Development of a University Undergraduate Course Sequence About the Extension System

Many undergraduates are interested in community-based programming, but at most land-grants undergraduates have little contact with Extension. This article describes a grant project that developed two undergraduate courses about Extension and community-based, experiential education. The academic-year course incorporates lecture, discussion, guest speakers, and hands-on activities. The summer-session course takes students to visit program sites in operation. In outcome evaluations, students gained significantly in their understanding of land-grants, Extension, and community programming, and gained confidence in working collaboratively, among other findings. Recommendations note that the success of similar courses requires involvement of county Extension personnel and balancing of several key factors

Untargeted lipidomic features associated with colorectal cancer in a prospective cohort.

BackgroundEpidemiologists are beginning to employ metabolomics and lipidomics with archived blood from incident cases and controls to discover causes of cancer. Although several such studies have focused on colorectal cancer (CRC), they all followed targeted or semi-targeted designs that limited their ability to find discriminating molecules and pathways related to the causes of CRC.MethodsUsing an untargeted design, we measured lipophilic metabolites in prediagnostic serum from 66 CRC patients and 66 matched controls from the European Prospective Investigation into Cancer and Nutrition (Turin, Italy). Samples were analyzed by liquid chromatography-high-resolution mass spectrometry (LC-MS), resulting in 8690 features for statistical analysis.ResultsRather than the usual multiple-hypothesis-testing approach, we based variable selection on an ensemble of regression methods, which found nine features to be associated with case-control status. We then regressed each selected feature on time-to-diagnosis to determine whether the feature was likely to be either a potentially causal biomarker or a reactive product of disease progression (reverse causality).ConclusionsOf the nine selected LC-MS features, four appear to be involved in CRC etiology and merit further investigation in prospective studies of CRC. Four other features appear to be related to progression of the disease (reverse causality), and may represent biomarkers of value for early detection of CRC

Meat intake, cooking-related mutagens and risk of colorectal adenoma in a sigmoidoscopy-based case-control study

Reported habits of red meat consumption, particularly red meat that has been cooked to the degree termed ‘well-done', is a positive risk factor for colorectal cancer. Under high, pyrolytic temperatures, heterocyclic amines (HCA) and benzo[a]pyrene (BP) molecules can form inside and on the surface of red meat, respectively. These compounds are precursors that are metabolically converted to compounds known to act as mutagens and carcinogens in animal models, yet their role in human colorectal carcinogenesis remains to be clarified. We investigated whether intake of these compounds is associated with risk of colorectal adenoma in the context of a polyp-screening study conducted in Southern California. Using a database of individual HCAs and BP in meats of various types and subjected to specified methods and degrees of cooking, we estimated nanogram consumption of 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine, 2-amino-3,4,8-trimethylimidazo[4,5-f] quinoxaline, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline and benzo[a]pyrene (BP). We observed a 6% increased risk of large (>1 cm) adenoma per 10 ng/day consumption of BP [OR = 1.06 (95% CI, 1.00-1.12), P (trend) = 0.04]. A major source of BP is red meat exposed to a naked flame, as occurs during the barbecuing process. Consistent with this finding an incremental increase of 10 g of barbecued red meat per day was associated with a 29% increased risk of large adenoma [OR = 1.29 (95% CI, 1.02-1.63), P (trend) = 0.04]. Individuals in the top quintile of barbecued red meat intake were at increased risk of large adenoma [OR = 1.90 (95% CI, 1.04-3.45)], compared with never consuming barbecued red meat. The consumption of oven-broiled red meat was inversely related to adenoma risk compared with non-consumers [OR = 0.49 (95% CI, 0.28-0.85)]. We did not identify any association with consumption of individual HCAs and colorectal adenoma risk. These results support the hypothesis that BP contributes to colorectal carcinogenesi

Associations between Prediagnostic Circulating Bilirubin Levels and Risk of Gastrointestinal Cancers in the UK Biobank

Evidence from experimental studies suggests that bilirubin, a metabolic by-product of hemoglobin breakdown, has anticancer activity and may, therefore, reduce the risk of gastrointestinal (GI) cancers. We conducted a prospective study among 440,948 participants in the UK Biobank and found that higher prediagnostic circulating bilirubin levels were robustly associated with a lower risk of developing esophageal adenocarcinoma, which is compatible with the antioxidant hypothesis of bilirubin. We further observed negative associations between bilirubin and risk of colorectal cancer, which were less robust and could be due to reverse causality, whereby undiagnosed cancer affects bilirubin levels. The observed positive associations between bilirubin and risk of hepatobiliary cancers may indicate underlying liver disease processes. No associations were found for cancers of the mouth, stomach, and pancreas. Bilirubin is a novel biomarker for disease development that is routinely measured in clinical settings. Provided that our findings are replicated in further studies, circulating bilirubin could serve as a future risk stratification marker for certain GI cancers. We investigated associations between serum levels of bilirubin, an endogenous antioxidant, and gastrointestinal cancer risk. In the UK Biobank, prediagnostic serum levels of total bilirubin were measured in blood samples collected from 440,948 participants. In multivariable-adjusted Cox proportional hazard regression, we estimated hazard ratios (HR) and 95% confidence intervals (CI) for associations between bilirubin levels and gastrointestinal cancer risk (colorectum, esophagus, stomach, mouth, pancreas, and liver). After a median follow-up of 7.1 years (interquartile range: 1.4), 5033 incident gastrointestinal cancer cases were recorded. In multivariable-adjusted models, bilirubin levels were negatively associated with risk of esophageal adenocarcinoma (EAC, HR per 1-SD increment in log-total bilirubin levels 0.72, 95%CI 0.56-0.92, p = 0.01). Weak and less robust negative associations were observed for colorectal cancer (CRC, HR per 1-SD increment in log-total bilirubin levels 0.95, 95%CI 0.88-1.02, p = 0.14). Bilirubin levels were positively associated with risk of hepatocellular carcinoma (HCC, HR per 1-SD increment in log-total bilirubin levels 2.07, 95%CI 1.15-3.73, p = 0.02) and intrahepatic bile duct (IBD) cancer (HR per 1-SD increment 1.67, 95%CI 1.07-2.62, p = 0.03). We found no associations with risks of stomach, oral, and pancreatic cancers. Prediagnostic serum levels of bilirubin were negatively associated with risk of EAC and positively associated with HCC and IBD cancer. Further studies are warranted to replicate our findings for specific GI cancers

Adiposity and cancer at major anatomical sites: umbrella review of the literature

Objective To evaluate the strength and validity of the evidence for the association between adiposity and risk of developing or dying from cancer. Design Umbrella review of systematic reviews and metaanalyses. Data sources PubMed, Embase, Cochrane Database of Systematic Reviews, and manual screening of retrieved references. Eligibility criteria Systematic reviews or meta-analyses of observational studies that evaluated the association between indices of adiposity and risk of developing or dying from cancer. Data synthesis Primary analysis focused on cohort studies exploring associations for continuous measures of adiposity. The evidence was graded into strong, highly suggestive, suggestive, or weak after applying criteria that included the statistical significance of the random effects summary estimate and of the largest study in a meta-analysis, the number of cancer cases, heterogeneity between studies, 95% prediction intervals, small study effects, excess significance bias, and sensitivity analysis with credibility ceilings. Results 204 meta-analyses investigated associations between seven indices of adiposity and developing or dying from 36 primary cancers and their subtypes. Of the 95 meta-analyses that included cohort studies and used a continuous scale to measure adiposity, only 12 (13%) associations for nine cancers were supported by strong evidence. An increase in body mass index was associated with a higher risk of developing oesophageal adenocarcinoma; colon and rectal cancer in men; biliary tract system and pancreatic cancer; endometrial cancer in premenopausal women; kidney cancer; and multiple myeloma. Weight gain and waist to hip circumference ratio were associated with higher risks of postmenopausal breast cancer in women who have never used hormone replacement therapy and endometrial cancer, respectively. The increase in the risk of developing cancer for every 5 kg/m2 increase in body mass index ranged from 9% (relative risk 1.09, 95% confidence interval 1.06 to 1.13) for rectal cancer among men to 56% (1.56, 1.34 to 1.81) for biliary tract system cancer. The risk of postmenopausal breast cancer among women who have never used HRT increased by 11% for each 5 kg of weight gain in adulthood (1.11, 1.09 to 1.13), and the risk of endometrial cancer increased by 21% for each 0.1 increase in waist to hip ratio (1.21, 1.13 to 1.29). Five additional associations were supported by strong evidence when categorical measures of adiposity were included: weight gain with colorectal cancer; body mass index with gallbladder, gastric cardia, and ovarian cancer; and multiple myeloma mortality. Conclusions Although the association of adiposity with cancer risk has been extensively studied, associations for only 11 cancers (oesophageal adenocarcinoma, multiple myeloma, and cancers of the gastric cardia, colon, rectum, biliary tract system, pancreas, breast, endometrium, ovary, and kidney) were supported by strong evidence. Other associations could be genuine, but substantial uncertainty remains. Obesity is becoming one of the biggest problems in public health; evidence on the strength of the associated risks may allow finer selection of those at higher risk of cancer, who could be targeted for personalised prevention strategies

from global food systems to individual exposures and mechanisms

Funding Information: This work was supported by Cancer Research UK [Ref: C33493/A29678] and World Cancer Research Fund International [Ref: IIG_FULL_2020_033]. Publisher Copyright: © 2022, The Author(s), under exclusive licence to Springer Nature Limited.Ultra-processed foods (UPFs) have become increasingly dominant globally, contributing to as much as 60% of total daily energy intake in some settings. Epidemiological evidence suggests this worldwide shift in food processing may partly be responsible for the global obesity epidemic and chronic disease burden. However, prospective studies examining the association between UPF consumption and cancer outcomes are limited. Available evidence suggests that UPFs may increase cancer risk via their obesogenic properties as well as through exposure to potentially carcinogenic compounds such as certain food additives and neoformed processing contaminants. We identify priority areas for future research and policy implications, including improved understanding of the potential dual harms of UPFs on the environment and cancer risk. The prevention of cancers related to the consumption of UPFs could be tackled using different strategies, including behaviour change interventions among consumers as well as bolder public health policies needed to improve food environments.publishersversionpublishe

Estrogen and progesterone-related gene variants and colorectal cancer risk in women

<p>Abstract</p> <p>Background</p> <p>Observational studies and randomized trials have suggested that estrogens and/or progesterone may lower the risk for colorectal cancer. Inherited variation in the sex-hormone genes may be one mechanism by which sex hormones affect colorectal cancer, although data are limited.</p> <p>Method</p> <p>We conducted a comprehensive evaluation of single nucleotide polymorphisms (SNPs) in genes encoding 3 hormone receptors (<it>ESR1, ESR2, PGR</it>) and 5 hormone synthesizers (<it>CYP19A1 and CYP17A1, HSD17B1, HSD17B2, HSD17B4</it>) among 427 women with incident colorectal cancer and 871 matched controls who were Caucasians of European ancestry from 93676 postmenopausal women enrolled in the Women's Health Initiative Observational cohort. A total of 242 haplotype-tagging and functional SNPs in the 8 genes were included for analysis. Unconditional logistic regression with adjustment for age and hysterectomy status was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs).</p> <p>Results</p> <p>We observed a weak association between the <it>CYP17A1 </it>rs17724534 SNP and colorectal cancer risk (OR per risk allele (A) = 1.39, 95% CI = 1.09-1.78, corrected p-value = 0.07). In addition, a suggestive interaction between rs17724534 and rs10883782 in 2 discrete LD blocks of <it>CYP17A1 </it>was observed in relation to colorectal cancer (empirical p value = 0.04). Moreover, one haplotype block of <it>CYP19A1 </it>was associated with colorectal cancer (corrected global p value = 0.02), which likely reflected the association with the tagging SNP, rs1902584, in the block.</p> <p>Conclusion</p> <p>Our findings offer some support for a suggestive association of <it>CYP17A1 </it>and <it>CYP19A1 </it>variants with colorectal cancer risk.</p