North Carolina Colon Cancer Study Research Articles

Racial Differences in Over-the-Counter Non-steroidal Anti-inflammatory Drug Use Among Individuals at Risk of Adverse Cardiovascular Events.

Black Americans are disproportionately affected by adverse cardiovascular events (ACEs). Over-the-counter (OTC) non-steroidal anti-inflammatory drugs (NSAIDs) confer increased risk for ACEs, yet racial differences in the use of these products remain understudied. This study sought to determine racial differences in OTC NSAID and high-potency powdered NSAID (HPP-NSAID) use. This retrospective analysis examined participants at risk of ACEs (defined as those with self-reported hypertension, diabetes, heart disease, or smoking history ≥ 20years) from the North Carolina Colon Cancer Study, a population-based case-control study. We used multivariable logistic regression models to assess the independent associations of race with any OTC NSAID use, HPP-NSAID use, and regular use of these products. Of the 1286 participants, 585 (45%) reported Black race and 701 (55%) reported non-Black race. Overall, 665 (52%) reported any OTC NSAID use and 204 (16%) reported HPP-NSAID use. Compared to non-Black individuals, Black individuals were more likely to report both any OTC NSAID use (57% versus 48%) and HPP-NSAID use (22% versus 11%). In multivariable analyses, Black (versus non-Black) race was independently associated with higher odds of both NSAID use (OR 1.4, 95% CI (1.1, 1.8)) and HPP-NSAID use (OR 1.8 (1.3, 2.5)). Black individuals at risk of ACEs had higher odds of any OTC NSAID and HPP-NSAID use than non-Black individuals, after controlling for pain and socio-economic status. Further research is necessary to identify potential mechanisms driving this increased use.

Abstract EP66: Racial Differences In The Use Of Over-the-counter Non-steroidal Anti-inflammatory Drugs Among Individuals At Risk Of Adverse Cardiovascular Events

Introduction: Over-the-counter (OTC) non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used despite conferring risk for adverse cardiovascular events (ACEs). ACEs disproportionately affect Black individuals, yet patterns of OTC NSAID and high-potency powder NSAID (HPP-NSAID) use among different racial groups remains understudied. Hypothesis: We hypothesized that use of OTC NSAIDs and HPP-NSAIDs is higher among Black individuals. Methods: We analyzed data from the North Carolina Colon Cancer study, a population-based case-control study in 1996-2000. Participants at risk of ACEs, defined as self-reported hypertension, diabetes, heart disease, or smoking history ≥ 20 years, were included in our analysis. Primary outcomes were any OTC NSAID use and HPP-NSAID use. Secondary outcomes included regular use of the primary outcome variables. Using multivariable logistic regression, we quantified the independent association of the outcomes with race after adjusting for age, sex, education, poverty, and pain interfering with daily activities. We investigated the effect modifications of poverty status and educational attainment separately on the noted associations. Results: Of the 1286 participants at risk for ACEs, 583 (45%) reported Black, 695 (54%) White, and 8 (<1%) Other race. Overall, 665 (52%) reported any NSAID use and 204 (16%) reported HPP-NSAID use. Any NSAID use was reported by 329 (57%) Black participants compared to 332 (48%) White participants. HPP-NSAID use was reported by 126 (22%) Black participants compared to 76 (11%) White participants. Of users, 174 (26%) reported regular NSAID use and 37 (18%) reported regular HPP-NSAID use; this pattern was similar across race. In multivariable analysis, Black (versus White) race was independently associated with higher odds of NSAID use (odds ratio [OR] 1.4 95% confidence interval [1.1, 1.8]). Pain interfering with daily activities (OR 1.4 [1.1, 1.8]) was also associated with NSAID use and older age was negatively associated with NSAID use (OR 0.96 [0.95, 0.97]). After adjustment, Black race was associated with HPP-NSAID use (OR 1.8 [1.3, 2.6]). Male sex (OR 1.6 [1.2, 2.3]) and being in or near poverty (OR 1.6 [1.0, 2.3]) were also independently associated with HPP-NSAID use and older age (OR 0.96 [0.94, 0.97]) and educational attainment of some college or greater (OR 0.5 [0.3, 0.7]) were negatively associated with HPP-NSAID use. The associations between race and either outcome were not significantly moderated by educational attainment nor poverty status. Conclusions: In this population-based study, Black individuals at risk of ACEs had higher odds of any NSAID and HPP-NSAID use than White participants, even after controlling for pain and socio-economic status. Further research is necessary to determine the impact of this differential use on established inequities in cardiovascular outcomes.

Lifestyle Factors, Colorectal Tumor Methylation, and Survival Among African Americans and European Americans

Differences in tumor characteristics might partially account for mortality disparities between African American (AA) and European American (EA) colorectal cancer patients. We evaluated effect modification by race for exposure and patient-outcomes associations with colorectal tumor methylation among 218 AA and 267 EA colorectal cancer cases from the population-based North Carolina Colon Cancer Study. Tumor methylation was assessed in CACNA1G, MLH1, NEUROG1, RUNX3, and SOCS1. We used logistic regression to assess whether associations between several lifestyle factors—intake of fruits, vegetables, folate, and non-steroidal anti-inflammatory drugs—and tumor methylation were modified by race. Proportional hazards models were used to evaluate whether race modified associations between tumor methylation and time to all-cause mortality. Greater fruit consumption was associated with greater odds of high NEUROG1 methylation among EA at methylation cut points of 15–35% (maximum OR 3.44, 95% CI 1.66, 7.13) but not among AA. Higher folate intake was associated with lower odds of high CACNA1G methylation among EAs but not AAs. Tumor methylation was not associated with all-cause mortality for either group. Race might modify associations between lifestyle factors and colorectal tumor methylation, but in this sample did not appear to modify associations between tumor methylation and all-cause mortality.

Abstract A76: Immune mechanisms and racial disparities in colon cancer

Abstract Background: Colorectal cancer (CRC) has a disproportionate impact on African Americans (AA). In CRC, AA often display more aggressive disease with poorer prognosis compared to Caucasian Americans (CA). The biological mechanisms involved in the observed racial disparities are not clear but it is strikingly evident that immune responses are critical towards the development, growth and metastasis of this tumor type. Anti-tumor immunity, characterized by anti-tumor TH1 cells and strong cytotoxic T lymphocyte (CTL) activity, has been shown quite elegantly in the literature to significantly improve disease-free survival in CA patients with CRC. Unfortunately, these studies have not included patients from various ethnic backgrounds, such as AA patients, although there is no reason at this time to believe that the role of anti-tumor immunity in protection of patients from their disease will be limited to CA patients. The proposed immune mechanism of the protection is the elimination of metastatic cells breaking away from the primary tumor, decreasing tumor recurrence. We hypothesize deficiencies in anti-tumor immunity may contribute to the racial disparity observed in CRC. Methods: We have used immunohistochemistry (IHC) on ~250 archived CRC samples from the North Carolina Colon Cancer Study to evaluate immune cell infiltration (CD8 and CD57), CTL activity (granzyme B, (GzmB)), and IL-17 production in situ. Also, using GzmB immunostainings, we analyzed the histological location of CTL activity, whether it was intratumoral vs. at the invasive borders of the CRC patient samples. The advantage of this population-based study that covered 33 counties in North Carolina is that 45% of the participants were AA while 55% were CA (self-proclaimed). The disadvantage to this study is that no follow-up data is available. All samples were tested for MSI and no MSI tumors were included in this study. Results: Our data reveal that the number of infiltrating CD8+ and CD57+ immune cells, as well as the number of cells making IL-17, do not vary statistically by race in these CRC samples. However, analyses of the histological location for infiltrating CTL activity revealed that the frequency of CA patients that are “high GzmB” responders (in the upper 50%) is significantly higher than AA in both the intratumoral regions (p=0.01) and the invasive borders (p=0.0003). In addition, we have seen that race may modulate the effect of IL-17 on anti-tumor immunity. When IL-17 is high, both races show a good correlation between GzmB expression and the presence of intraepithelial CD8+ immune cells (0.80 and 0.82 for AA and CA, respectively). When IL-17 is low, however, this association seems to break down in AA but not in CA patients (0.53 vs. 0.88, respectively; the results reach marginal statistical significance at p=0.077). The data suggest that when IL-17 levels are low, AA patients do not have as much GzmB expression in their infiltrating immune cells as CA patients. Further studies to investigate the role of IL-17 and how it might influence anti-tumor immunity by race are definitely warranted. Conclusion: Our data to date indicate that the number of AA patients with high numbers of GzmB expressing cells infiltrating their tumors in intratumoral as well as invasive border regions is significantly lower than what is observed in CA patients. In addition, IL-17 may have a modulatory effect on anti-tumor cytotoxicity by race. These observations support our hypothesis that immune processes may contribute to the racial disparities observed in colorectal cancer. Acknowledgements: The authors acknowledge the contributions of R Basa, V Davies, X Li, B Murali, J Shah, B Yang and M Kinseth to these studies. This study was funded by the NCI Comprehensive Partnerships to Reduce Cancer Health Disparities (CPRCHD) grants (U54CA132384 and U54CA132379) and by 1U01CA162147 (to KLM and JMC). Citation Format: Mohammad W. Khan, Mengxi Tian, John M. Carethers, Kathleen L. McGuire. Immune mechanisms and racial disparities in colon cancer. [abstract]. In: Proceedings of the AACR Special Conference: Tumor Immunology and Immunotherapy: A New Chapter; December 1-4, 2014; Orlando, FL. Philadelphia (PA): AACR; Cancer Immunol Res 2015;3(10 Suppl):Abstract nr A76.

IGF2RGenetic Variants, Circulating IGF2 Concentrations and Colon Cancer Risk in African Americans and Whites

TheMannose 6 Phosphate/Insulin-like Growth Factor Receptor-2 (IGF2R)encodes a type-1 membrane protein that modulates availability of the potent mitogen, IGF2. We evaluated the associations betweenIGF2Rnon-synonymous genetic variants (c.5002G>A, Gly1619Arg(rs629849), and c.901C>G, Leu252Val(rs8191754)), circulating IGF2 levels, and colon cancer (CC) risk among African American and White participants enrolled in the North Carolina Colon Cancer Study (NCCCS). Generalized linear models were used to compare circulating levels of IGF2 among 298 African American and 518 White controls. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association ofIGF2Rgenetic variants and CC risk. Women homozygous for theIGF2Rc.5002 G>A allele, had higher mean levels of circulating IGF2, 828 (SD=321) ng/ml compared to non-carriers, 595 (SD=217) ng/ml (p-value=0.01). This pattern was not apparent in individuals homozygous for theIGF2Rc.901 C>G variant. Whites homozygous for theIGF2Rc.901 C>G variant trended towards a higher risk of CC, OR=2.2 [95% CI(0.9–5.4)], whereas carrying theIGF2Rc.5002 G>A variant was not associated with CC risk. Our findings support the hypothesis that being homozygous for theIGF2Rc.5002 G>A modulates IGF2 circulating levels in a sex-specific manner, and while carrying theIGF2Rc.901 C>G may increase cancer risk, the mechanism may not involve modulation of circulating IGF2.

IGF2R genetic variants, circulating IGF2 concentrations and colon cancer risk in African Americans and Whites.

The Mannose 6 Phosphate/Insulin-like Growth Factor Receptor-2 (IGF2R) encodes a type-1 membrane protein that modulates availability of the potent mitogen, IGF2. We evaluated the associations between IGF2R non-synonymous genetic variants (c.5002G>A, Gly1619Arg(rs629849), and c.901C>G, Leu252Val(rs8191754)), circulating IGF2 levels, and colon cancer (CC) risk among African American and White participants enrolled in the North Carolina Colon Cancer Study (NCCCS). Generalized linear models were used to compare circulating levels of IGF2 among 298 African American and 518 White controls. Logistic regression models were used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association of IGF2R genetic variants and CC risk. Women homozygous for the IGF2R c.5002 G>A allele, had higher mean levels of circulating IGF2, 828 (SD=321) ng/ml compared to non-carriers, 595 (SD=217) ng/ml (p-value=0.01). This pattern was not apparent in individuals homozygous for the IGF2R c.901 C>G variant. Whites homozygous for the IGF2R c.901 C>G variant trended towards a higher risk of CC, OR=2.2 [95% CI(0.9–5.4)], whereas carrying the IGF2R c.5002 G>A variant was not associated with CC risk. Our findings support the hypothesis that being homozygous for the IGF2R c.5002 G>A modulates IGF2 circulating levels in a sex-specific manner, and while carrying the IGF2R c.901 C>G may increase cancer risk, the mechanism may not involve modulation of circulating IGF2.

Inverse Relationship Between Moderate Alcohol Intake and Rectal Cancer: Analysis of the North Carolina Colon Cancer Study

The relationship between alcohol intake and rectal cancer is uncertain. We sought to evaluate whether alcohol consumption is associated with distal colorectal cancer and rectal cancer specifically. Data on alcohol intake were examined from the North Carolina Colon Cancer Study, a population-based case-control study of distal colorectal cancer. This study encompassed 33 counties in the central and eastern part of North Carolina. Cases had adenocarcinoma of the rectum, rectosigmoid, and sigmoid colon. Controls were frequency-matched on age, race, and sex. Demographic and dietary intake data were collected with use of a validated questionnaire. Logistic regression was used to estimate odds ratios for the relationship between alcohol consumption and distal colorectal cancer. Included in the study were 1033 cases and 1011 controls. The odds ratio for rectal cancer comparing any vs no alcohol intake was 0.73 (95% CI 0.60, 0.90), adjusted for age, sex, race, smoking status, obesity, education, red meat intake, use of nonsteroidal anti-inflammatory medications, and family history of colorectal cancer. The odds ratio for moderate alcohol (≤14 g/day) was 0.66 (95% CI 0.53, 0.82), whereas the odds ratio for heavy alcohol (>14 g/day) was 0.93 (95% CI 0.70, 1.23). Moderate beer and wine intakes were also inversely associated with distal colorectal cancer: odds ratios 0.76 (95% CI 0.60, 0.96) and 0.69 (95% CI 0.56, 0.86). This was a retrospective, observational study. Residual confounding is possible. In this study, moderate alcohol intake (especially wine) was inversely associated with distal colorectal cancer.

Inverse Relationship Between Moderate Alcohol Intake and Rectal Cancer: Analysis of the North Carolina Colon Cancer Study

Inverse Relationship Between Moderate Alcohol Intake and Rectal Cancer: Analysis of the North Carolina Colon Cancer Study

Trans-Fatty acid consumption and its association with distal colorectal cancer in the North Carolina Colon Cancer Study II

trans-Fatty acid consumption and its association with distal colorectal cancer in the North Carolina Colon Cancer Study II

Trans-Fatty acid consumption and its association with distal colorectal cancer in the North Carolina Colon Cancer Study II

Recently, the potential health effects of trans-fatty acid consumption have raised concerns. A few studies have examined the risk of colorectal cancer with increasing consumption of trans-fatty acids, but none investigated the risk of rectal cancer, which may have different risk factors than colon cancer. Our objective was to explore the relationship between trans-fatty acid consumption and distal colorectal (sigmoid, rectosigmoid, and rectal) cancer using a case-control study of Whites (n = 1,516) and African Americans (n = 392) in North Carolina from 2001 to 2006. Matched cases and controls were interviewed about demographic information, lifestyle factors, and diet. White cases reported higher mean consumption of trans-fatty acid than White controls, but mean consumption was similar for African American cases and controls. Relative to the lowest quartile, the highest quartiles of energy-adjusted trans-fatty acid consumption were positively associated with distal colorectal cancer for Whites [adjusted ORs for the third and fourth quartiles are 1.54 (95%CI: 1.12, 2.13) and 1.45 (95%CI: 1.04, 2.03), respectively]. Consumption was not associated with distal colorectal cancer in African Americans [adjusted ORs for the third and fourth quartiles are 0.98 (95%CI: 0.47, 2.05) and 0.87 (95%CI 0.42, 1.81), respectively]. In conclusion, high consumption of trans-fatty acids was positively associated with distal colorectal cancer among Whites.

Associations Between Trans Fatty Acid Consumption and Colon Cancer Among Whites and African Americans in the North Carolina Colon Cancer Study I

Disparities in incidence andmortality rates of colon cancer exist between Whites and African Americans. Prior studies examined the association between trans fatty acid consumption and colorectal cancer, but none assessed this possible relationship within a large study population of African Americans and Whites. Using data from a population-based, case-control study in North Carolina, we investigated this association with attention to possible racial differences. Cases and matched controls were queried on demographic characteristics, lifestyle factors, medical history, and diet.Cases reported higher daily consumption (g/day) of trans fatty acids (mean = 5.9, SD = 2.9, median = 5.5, IQR = 3.8−7.5) compared to controls (mean = 5.2, SD = 2.4, median = 4.7, IQR = 3.5−6.4). Energy-adjusted trans fatty acid consumption was not associated with colon cancer. Compared to participants in the lowest quartile of consumption, those in the highest quartile had an adjusted odds ratio of 1.01 (95% confidence interval 0.69, 1.49) for Whites and 0.99 (95% confidence interval 0.61, 1.62) for African Americans. No association was found between increased consumption of trans fatty acid and specific tumor location (proximal or distal colon). In conclusion, trans fatty acid consumption is not associated with colon cancer and does not contribute to disparities in colon cancer rates.

Selenium, Folate, and Colon Cancer

Selenium is an essential trace element that has been implicated in cancer risk; however, study results have been inconsistent with regard to colon cancer. Our objectives were to 1) investigate the association between selenium and colon cancer, 2) evaluate possible effect measure modifiers, and 3) evaluate potential biases associated with the use of postdiagnostic serum selenium measures. The North Carolina Colon Cancer Study is a large population-based, case-control study of colon cancer in North Carolina between 1996 and 2000 (n = 1,691). Nurses interviewed patients about diet and lifestyle and drew blood specimens, which were used to measure serum selenium. Individuals who had both high serum selenium (> 140 mcg/l) and high reported folate (> 354 mcg/day) had a reduced relative risk of colon cancer [odds ratio (OR) = 0.5, 95% confidence interval (CI) = 0.4–0.8). The risk of colon cancer for those with high selenium and low folate was approximately equal to the risk among those with low selenium and low folate (OR = 1.1, 95% CI = 0.7–1.5) as was the risk for those with low selenium and high folate (OR = 0.9, 95% CI = 0.7–1.2). We did not find evidence of bias due to weight loss, stage at diagnosis, or time from diagnosis to selenium measurement. High levels of serum selenium and reported folate jointly were associated with a substantially reduced risk of colon cancer. Folate status should be taken into account when evaluating the relation between selenium and colon cancer in future studies. Importantly, weight loss, stage at diagnosis, or time from diagnosis to blood draw did not appear to produce strong bias in our study.

Dietary Patterns and Colon Cancer Risk in Whites and African Americans in the North Carolina Colon Cancer Study

We examined associations of dietary patterns with colon cancer risk in African Americans and Whites from a case-control study in North Carolina. Incident colon cancer cases, 40 to 80 yr (n = 636), and matched controls (n = 1,042) were interviewed in person to elicit information on potential colon cancer risk factors. A validated food frequency questionnaire adapted to include regional foods captured diet over the year prior to diagnosis (cases) or interview date (controls). Three meaningful intake patterns were identified in both Whites and African Americans: “Western-Southern,” “fruit-vegetable,” and “metropolitan.” Compared to the Western-Southern pattern, the fruit-vegetable and metropolitan patterns were associated with more healthful dietary behaviors (e.g., higher vegetable intake and lower red meat consumption), and demographic/lifestyle characteristics typically correlated with low colon cancer risk, for example, lower BMI, higher education, and higher NSAID use. The fruit-vegetable pattern was significantly inversely associated with colon cancer risk in Whites (OR = 0.4, 95% CI = 0.3–0.6) and the metropolitan pattern with a nonsignificant 30% risk reduction in both Whites and African Americans after adjustment for education. The Western-Southern pattern was not associated with colon cancer risk. These findings may explain some of the racial differences in colon cancer incidence and underscore the importance of examining diet-cancer associations in different population subgroups.

Dietary Patterns and Colon Cancer Risk in Whites and African Americans in the North Carolina Colon Cancer Study

Dietary Patterns and Colon Cancer Risk in Whites and African Americans in the North Carolina Colon Cancer Study

Associations Between Trans Fatty Acid Consumption and Colon Cancer Among Whites and African Americans in the North Carolina Colon Cancer Study I

Associations Between Trans Fatty Acid Consumption and Colon Cancer Among Whites and African Americans in the North Carolina Colon Cancer Study I

Rural‐Urban Differences in Colon Cancer Risk in Blacks and Whites: The North Carolina Colon Cancer Study

Geographic and racial variations in cancer incidence have been observed. Studies of colorectal carcinoma indicate a higher incidence and mortality rate for blacks than for whites in the United States. We evaluated the effect of rural versus urban residence on colon cancer risk and stage of disease at diagnosis in blacks and whites. Interviews were conducted with 558 colon cancer cases and 952 controls enrolled in the North Carolina Colon Cancer Study, a population-based case-control study of blacks and whites residing in 33 contiguous counties. Residence in a rural area was associated with increased colon cancer risk (odds ratio, 1.4; 95% confidence interval, 1.1-1.8). This association was no longer significant after controlling for recent use of colorectal cancer screening tests (odds ratio, 1.2; 95% confidence interval, 0.9-1.6). Risk estimates were not modified by race nor were they markedly different for extent of disease at diagnosis. However, colorectal cancer screening rates were lower for blacks than for whites. Our findings suggest that rural blacks and whites are at increased risk of colon cancer regardless of stage of disease at diagnosis than their urban counterparts; this relationship may be mediated by screening behavior.

5,10-Methylenetetrahydrofolate Reductase 677 and 1298 Polymorphisms, Folate Intake, and Microsatellite Instability in Colon Cancer

The 5,10-methylenetetrahydrofolate reductase (MTHFR) gene plays a critical role in folate metabolism. Studies on the association between MTHFR polymorphisms and length changes in short tandem repeat DNA sequences [microsatellite instability (MSI)] are inconsistent. Using data from colon cancer cases (n=503) enrolled as part of an existing population-based case-control study, we investigated the association between MTHFR 677 and MTHFR 1298 polymorphisms and MSI. We also examined whether the association was modified by folate intake. Participants were case subjects enrolled as part of the North Carolina Colon Cancer Study. Consenting cases provided information about lifestyle and diet during in-home interviews as well as blood specimens and permission to obtain tumor blocks. DNA from normal and tumor tissue sections was used to determine microsatellite status (MSI). Tumors were classified as MSI if two or more microsatellite markers (BAT25, BAT26, D5S346, D2S123, and D17S250) had changes in the number of DNA sequence repeats compared with matched nontumor tissue. Tumors with one positive marker (MSI-low) or no positive markers (microsatellite stable) were grouped together as non-MSI tumors (microsatellite stable). MTHFR 677 and MTHFR 1298 genotypes were determined by real-time PCR using the 5' exonuclease (Taqman) assay. Logistic regression was used to calculate odds ratio (OR) and 95% confidence intervals (95% CI). MSI was more common in proximal tumors (OR, 3.8; 95% CI, 1.7-8.4) and in current smokers (OR, 4.0; 95% CI, 1.6-9.7). Compared with MTHFR 677 CC referent, MTHFR 677 CT/TT genotype was inversely associated with MSI among White cases (OR, 0.36; 95% CI, 0.16-0.81) but not significant among African Americans. Although not statistically significant, a similar inverse association was observed between MTHFR 677 CT/TT genotype and MSI among the entire case subjects (OR, 0.54; 95% CI, 0.26-1.10). Among those with adequate folate intake (>400 microg total folate), we found strong inverse associations between combined MTHFR genotypes and MSI (677 CC+1298 AC/CC, OR, 0.09; 95% CI, 0.01-0.59; 677 CT/TT+1298 AA, OR, 0.13; 95% CI, 0.02-0.85) compared with the combined wild-type genotypes (677 CC+1298 AA). This protective effect was not evident among those with low folate (<400 microg total folate) intake. Our results suggest that MTHFR variant genotypes are associated with reduced risk of MSI tumors under conditions of adequate folate intake, although the data are imprecise due to small numbers. These results indicate that the relationship between MTHFR genotypes and MSI is influenced by folate status.

Diet, lifestyle, and genomic instability in the North Carolina Colon Cancer Study.

Microsatellite instability (MSI) is one form of genomic instability that occurs in 10% to 20% of sporadic colon tumors and almost all hereditary nonpolyposis colon cancers. However, little is known about how environmental factors (e.g., diet) may influence MSI in sporadic colon cancer. We used data from a population-based case-control study in North Carolina (486 colon cancer cases and 1,048 controls) to examine associations of diet (total energy, macronutrients, micronutrients, and food groups) with MSI. In-person interviews elicited information on potential colon cancer risk factors, and a previously validated food frequency questionnaire adapted to include regional foods was used to assess diet over the year before diagnosis or interview date. MSI was classified as MSI-high (MSI-H) and MSI-low or microsatellite stable (MSI-L/MSS). Multivariate logistic regression models estimated energy-adjusted and non-energy-adjusted odds ratios (OR). Ten percent of the cases (n = 49) had MSI-H tumors (29% African American). The strongest associations between diet and MSI were observed in case-control comparisons: there was a robust inverse association between MSI-H status and beta-carotene [OR, 0.4; 95% confidence interval (95% CI), 0.2-0.9] and positive associations with energy-adjusted refined carbohydrates (OR, 2.2; 95% CI, 0.9-5.4) and non-energy-adjusted read meat intake (OR, 2.0; 95% CI, 0.9-4.2). Compared with controls, MSI-L/MSS tumors were statistically significantly associated with energy-adjusted vitamin C, vitamin E, calcium, dietary fiber, and dark green vegetables and positively associated with total energy intake (all Ps for trend < 0.05). In case-case comparisons, no dietary factors were significantly differently related to MSI-H compared with MSI-L/MSS tumors. Refined carbohydrate and red meat consumption may promote development of MSI-H tumors, whereas beta-carotene may be associated with lower risk.

Social Ties and Colorectal Cancer Screening among Blacks and Whites in North Carolina

AbstractFew studies have examined the relationship between social networks and colorectal cancer screening in diverse populations. Prior research suggests that the type of social support as well as the amount or frequency of support available from one's social network may be associated with health outcomes. Therefore, the current study examined relationships between both structural (i.e., quantitative aspects of the social network, such as number of ties and frequency of contact with ties) and functional (i.e., functions provided by social network ties, such as offering emotional or instrumental support) aspects of social ties and utilization of colorectal cancer screening tests. Analyses included 697 randomly selected Blacks and Whites ages 51 to 80 years enrolled as controls in the North Carolina Colon Cancer Study. Social tie and screening information was obtained from face-to-face interviews. Forty-seven percent of participants (40% Blacks and 51% Whites) reported use of one of the options for colorectal cancer screening according to the guidelines at that time. Compared with those with the fewest social connections, those who were most socially connected were more likely to report recent use of colorectal cancer screening [odds ratio (OR), 3.2; 95% confidence interval (95% CI), 1.7-6.2]. This association was stronger among Blacks (OR, 3.8; 95% CI, 1.3-10.7) than Whites (OR, 2.9; 95% CI, 1.2-6.9; P for interaction = 0.006). There were also positive associations between being a church group (OR, 1.9; 95% CI, 1.4-2.7) and other group member (OR, 1.6; 95% CI, 1.1-2.2) and screening. Neither emotional (e.g., offering reassurance that one is cared for) nor instrumental (e.g., giving material assistance) support was associated with screening behavior. These data suggest that structural rather than functional aspects of social ties may be important in influencing colorectal cancer screening behavior.

Longitudinal Changes in Lifestyle Behaviors and Health Status in Colon Cancer Survivors

Abstract Lifestyle changes in persons diagnosed with cancer are important because they may impact prognosis, co-morbidities, and survival. This report describes longitudinal changes in lifestyle behaviors and health status among colon cancer survivors (n = 278) and population-based controls (n = 459) in North Carolina (39% African American), and examines demographic and psychosocial correlates of healthy lifestyle changes following a colon cancer diagnosis. Data are from surveys of a population-based cohort of colon cancer patients on diagnosis (the North Carolina Colon Cancer Study, NCCCS) and approximately 2 years post-diagnosis [the North Carolina Strategies to Improve Diet, Exercise, and Screening Study (NC STRIDES)], and population-based controls. Both studies collected information on demographic/lifestyle characteristics and medical history. The NCCCS reflects pre-diagnosis or pre-interview patterns, whereas NC STRIDES queried on current practices. Between the NCCCS and NC STRIDES, colon cancer survivors reported significant increases in vegetable intake, physical activity, and supplement use (all P &amp;lt;0.01) and a non-statistically significant increase in fruit/juice consumption (0.1 serving), with larger fruit/vegetable changes in African Americans than Whites. Controls increased physical activity and supplement use and fewer reported arthritic symptoms (P &amp;lt; 0.05). Survivors who were older and female had an almost 3 times higher likelihood of having used at least one new dietary supplement post-diagnosis, whereas being retired correlated with increased vegetable intake, all P &amp;lt; 0.05. Having more barriers to increasing fruit/vegetable intake was inversely associated with taking a new supplement (P &amp;lt; 0.05 only in controls). Colon cancer survivors reported making significant improvements in multiple health-related behaviors. Health care providers should communicate with persons diagnosed with colon cancer to ensure that they are making healthy lifestyle changes.