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The overall survival rate of prostate cancer (PCa) has improved over the past decades. However, huge socioeconomic and racial disparities in overall and prostate cancer-specific mortality exist. The neighborhood-level factors including socioeconomic disadvantage and lack of access to care may contribute to disparities in cancer mortality. This study examines the impact of neighborhood deprivation on mortality among PCa survivors.North Carolina-Louisiana Prostate Cancer Project (PCaP) data were used. A total of 2113 men, 1046 AA and 1067 EA, with PCa were included in the analysis. Neighborhood deprivation was measured by the Area Deprivation Index (ADI) at the census block group level using data from the US Census Bureau. Quintiles of ADI were created. Cox proportional hazards and competing risk models with mixed effects were performed to estimate the effect of neighborhood deprivation on all-cause and PCa-specific mortality adjusted for age, race, study site, insurance status, and comorbidities.Participants living in the most deprived neighborhoods had an increased risk for all-cause mortality (quintiles 4 + 5: adjusted hazard ratio [aHR] = 1.51, 95% confidence interval [CI] = 1.16-1.96) compared to those in the least deprived (quintile 1) neighborhoods. The risk of prostate cancer-specific mortality was also higher among those living in the deprived neighborhoods (quintiles 4 + 5: aHR = 1.90, 95% CI = 1.10-3.50) than those in the least deprived neighborhood.The findings suggest neighborhood-level resources or health interventions are essential to improve survival among men with PCa. Additional research should focus on the mechanisms of how the neighborhood environment affects mortality.

Patient and clinical characteristics of Caucasian and African American statin users and non-users.

Logistic regression analysis of associations between statin use and prostate cancer aggressiveness, additionally adjusted for education, income and family history of prostate cancer.

Background: Although statin use has been associated with reduced prostate cancer aggressiveness, the impact of race and patient characteristics on this association is not well understood. We examined the association between statin use and prostate cancer aggressiveness in Caucasians (CA) and African Americans (AA) and explored effect modification by health-seeking behaviors associated with statin use.Methods: Of 1,930 cases from The North Carolina-Louisiana Prostate Cancer Project, 344 (18%) were classified as aggressive based on clinical criteria. Utilizing nonaggressive cases as referent, logistic regression was used to examine the association between statin use and prostate cancer aggressiveness, overall and stratified by race. Smoking and prostate cancer screening were examined as effect modifiers of this association.Results: There was an inverse association between statin use and prostate cancer aggressiveness [OR, 0.74; 95% confidence interval (CI), 0.56–0.96], with comparable effect estimates in both races. Although not statistically significant, statin use was associated with reduced ORs for aggressive prostate cancer in never-screened men (OR, 0.79; 95% CI, 0.45–1.39), men screened at low/recommended frequency (≤once/year; OR, 0.66; 95% CI, 0.41–1.06), and men screened at high frequency (>once/year; OR, 0.78; 95% CI, 0.53–1.15). Inverse associations between statins and aggressive prostate cancer were strongest in never smokers (OR, 0.42; 95% CI, 0.25–0.72), attenuated in former smokers (OR, 0.84; 95% CI, 0.59–1.19), and absent in current smokers (OR, 1.36; 95% CI, 0.70–2.64).Conclusions: Statin use was associated with reduced prostate cancer aggressiveness in CA and AAs, with strongest inverse associations in nonsmokers.Impact: Health-seeking behaviors associated with statin use should be considered when examining the impact of statins on prostate cancer aggressiveness. Cancer Epidemiol Biomarkers Prev; 25(4); 670–7. ©2016 AACR.

Logistic regression analysis of associations between statin use and prostate cancer aggressiveness, excluding men using non-statin cholesterol-lowering drugs.

Financial toxicity (FT) is a growing concern among cancer survivors that adversely affects the quality of life and survival. Individuals diagnosed with aggressive cancers are often at a greater risk of experiencing FT. The objectives of this study were to estimate FT among prostate cancer (PCa) survivors after 10-15 years of diagnosis, assess the relationship between PCa aggressiveness at diagnosis and FT, and examine whether current cancer treatment status mediates the relationship between PCa aggressiveness and FT.PCa patients enrolled in the North Carolina-Louisiana Prostate Cancer Project (PCaP) were recontacted for long-term follow-up. The prevalence of FT in the PCaP cohort was estimated. FT was estimated using the COmprehensive Score for Financial Toxicity, a validated measure of FT. The direct effect of PCa aggressiveness and an indirect effect through current cancer treatment on FT was examined using causal mediation analysis.More than one-third of PCa patients reported experiencing FT. PCa aggressiveness was significantly independently associated with high FT; high aggressive PCa at diagnosis had more than twice the risk of experiencing FT than those with low or intermediate aggressive PCa (adjusted odds ratio [aOR] = 2.13, 95% CI = 1.14-3.96). The proportion of the effect of PCa aggressiveness on FT, mediated by treatment status, was 10%, however, the adjusted odds ratio did not indicate significant evidence of mediation by treatment status (aOR = 1.05, 95% CI = 0.95-1.20).Aggressive PCa was associated with high FT. Future studies should collect more information about the characteristics of men with high FT and identify additional risk factors of FT.

To better understand health care utilization and develop decision support tools, methods for identifying patients with suspected genetic diseases (GDs) are needed. Previous studies had identified inpatient-relevant International Classification of Diseases (ICD) codes that were possibly, probably, or definitely indicative of GDs. We assessed whether these codes identified GD-related inpatient, outpatient, and emergency department encounters among pediatric patients with suspected GDs from a previous study (the North Carolina Clinical Genomic Evaluation by Next-Generation Exome Sequencing [NCGENES] study).Using the electronic medical records of 140 pediatric patients from the NCGENES study, we characterized the presence of ICD codes representing possible, probable, or definite GD-related diagnoses across encounter types. In addition, we examined codes from encounters for which initially no GD-related codes had been found and determined whether these codes were indicative of a GD.Among NCGENES patients with visits between 2014 and 2017, 92% of inpatient, 75% of emergency department, and 63% of outpatient encounters included ≥1 GD-related code. Encounters with highly specific (ie, definite) GD codes had fewer low-specificity GD codes than encounters with only low-specificity GD codes. We identified an additional 32 ICD-9 and 56 ICD-10 codes possibly indicative of a GD.Code-based strategies can be refined to assess health care utilization among pediatric patients and may contribute to a systematic approach to identify patients with suspected GDs.

Background The early diagnosis and treatment of depression are cancer care priorities. These priorities are critical for prostate cancer survivors because men rarely seek mental health care. However, little is known about the epidemiology of depression in this patient population. The goal of this study was to describe the prevalence and predictors of probable depression in prostate cancer survivors. Methods The data were from a population-based cohort of North Carolinian prostate cancer survivors who were enrolled from 2004 to 2007 in the North Carolina-Louisiana Prostate Cancer Project (n = 1031) and were prospectively followed annually from 2008 to 2011 in the Health Care Access and Prostate Cancer Treatment in North Carolina study (n = 805). Generalized estimating equations were used to evaluate an indicator of probable depression (Short Form 12 mental composite score ≤48.9; measured at enrollment and during the annual follow-up) as a function of individual-level characteristics within the longitudinal data set. Results The prevalence of probable depression fell from 38% in the year of the cancer diagnosis to 20% 6 to 7 years later. Risk factors for probable depression throughout the study were African American race, unemployment, low annual income, younger age, recency of cancer diagnosis, past depression, comorbidities, treatment decisional regret, and nonadherence to exercise recommendations. Conclusions Depression is a major challenge for prostate cancer survivors, particularly in the first 5 years after the cancer diagnosis. To the authors' knowledge, this is the first study to demonstrate an association between treatment decisional regret and probable depression.

Background Appropriate depression care is a cancer‐care priority. However, many cancer survivors live with undiagnosed and untreated depression. Prostate cancer survivors may be particularly vulnerable, but little is known about their access to depression care. The goal of this study was to describe patterns and predictors of clinical diagnosis and treatment of depression in prostate cancer survivors. Methods Generalized estimating equations were used to evaluate indicators of self‐reported clinical diagnosis and treatment depression as a function of individual‐level characteristics within a longitudinal dataset. The data were from a population‐based cohort of North Carolinian prostate cancer survivors who were enrolled from 2004 to 2007 on the North Carolina‐Louisiana Prostate Cancer Project (N = 1,031), and prospectively followed annually from 2008 to 2011 on the Health Care Access and Prostate Cancer Treatment in North Carolina (N = 805). Results The average rate of self‐reported clinical diagnosis of depression was 44% (95% CI: 39%‐49%), which declined from 60% to 40% between prostate cancer diagnosis and 5‐7 years later. Factors associated with lower odds of self‐reported clinical diagnosis of depression include African‐American race, employment, age at enrollment, low education, infrequent primary care visits, and living with a prostate cancer diagnosis for more than 2 years. The average rate of self‐reported depression treatment was 62% (95% CI: 55%‐69%). Factors associated with lower odds of self‐reported depression treatment included employment and living with a prostate cancer diagnosis for 2 or more years. Conclusion Prostate cancer survivors experience barriers when in need of depression care.

Background Exome sequencing (ES) has probable utility for shortening the diagnostic odyssey of children with suspected genetic disorders. This report describes the design and methods of a study evaluating the potential of ES as a routine clinical tool for pediatric patients who have suspected genetic conditions and who are in the early stages of the diagnostic odyssey. Methods The North Carolina Clinical Genomic Evaluation by Next-generation Exome Sequencing (NCGENES) 2 study is an interdisciplinary, multi-site Phase III randomized controlled trial of two interventions: educational pre-visit preparation (PVP) and offer of first-line ES. In this full-factorial design, parent-child dyads are randomly assigned to one of four study arms (PVP + usual care, ES + usual care, PVP + ES + usual care, or usual care alone) in equal proportions. Participants are recruited from Pediatric Genetics or Neurology outpatient clinics in three North Carolina healthcare facilities. Eligible pediatric participants are Discussion NCGENES 2 will contribute valuable knowledge concerning technical, clinical, psychosocial, and health economic issues associated with using early diagnostic ES to shorten the diagnostic odyssey of pediatric patients with likely genetic conditions. Results will inform efforts to engage diverse populations in genomic medicine research and generate evidence that can inform policy, practice, and future research related to the utility of first-line diagnostic ES in health care. Trial registration ClinicalTrials.govNCT03548779. Registered on June 07, 2018.

RESEARCH OBJECTIVE: Racial disparities in health care experiences and access are well‐documented. Yet, little is known regarding racial variations in the confluence of multiple health care access (HCA) experiences among cancer patients. We identified cancer patient subgroups with similar, co‐occurring HCA experiences, and evaluated racial differences in HCA subgroup membership. STUDY DESIGN: We used data from the University of North Carolina Health Registry/Cancer Survivorship Cohort. Participants completed a baseline questionnaire assessing demographics, health history, health‐related quality of life, and health care experiences. HCA was assessed along five domains (ie, doctor interpersonal manner, doctor communication, financial burden, time spent with doctor, and accessibility/convenience) using the RAND Patient Satisfaction Questionnaire. We used latent profile analysis to identify subgroups of patients with similar HCA experiences. Modified Poisson regressions were estimated to assess racial differences in HCA subgroup membership, adjusting for patient clinical and demographic characteristics. POPULATION STUDIED: Black and white breast, gastrointestinal, genitourinary, and head/neck cancer patients aged 18 or older and enrolled in the University of North Carolina Health Registry/Cancer Survivorship Cohort during 2010 to 2016. PRINCIPAL FINDINGS: Our analysis included 393 black (14.8%) and 2265 white (85.2%) participants. The latent profile analysis resulted in an optimal solution of 5 HCA profiles/subgroups, ranging from Low HCA to High HCA. Members of profile 1 (6.0% of sample) reported “Low” HCA along all HCA domains. Profile 2 (10.8%) consisted of individuals reporting low scores on every HCA domain except “financial burden,” where scores were moderate. Profile 3 (49.9%) members exhibited moderate scores on each HCA domain, while members of profile 4 (11.7%%) reported moderate HCA scores on most HCA domains, with the exception of low scores on “financial burden.” Profile 5 (21.7%) was comprised of patients reporting “High” HCA along every HCA domain. In unadjusted chi‐square comparisons, black patients were more likely to be in the “Low” HCA group (Profile 1) than whites (11.11% vs 5.3%, P

PURPOSE: Obesity may alter mononuclear phagocyte system (MPS) function and the pharmacology and efficacy of nanoparticles therapies, such as PEGylated liposomal doxorubicin (PLD). We aimed to evaluate relationships between hormone and chemokine mediators of MPS function and the pharmacokinetic (PK) exposure of PLD in obese and normal weight patients with ovarian and endometrial cancer. METHODS: Hormone and chemokine mediators in obese and normal weight ovarian and endometrial cancer patients were measured. A separate pharmacology study was performed that evaluated the relationship between serum hormone concentrations, MPS function, and PK disposition of PLD in refractory ovarian cancer patients. RESULTS: Univariate analysis revealed a significant relationship between serum estradiol and body mass index (OR: 8.64, 95% CI: 2.67–28.0, p

BACKGROUND: Statin use is associated with lower advanced prostate cancer risk and reduced prostate cancer-specific mortality, but prior studies were conducted mainly in white men. We examined the effect of statin use on risk of prostate cancer progression in a population-based, minority-enriched cohort.METHODS: We used data from prostate cancer cases (45% African American) diagnosed between 2004 and 2007 who participated in the Health Care Access and Prostate Cancer Treatment in North Carolina cohort (HCaP-NC). We abstracted statin use at diagnosis. Men reported if they had ever been diagnosed with high cholesterol. Multivariable Cox proportional hazards analysis was used to examine associations between statin use and risk of prostate cancer progression (biochemical recurrence or secondary treatment), overall and by race. In secondary analysis, we examined the association between high cholesterol and risk of progression, overall, and by statin use.RESULTS: Of 669 men, 244 (36%) were statin users at diagnosis. During 3.8 years median follow-up, 138 men experienced prostate cancer progression. There was no association between statin use and risk of progression, either overall (HR 1.03; 95%CI 0.72-1.46) or stratified by race. High cholesterol was inversely associated with risk of progression, particularly among statin users (HR 0.43; 95%CI 0.20-0.94; p-interaction = 0.22) and in men with higher perceived access to care (HR 0.57; 95%CI 0.36-0.90; p-interaction = 0.03). Study limitations included a relatively small sample size, short follow-up, and lack of data regarding post diagnosis statin use.CONCLUSIONS: Statin use at diagnosis was not associated with prostate cancer progression in the population-based, minority-enriched HCaP-NC. Greater healthcare engagement, including actively controlling serum cholesterol, may be linked to better prostate cancer-specific outcomes.

The metabolic landscape of the prostate changes with malignant transformation, and metabolomics is a means of identifying diagnostic and prognostic biomarkers for prostate cancer. Epidemiology and registry studies containing archival formalin-fixed paraffin-embedded (FFPE) specimens are a rich resource for this work but this method of tissue preservation presents a challenge due to loss of metabolites. We optimized global metabolic profiling in FFPE tissue and identified metabolites distinguishing tumor from normal prostate tissue, and aggressive from non-aggressive prostate cancer. For optimization of metabolomics in FFPE tissues, we obtained matched frozen and FFPE tumor tissue from 62 prostate cancer cases who underwent radical prostatectomy (RP) at the University of North Carolina (UNC) hospital, of which 24 also had adjacent normal prostate tissue. To identify metabolites associated with tumor aggressiveness, we obtained matched tumor and normal FFPE tissue from 60 prostate cancer patients (Gleason ≥4+3, n=30; Gleason ≤3+4, n=30) who underwent RP participating in the UNC Health Registry/Cancer Survivorship Cohort. Following log transformation and imputation of missing values with the minimum observed value for each compound, Welch's two-sample t-test was used to identify biochemicals that differed significantly between groups. Random forest analysis evaluated predictive accuracy of metabolites for distinguishing tumor from normal prostate tissue. We identified 768 compounds of known identity in frozen and 119 in matched FFPE tissues. Therefore, only 15% of the metabolites detected in frozen samples were recovered from corresponding FFPE tissue, with 80% of these common to both FFPE and matched frozen tissues. We found a predictive accuracy of 78% and 67% for frozen and FFPE tissue, respectively, for distinguishing tumor from normal. Of 39 metabolites significantly altered between matched tumor and normal FFPE tissue, 47% belonged to the lipid class, and despite a greater number of significantly altered metabolites in frozen tissue (246), the proportion belonging to the lipid class was similar (50%). Citrate, integral to normal prostate metabolism, and citrulline, involved in nitric oxide synthesis, had significantly lower levels in aggressive versus non-aggressive tumors. Cell membrane phospholipids were found at significantly higher levels in aggressive tumors. Common patterns of altered metabolites in tumor vs. normal prostate were observed irrespective of tissue preservation method, despite loss of a large proportion of metabolites during the process of FFPE. As such, FFPE studies are feasible particularly when lipid metabolism is of interest as this class appears one of the best preserved in FFPE. This work will pave the way for incorporating metabolomics profiling of FFPE specimens into epidemiology and registry-based studies of prostate cancer. Citation Format: Sophia Rachael Halliday, Linnea T. Olsson, Alina Hamilton, Sivapriya Ramamoorthy, Jason Kitchen, Erin Kirk, Laura Farnan, Adrian Gerstel, Melissa A. Troester, Jannette T. Bensen, Sara E. Wobker, Emma Allott. Metabolomics profiling of formalin-fixed paraffin-embedded prostate tissues [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2021; 2021 Apr 10-15 and May 17-21. Philadelphia (PA): AACR; Cancer Res 2021;81(13_Suppl):Abstract nr 2347.

Background: Although statin use has been associated with reduced prostate cancer aggressiveness, the impact of race and patient characteristics on this association is not well understood. We examined the association between statin use and prostate cancer aggressiveness in Caucasians (CA) and African Americans (AA) and explored effect modification by health-seeking behaviors associated with statin use. Methods: Of 1,930 cases from The North Carolina-Louisiana Prostate Cancer Project, 344 (18%) were classified as aggressive based on clinical criteria. Utilizing nonaggressive cases as referent, logistic regression was used to examine the association between statin use and prostate cancer aggressiveness, overall and stratified by race. Smoking and prostate cancer screening were examined as effect modifiers of this association. Results: There was an inverse association between statin use and prostate cancer aggressiveness [OR, 0.74; 95% confidence interval (CI), 0.56–0.96], with comparable effect estimates in both races. Although not statistically significant, statin use was associated with reduced ORs for aggressive prostate cancer in never-screened men (OR, 0.79; 95% CI, 0.45–1.39), men screened at low/recommended frequency (≤once/year; OR, 0.66; 95% CI, 0.41–1.06), and men screened at high frequency (>once/year; OR, 0.78; 95% CI, 0.53–1.15). Inverse associations between statins and aggressive prostate cancer were strongest in never smokers (OR, 0.42; 95% CI, 0.25–0.72), attenuated in former smokers (OR, 0.84; 95% CI, 0.59–1.19), and absent in current smokers (OR, 1.36; 95% CI, 0.70–2.64). Conclusions: Statin use was associated with reduced prostate cancer aggressiveness in CA and AAs, with strongest inverse associations in nonsmokers. Impact: Health-seeking behaviors associated with statin use should be considered when examining the impact of statins on prostate cancer aggressiveness. Cancer Epidemiol Biomarkers Prev; 25(4); 670–7. ©2016 AACR.

Background Racial disparities in time-to-treatment exist among cancer patients, with patients of color being more likely to experience treatment delays. Such racial differences in treatment initiation are likely on the causal pathway to inequities in treatment outcomes. Emerging research has documented racial differences in financial burden, but little is known about the contribution of financial burden to disparities in treatment delays. In this study, we evaluated whether financial burden partly accounted for racial disparities in time to treatment initiation among a cohort of cancer survivors. Methods We used cross-sectional data of patients enrolled in the University of North Carolina Health Registry/Cancer Survivorship Cohort (HR/CSC) between 2010 and 2016. The sample for this study was limited to cancer patients and survivors who identified as non-Hispanic White or Black, received a diagnosis for breast, genitourinary, gastrointestinal, or head or neck cancer, and completed a questionnaire at least 30 days following their diagnosis (N=2,123). Time to treatment was measured in number of days from diagnosis to start of first course of treatment, ascertained from the medical record. Initial treatment was either surgery, chemotherapy, radiation, or hormonal therapy, depending on the clinical indication. Financial burden was assessed using the Patient Satisfaction Questionairre-18 on the self-reported satisfaction with the financial aspects of care (>3.5 is satisfied; Citation Format: Wendi Elkins, Olive Mbah, Jeannette T Benson, Laura Farnan, Neda Padilla, Sam Cykert, Bryce B Reeve, Giselle Corbie-Smith, Cleo A. Samuel. Impact of racial differences in financial burden on time to treatment [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr D071.

PURPOSE: Metformin has been associated with a reduced incidence of prostate cancer and improved prostate cancer outcomes. However, whether race modifies the association between metformin use and prostate cancer aggressiveness remains uncertain. The association between metformin use and prostate cancer aggressiveness was examined separately in Black Americans (Blacks) and White Americans (Whites). METHODS: The study population consisted of 305 Black and 195 White research participants with incident prostate cancer and self-reported diabetes from the North Carolina-Louisiana Prostate Cancer Project (PCaP). High aggressive prostate cancer was defined using a composite measure of Gleason sum, prostate-specific antigen, and clinical stage. Multivariable logistic regression was used to assess the association between metformin use and high aggressive prostate cancer at diagnosis, separately among Whites and Blacks, with adjustment for age, screening history, site, education, insurance, and body mass index. RESULTS: Metformin use was associated positively with high aggressive prostate cancer in Blacks (OR: 2.01; 95% CI: 1.05, 3.83). By contrast, a weak inverse association between metformin use and high aggressive prostate cancer was found in Whites (OR: 0.80, 95% CI: 0.34, 1.85). CONCLUSIONS: The association between metformin use and prostate cancer aggressiveness may be modified by race.

BACKGROUND The role of race in modifying the association among diabetes, obesity, and prostate cancer (CaP) progression is not well studied. We evaluated diabetes and obesity in association with time to CaP progression in White Americans (Whites) and Black Americans (Blacks). METHODS Our study sample consisted of 363 White and 284 Black research participants from the Health Care Access and CaP Treatment in North Carolina (HCaP-NC) cohort. The association between self-reported diabetes or obesity and CaP progression (mean follow-up time approximately 5 years) was assessed using Cox proportional hazards modeling, with adjustment for potential confounders. Stratum-specific hazard ratio (HR) estimates for Whites and Blacks were evaluated. RESULTS Self-reported diabetes was not associated with CaP progression in the cohort as a whole (HR: 0.86, 95%CI: 0.54, 1.35), or among racially defined groups (Whites, HR: 1.03, 95%CI: 0.50, 2.13 or Blacks, HR: 0.77, 95%CI: 0.43, 1.39). Obesity was positively associated with CaP progression among Whites, in models including (HR: 1.79, 95%CI: 1.08, 2.97), and excluding (HR: 1.80, 95%CI: 1.09, 2.96) diabetes as a covariate. No association was observed between obesity and CaP progression in Blacks or the cohort as whole. CONCLUSIONS Self-reported diabetes was not associated with CaP progression In HCaP-NC. Obesity was associated with CaP progression only among White research participants. Prostate 77:878–887, 2017. © 2017 Wiley Periodicals, Inc.

BACKGROUND: Epidemiologic and laboratory evidence supports a role for cholesterol in prostate cancer (PC). Dietary saturated fat content impacts serum cholesterol levels. However, epidemiologic associations between saturated fat and PC aggressiveness are inconsistent. We hypothesized that high saturated fat intake would be associated with increased PC aggressiveness, and that statin use would modify this association.METHODS: Of 1854 PC cases in the North Carolina-Louisiana PC Project, 321 (17%) were classified as high aggressive (Gleason sum ⩾8, PSA>20 ng ml-1, or Gleason sum ⩾7 and clinical stage T3-4) or low/intermediate aggressive (all other cases). Using low/intermediate aggressive cases as the referent group, we examined the association between tertiles of total fat-adjusted saturated fat intake and high aggressive PC using logistic regression, overall and stratified by race and statin use. We examined total fat-adjusted polyunsaturated and monounsaturated fatty acids (PUFA and MUFA, respectively), trans fat and cholesterol intake in secondary analysis.RESULTS: High total fat-adjusted saturated fat intake was associated with an elevated odds ratio (OR) for aggressive PC (ORT3vsT1 1.51; 95% CI 1.10-2.06; P-trend=0.009), with an attenuated association in statin users (ORT3vsT1 1.16; 95% CI 0.67-2.01; P-trend=0.661) compared with non-users (ORT3vsT1 1.71; 95% CI 1.16-2.51; P-trend=0.053). High total fat-adjusted cholesterol intake was associated with aggressive PC in European Americans (ORT3vsT1 1.62; 95% CI 1.02-2.58; P-trend=0.056), but not African Americans (ORT3vsT1 0.92; 95% CI 0.60-1.42; P-trend=0.750). High total fat-adjusted PUFA was inversely associated with PC aggressiveness (ORT3vsT1 0.75; 95% CI 0.55-1.03), although this was not significant. No associations were found between total fat-adjusted MUFA or trans fat and PC aggressiveness.CONCLUSIONS: High total fat-adjusted saturated fat intake was associated with increased PC aggressiveness, with a suggestion of a stronger effect in men not using statins. The association between total fat-adjusted cholesterol intake and PC aggressiveness was most pronounced in European Americans.

Few studies have investigated the role of race in the association of diabetes and obesity with prostate cancer aggressiveness. Here we evaluate the independent association between diabetes and obesity with prostate cancer aggressiveness in White Americans and Black Americans.Our cross-sectional, case-only study consisted of 1,058 White Americans and 991 Black Americans from the North Carolina-Louisiana Prostate Cancer (PCaP) project. Diabetes status was determined by self-report. Obesity was determined using body mass index and calculated based on anthropometric measurements. High aggressive prostate cancer was defined as Gleason sum ≥8, or prostate-specific antigen20 ng/ml, or Gleason sum = 7 and clinical stage cT3-cT4. The association between diabetes and obesity with high aggressive prostate cancer at diagnosis was evaluated using multivariable logistic regression and adjusted for potential confounders.Diabetes was not associated with high aggressive prostate cancer in the overall sample (OR 1.04; 95% CI 0.79, 1.37), White Americans (OR 1.00; 95% CI 0.65, 1.57) or Black Americans (OR 1.07; 95% CI 0.75, 1.53). Obesity, independent of diabetes, was positively associated with high aggressive prostate cancer in White Americans (OR 1.98; 95% CI 1.14, 3.43), but not in the overall sample (OR 1.37; 95% CI 0.99, 1.92) or Black Americans (OR 1.09; 95% CI 0.71, 1.67).Diabetes was not associated with prostate cancer aggressiveness, overall, or in either race group. Obesity, independent of diabetes, was associated with high aggressive prostate cancer only in White Americans.

Introduction: Epidemiologic data support a positive association between hypercholesterolemia and aggressive prostate cancer, and an inverse association between statin use and aggressive prostate cancer. Saturated fat intake is an important dietary determinant of serum cholesterol levels. However, epidemiologic evidence supporting a role for saturated fat in prostate cancer aggressiveness is mixed. We hypothesized that high saturated fat intake would be associated with increased prostate cancer aggressiveness, and that this association would be modified by statin use. Methods: Of 1,854 prostate cancer cases in the North Carolina-Louisiana Prostate Cancer Project (PCaP), 321 (17%) were classified as high aggressive based on clinical criteria. Saturated fat intake was adjusted for total fat intake using the residual method, and categorized into tertiles based on the distribution among all research subjects. Using low and intermediate aggressive cases as the reference group, logistic regression was used to examine the association between tertiles of saturated fat intake and prostate cancer aggressiveness, overall and stratified by race and by statin use. In addition to demographic and screening variables, energy-adjusted total fat intake and energy intake were included as covariates in our models. In secondary analysis, we examined associations for total fat, monounsaturated and polyunsaturated fatty acids (MUFA and PUFA, respectively), trans fat, and cholesterol intake. Results: High saturated fat intake was associated with an elevated odds ratio (OR) for aggressive prostate cancer (ORupper tertile (T3) vs. lower (T1) 1.44; 95% CI 1.06-1.96; p-trend = 0.020). The magnitude of this association was weaker in statin users (ORT3 vs. T1 1.10; 95% CI 0.63-1.91; p-trend = 0.790) compared to men not using statins (ORT3 vs. T1 1.63; 95% CI 1.11-2.37; p-trend = 0.015). There was a suggestion of a positive association between high cholesterol intake and aggressive prostate cancer among all men (ORT3 vs. T1 1.28; 95% CI 0.94-1.75; p-trend = 0.074), and this association was more pronounced in European Americans (ORT3 vs. T1 1.82; 95% CI 1.15-2.88; p-trend = 0.012). Elevated PUFA intake was inversely associated with prostate cancer aggressiveness (ORT3 vs. T1 0.66; 95% CI 0.48-0.90; p-trend = 0.009), with similar effect estimates in both races. There were no associations between trans fat or MUFA and prostate cancer aggressiveness. Conclusions: Elevated intake of saturated fat was positively associated, while high intake of PUFA was inversely associated, with aggressive prostate cancer. Weaker associations between saturated fat and prostate cancer aggressiveness in statin users suggest that the impact of saturated fat on serum cholesterol levels may be one potential mechanism by which saturated fat impacts prostate cancer aggressiveness. Citation Format: Emma H. Allott, Lenore Arab, L. Joseph Su, Laura Farnan, Elizabeth T.H. Fontham, James L. Mohler, Jeannette T. Bensen, Susan E. Steck. Saturated fat intake and prostate cancer aggressiveness: Results from the population-based North Carolina-Louisiana prostate cancer project. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1760.

BACKGROUND: The current study examined how patients' sociodemographic, cancer-related, and subjective affective factors impacted their role in treatment decision-making. METHODS: The patient sample (N = 788) was taken from a prospective follow-up study of a population-based cohort. Participants included 343 African American and 445 Caucasian-American patients with clinically localized prostate cancer. Multinomial logistic regression was used to investigate relations between the explanatory variables and the nominal 3-level decision-making variable: patient-only, patient-physician shared, and physician-only. RESULTS: Approximately 41% of patients reported patient-only decision-making, 45% reported shared decision-making, and 13% reported physician-only decision-making. The odds of patient-only over physician-only decision-making were greater for younger men (vs those aged ≥ 65 years) (odds ratio [OR], 1.68; 95% confidence interval [95% CI], 1.03-2.74), and were less for men with high (vs low) cancer aggressiveness (OR,0.29; 95% CI, 0.15-0.55). The odds of shared over physician-only decision-making were less for men with high (vs low) cancer aggressiveness (OR, 0.40; 95% CI, 0.22-0.73). Greater odds of patient-only and shared decision-making also were found to be associated with greater concerns about the physical impact of treatment and having enough time for decision-making and lower scores of receiving advice from others. CONCLUSIONS: The findings of the current study indicate that, to facilitate a more patient-oriented decision-making process regarding treatment in those with clinically localized prostate cancer, clinicians need to tailor their interventions according to patient age and cancer aggressiveness, help reduce patient concerns and misconceptions regarding the physical impact of treatments, allow sufficient time for patients to consider treatment options, and assist patients in balancing advice and information received from different sources. Cancer 2013. © 2012 American Cancer Society.