenopausal breast cancer risk, with summary relative risks of approximately 1.15. We analyzed data from the Southern Community Cohort Study (SCCS) following an underserved population with high diabetes prevalence to prospectively examine whether diabetes was associated with subsequent postmenopausal breast cancer risk and whether obesity modified this effect.Methods: Women with incident breast cancer were identified through linkage with state cancer registries and the National Death Index (213 white, 418 black cases). Person-years were calculated from date of entry into the SCCS until the earliest of date of breast cancer diagnosis, date of death, or date of last follow-up (8,277 white, 16,458 black noncases). Data on diabetes diagnosis were obtained through baseline and follow-up surveys. Cox regression was applied to examine the association between diabetes and postmenopausal breast cancer risk.Results: After adjustment for confounding, there was no association between self-reported diabetes and postmenopausal breast cancer risk among white (hazard ratio [HR] 1.02, 95% confidence interval [CI] 0.75-1.40) or black (HR 1.00, 95% CI 0.81-1.22) women. Nor was there evidence that obesity modified the effect of diabetes on postmenopausal breast cancer in women of either race.Conclusions: We found no evidence of the hypothesized increased risk of breast cancer among women with diabetes. The breast cancer risks among those with diabetes in this population suggest that the association between these two illnesses is complex. [ABSTRACT FROM AUTHOR]

Background: Parity is widely recognized as protective for breast cancer, but breast cancer risk may be increased shortly after childbirth. Whether this risk varies with breastfeeding, family history of breast cancer, or specific tumor subtype has rarely been evaluated.Objective: To characterize breast cancer risk in relation to recent childbirth.Design: Pooled analysis of individual-level data from 15 prospective cohort studies.Setting: The international Premenopausal Breast Cancer Collaborative Group.Participants: Women younger than 55 years.Measurements: During 9.6 million person-years of follow-up, 18 826 incident cases of breast cancer were diagnosed. Hazard ratios (HRs) and 95% CIs for breast cancer were calculated using Cox proportional hazards regression.Results: Compared with nulliparous women, parous women had an HR for breast cancer that peaked about 5 years after birth (HR, 1.80 [95% CI, 1.63 to 1.99]) before decreasing to 0.77 (CI, 0.67 to 0.88) after 34 years. The association crossed over from positive to negative about 24 years after birth. The overall pattern was driven by estrogen receptor (ER)-positive breast cancer; no crossover was seen for ER-negative cancer. Increases in breast cancer risk after childbirth were pronounced when combined with a family history of breast cancer and were greater for women who were older at first birth or who had more births. Breastfeeding did not modify overall risk patterns.Limitations: Breast cancer diagnoses during pregnancy were not uniformly distinguishable from early postpartum diagnoses. Data on human epidermal growth factor receptor 2 (HER2) oncogene overexpression were limited.Conclusion: Compared with nulliparous women, parous women have an increased risk for breast cancer for more than 20 years after childbirth. Health care providers should consider recent childbirth a risk factor for breast cancer in young women.Primary Funding Source: The Avon Foundation, the National Institute of Environmental Health Sciences, Breast Cancer Now and the UK National Health Service, and the Institute of Cancer Research. [ABSTRACT FROM AUTHOR]

Motivation The use of single nucleotide polymorphism (SNP) interactions to predict complex diseases is getting more attention during the past decade, but related statistical methods are still immature. We previously proposed the SNP Interaction Pattern Identifier (SIPI) approach to evaluate 45 SNP interaction patterns/patterns. SIPI is statistically powerful but suffers from a large computation burden. For large-scale studies, it is necessary to use a powerful and computation-efficient method. The objective of this study is to develop an evidence-based mini-version of SIPI as the screening tool or solitary use and to evaluate the impact of inheritance mode and model structure on detecting SNP–SNP interactions. Results We tested two candidate approaches: the 'Five-Full' and 'AA9int' method. The Five-Full approach is composed of the five full interaction models considering three inheritance modes (additive, dominant and recessive). The AA9int approach is composed of nine interaction models by considering non-hierarchical model structure and the additive mode. Our simulation results show that AA9int has similar statistical power compared to SIPI and is superior to the Five-Full approach, and the impact of the non-hierarchical model structure is greater than that of the inheritance mode in detecting SNP–SNP interactions. In summary, it is recommended that AA9int is a powerful tool to be used either alone or as the screening stage of a two-stage approach (AA9int+SIPI) for detecting SNP–SNP interactions in large-scale studies. Availability and implementation The 'AA9int' and 'parAA9int' functions (standard and parallel computing version) are added in the SIPI R package, which is freely available at https://linhuiyi.github.io/LinHY%5fSoftware/. Supplementary information Supplementary data are available at Bioinformatics online. [ABSTRACT FROM AUTHOR]

Background: Self-reported smoking is the principal measure used to assess lung cancer risk in epidemiological studies. We evaluated if circulating cotinine-a nicotine metabolite and biomarker of recent tobacco exposure-provides additional information on lung cancer risk.Methods: The study was conducted in the Lung Cancer Cohort Consortium (LC3) involving 20 prospective cohort studies. Pre-diagnostic serum cotinine concentrations were measured in one laboratory on 5364 lung cancer cases and 5364 individually matched controls. We used conditional logistic regression to evaluate the association between circulating cotinine and lung cancer, and assessed if cotinine provided additional risk-discriminative information compared with self-reported smoking (smoking status, smoking intensity, smoking duration), using receiver-operating characteristic (ROC) curve analysis.Results: We observed a strong positive association between cotinine and lung cancer risk for current smokers [odds ratio (OR ) per 500 nmol/L increase in cotinine (OR500): 1.39, 95% confidence interval (CI): 1.32-1.47]. Cotinine concentrations consistent with active smoking (≥115 nmol/L) were common in former smokers (cases: 14.6%; controls: 9.2%) and rare in never smokers (cases: 2.7%; controls: 0.8%). Former and never smokers with cotinine concentrations indicative of active smoking (≥115 nmol/L) also showed increased lung cancer risk. For current smokers, the risk-discriminative performance of cotinine combined with self-reported smoking (AUCintegrated: 0.69, 95% CI: 0.68-0.71) yielded a small improvement over self-reported smoking alone (AUCsmoke: 0.66, 95% CI: 0.64-0.68) (P = 1.5x10-9).Conclusions: Circulating cotinine concentrations are consistently associated with lung cancer risk for current smokers and provide additional risk-discriminative information compared with self-report smoking alone. [ABSTRACT FROM AUTHOR]

Objectives To examine the association between neighbourhood deprivation and lung cancer risk. Design Nested case-control study. setting Southern Community Cohort Study of persons residing in 12 states in the southeastern USA. Participants 1334 cases of lung cancer and 5315 controls. Primary outcome measure Risk of lung cancer. results After adjustment for smoking status and other confounders, and additional adjustment for individual-level measures of socioeconomic status (SES), there was no monotonic increase in risk with worsening deprivation score overall or within sex and race groups. There was an increase among current and shorter term former smokers (p=0.04) but not among never and longer term former smokers. There was evidence of statistically significant interaction by sex among whites, but not blacks, in which the effect of worsening deprivation on lung cancer existed in males but not in females. Conclusions Area-level measures of SES were associated with lung cancer risk in current and shorter term former smokers only in this population. [ABSTRACT FROM AUTHOR]

Background: Despite declining colorectal cancer (CRC) incidence and mortality rates in the U.S., significant geographic and racial disparities in CRC death rates remain. Differences in guideline-concordant CRC screening rates may explain some of these disparities. We aim to assess individual and neighborhood-level predictors of guideline-concordant CRC screening within two cohorts of individuals located within CRC mortality geographic hotspot regions in the U.S. Methods: A total of 36,901 participants from the Southern Community Cohort Study and 4,491 participants from the Ohio Appalachia CRC screening study were included in this study. Self-reported date of last CRC screening was used to determine if the participant was within guidelines for screening. Logistic regression models were utilized to determine the association of individual-level predictors, neighborhood deprivation, and residence in hotspot regions on the odds of being within guidelines for CRC screening. Results: Lower household income, lack of health insurance, and being a smoker were each associated with lower odds of being within guidelines for CRC screening in both cohorts. Area-level associations were less evident, although up to 15% lower guideline adherence was associated with residence in neighborhoods of greater deprivation and in the Lower Mississippi Delta, one of the identified CRC mortality hotspots. Conclusion: These results reveal the adverse effects of lower area-level and individual socioeconomic status on adherence to CRC guideline screening. [ABSTRACT FROM AUTHOR]

Circulating vitamin B6 levels have been found to be inversely associated with lung cancer. Most studies have focused on the B6 form pyridoxal 5′‐phosphate (PLP), a direct biomarker influenced by inflammation and other factors. Using a functional B6 marker allows further investigation of the potential role of vitamin B6 status in the pathogenesis of lung cancer. We prospectively evaluated the association of the functional marker of vitamin B6 status, the 3‐hydroxykynurenine:xanthurenic acid (HK:XA) ratio, with risk of lung cancer in a nested case–control study consisting of 5,364 matched case–control pairs from the Lung Cancer Cohort Consortium (LC3). We used conditional logistic regression to evaluate the association between HK:XA and lung cancer, and random effect models to combine results from different cohorts and regions. High levels of HK:XA, indicating impaired functional B6 status, were associated with an increased risk of lung cancer, the odds ratio comparing the fourth and the first quartiles (OR4thvs.1st) was 1.25 (95% confidence interval, 1.10–1.41). Stratified analyses indicated that this association was primarily driven by cases diagnosed with squamous cell carcinoma. Notably, the risk associated with HK:XA was approximately 50% higher in groups with a high relative frequency of squamous cell carcinoma, i.e., men, former and current smokers. This risk of squamous cell carcinoma was present in both men and women regardless of smoking status. [ABSTRACT FROM AUTHOR]

Background: Obesity is known to be a major risk factor for diabetes, but the magnitude of risk and variation between blacks and whites are less well documented in populations heavily affected by obesity. Herein we assess rates and risks of incident diabetes in a diverse southern population where obesity is common. Methods: A total of 24,000 black and 14,064 white adults aged 40–79 in the Southern Community Cohort Study with no self-reported diabetes at study enrollment during 2002–2009 was followed for up to 10 (median 4.5) years. Incidence rates, odds ratios (OR) and accompanying 95% confidence intervals (CI) for medication-treated incident diabetes were determined according to body mass index (BMI) and other characteristics, including tobacco and alcohol consumption, healthy eating and physical activity indices, and socioeconomic status (SES). Results: Risk of incident diabetes rose monotonically with increasing BMI, but the trends differed between blacks and whites (pinteraction < .0001). Adjusted ORs (CIs) for diabetes among those with BMI≥40 vs 20–25 kg/m2 were 11.9 (8.4–16.8) for whites and 4.0 (3.3–4.8) for blacks. Diabetes incidence was more than twice as high among blacks than whites of normal BMI, but the racial difference became attenuated as BMI rose, with estimated 5-year probabilities of developing diabetes approaching 20% for both blacks and whites with BMI≥40 kg/m2. Diabetes risk was also associated with low SES, significantly (pinteraction≤.02) more so for whites, current cigarette smoking, and lower healthy eating and physical activity indices, although high BMI remained the predominant risk factor among both blacks and whites. From baseline prevalence and 20-year projections of the incidence trends, we estimate that the large majority of surviving cohort participants with BMI≥40 kg/m2 will be diagnosed with diabetes. Conclusions: Even using conservative criteria to ascertain diabetes incidence (i.e., requiring diabetes medication use and ignoring undiagnosed cases), rates of obesity-associated diabetes were exceptionally high in this low-income adult population. The findings indicate that effective strategies to halt the rising prevalence of obesity are needed to avoid substantial increases in diabetes in coming years. [ABSTRACT FROM AUTHOR]