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Biomedical subjects

Elizabeth A Platz

Publications and source records attributed to Elizabeth A Platz.

At least 19 recordsLinked to original sources

Plasma signals of lung tumor promotion for molecular cancer prevention.

Predicting lung cancer risk would enhance prevention trials. Although the Canakinumab Anti-inflammatory Thrombosis Outcome Study (CANTOS) trial demonstrated reduced lung cancer incidence with interleukin (IL)-1β inhibition, the high number needed to treat (NNT) to prevent lung cancer limits its use in unselected populations. Using machine learning, we identified a 14-protein plasma signature predicting lung cancer more than 5 years before diagnosis. The signature, validated across eight cohorts, was elevated in current smokers and individuals exposed to particulate matter (PM) and linked to lung myeloid and alveolar cells. In epidermal growth factor receptor (EGFR)-driven lung adenocarcinoma, diverse epithelial lineages converged on a keratin8+/claudin4+ alveolar transitional state (KAC), whose transcriptional programs correlated with signature emergence. Components of the signature were induced by PM, oncogenic EGFR, or IL-1β, whereas IL-1β inhibition restrained PM-driven KAC expansion and early tumorigenesis. In CANTOS, the signature identified individuals who seemed to benefit more from anti-IL-1β therapy, lowering the NNT threshold and nominating circulating signals of tumor promotion for prevention.

Humans↗

MyGeneRisk Colon: A Web-Based Tool for Personalized Colorectal Cancer Risk Prediction Based on Genetics and Lifestyle.

Colorectal cancer (CRC) is a leading cause of cancer-related death, with incidence rising substantially among individuals under 50 years of age. Polygenic risk scores (PRS) hold promise for identifying high-risk individuals; when combined with lifestyle factors, they substantially improve prediction accuracy compared with models based on lifestyle factors alone. However, few clinical tools currently exist that facilitate this integrated, PRS-enhanced risk assessment. To bridge this gap, we developed MyGeneRisk Colo n, a publicly accessible web portal that delivers individualized CRC risk prediction by incorporating genetic, demographic, family history, and lifestyle factors. This paper details the development of the underlying risk prediction model, the portal's architecture and data security, our reporting framework, and engagement with a community advisory panel. Designed as a user-friendly platform, MyGeneRisk Colon aims to effectively communicate personalized CRC risk profiles and educate users and healthcare providers about prevention strategies.

Journal Article↗

Genetic risk factors modulate the association between physical activity and colorectal cancer.

BACKGROUND: Physical activity (PA) is an established protective factor for colorectal cancer (CRC), but it is unclear if genetic variants modify this effect. To investigate this possibility, we conducted a genome-wide gene-PA interaction analysis. METHODS: Using logistic regression and two-step and joint tests, we analyzed interactions between common genetic variants across the genome and PA in relation to CRC risk. Self-reported PA levels were categorized as active (&#x2265; 8.75 MET-h/wk) vs. inactive (< 8.75 MET-h/wk) and as study- and sex-specific quartiles of activity. RESULTS: PA had an overall protective effect on CRC (OR [active vs. inactive] = 0.85; 95%CI = 0.81-0.90). The two-step GxE method identified an interaction between rs4779584, an intergenic variant near the GREM1 and SCG5 genes, and PA for CRC risk (p-interaction = 2.6&#xd7;10- 8). Stratification by genotype at this locus showed a significant reduction in CRC risk by 20% in active vs. inactive participants with the CC genotype (OR = 0.80; 95%CI = 0.75-0.85), but no significant PA-CRC association among CT or TT carriers. When PA was modeled as quartiles, the 1-d.f. GxE test identified that rs56906466, an intergenic variant near the KCNG1 gene, modified the association between PA and CRC (p-interaction = 3.5&#xd7;10- 8). Stratification at this locus showed that increase in PA (highest vs. lowest quartile) was associated with a lower CRC risk solely among TT carriers (OR = 0.77; 95%CI = 0.72-0.82). CONCLUSIONS: In summary, we identified two genetic variants that modified the association between PA and CRC risk. One of them, related to GREM1 and SCG5, suggests that the bone morphogenetic protein (BMP)-related, inflammatory, and/or insulin signaling pathways may be associated with the protective influence of PA on colorectal carcinogenesis.

GWAS↗

A prospective cohort study of red wine consumption and risk of prostate cancer.

In light of recent, strong inverse findings between lifetime red wine consumption and prostate cancer among younger men, we revisited our previous cohort analysis to more thoroughly investigate red wine consumption and prostate cancer in the Health Professionals Follow-up Study (HPFS). In 1986, HPFS participants reported their average consumption of red wine, white wine, beer and liquor during the past year, and their change in alcohol consumption over the prior 10 years. Prostate cancer diagnoses were ascertained on each biennial questionnaire and confirmed by medical record review. Between 1986 and 2002, 3,348 cases of prostate cancer were diagnosed among 45,433 eligible participants. Using men who did not consume red wine as the reference, no linear trend was observed between red wine consumption and prostate cancer in the full analytic cohort (p-trend = 0.57). Among men with unchanged alcohol consumption in the prior 10 years, and those additionally <65 years of age, slightly lower risks were observed for men who consumed 4 glasses/week, resulting in a lack of linear trend. These findings suggest that red wine does not contribute appreciably to the etiology of prostate cancer.

Adult↗

Mismatch repair polymorphisms and the risk of colorectal cancer.

Rare germline variants in mismatch repair genes have been linked to hereditary nonpolyposis colorectal cancer; however, it is unknown whether common polymorphisms in these genes alter the risk of colorectal cancer. To examine the association between common variants in mismatch repair genes and colorectal cancer, we conducted a case-cohort study within the CLUE II cohort. Four single nucleotide polymorphisms in 3 mismatch repair genes (MSH3 R940Q, MSH3 T1036A, MSH6 G39E and MLH1 I219V) were genotyped in 237 colorectal cancer cases and a subcohort of 2,189 participants. Incidence rate ratios (RRs) and 95% confidence intervals (95% CIs) for each polymorphism were estimated. The MSH3 1036A variant was found to be associated with an increased risk of colorectal cancer (RR=1.28, 95% CI: 0.94-1.74 and RR=1.65, 95% CI: 1.01-2.70 for the AT and TT genotypes, respectively, with p(trend)=0.02), particularly proximal colon cancer. Although the MSH3 940Q variant was only weakly associated with colorectal cancer overall (p(trend)=0.07), it was associated with a significant increased risk of proximal colon cancer (RR=1.69, 95% CI: 1.10-2.61 and RR=2.68, 95% CI: 0.96-7.47 for the RQ and QQ genotypes, respectively with p(trend)=0.005). Processed meat intake appeared to modify the association between the MSH3 polymorphisms and colorectal cancer (p(interaction) < 0.10 for both). No association was observed with the MSH6 and MLH1 polymorphisms overall. This study suggests that common polymorphisms in the mismatch repair gene, MSH3, may increase the risk of colorectal cancer, especially proximal colon cancer.

Adaptor Proteins, Signal Transducing↗

Statin drugs and risk of advanced prostate cancer.

BACKGROUND: Statins are commonly used cholesterol-lowering drugs that have proapoptotic and antimetastatic activities that could affect cancer risk or progression. Results from previous epidemiologic studies of the association between statin use and cancer have been inconsistent. We investigated the association of statin use with total and advanced prostate cancer, the latter being the most important endpoint to prevent. METHODS: We analyzed data from an ongoing prospective cohort study of 34,989 US male health professionals who were cancer free in 1990 and were followed to 2002. Participants reported their use of cholesterol-lowering drugs on biennial questionnaires. Prostate cancer diagnosis was confirmed by medical record review. Multivariable-adjusted relative risks (RRs) were estimated from Cox proportional hazards regression models. Statistical tests were two-sided. RESULTS: During 376,939 person-years of follow-up, we ascertained 2579 prostate cancer cases, 316 of which were advanced (regionally invasive, metastatic, or fatal). The age-standardized incidence rates of advanced prostate cancer were 38 and 89 per 100,000 person-years in current statin users and in past or never users, respectively. The multivariable-adjusted relative risk of advanced disease was 0.51 (95% confidence interval [CI] = 0.30 to 0.86) and of metastatic or fatal disease was 0.39 (95% CI = 0.19 to 0.77) for current statin use compared with no current use. The associations remained after adjusting for prostate-specific antigen screening history (advanced disease: RR = 0.57, 95% CI = 0.30 to 1.11; metastatic or fatal disease: RR = 0.35, 95% CI = 0.14 to 0.92). Risk of advanced disease was lower with longer statin use (P(trend) = .003); compared with never use, the relative risk for less than 5 years of use was 0.60 (95% CI = 0.35 to 1.03) and for 5 or more years of use was 0.26 (95% CI = 0.08 to 0.83). We found no association between statin use and risk of total prostate cancer (RR = 0.96, 95% CI = 0.85 to 1.09). CONCLUSIONS: In this cohort of male health professionals, use of statin drugs was not associated with risk of prostate cancer overall but was associated with a reduced risk of advanced (especially metastatic or fatal) prostate cancer.

Aged↗

The metabolic syndrome is associated with reduced risk of prostate cancer.

Diabetes is associated with reduced risk of prostate cancer, but whether the metabolic syndrome is associated with prostate cancer is not established. The authors assessed this association in the Atherosclerosis Risk in Communities (ARIC) Study, comprising 6,429 men in four US communities initially with no history of cancer and aged 45-64 years. Metabolic syndrome and other risk factors were assessed in 1987-1989. Follow-up for prostate cancer incidence (n = 385 through 2000) was accomplished through cancer registry and hospital linkage. At baseline, 1,871 men (29.5%) had the metabolic syndrome. After the authors adjusted for other risk factors, men with the metabolic syndrome (> or =3 components) were significantly less likely to develop prostate cancer (relative risk = 0.77, 95% confidence interval: 0.60, 0.98) than men without the metabolic syndrome. Diabetes was negatively associated with prostate cancer, although the confidence interval included 1 (relative risk = 0.73, 95% confidence interval: 0.51, 1.05). When diabetic participants were excluded, the inverse association between metabolic syndrome and prostate cancer incidence was slightly strengthened. In this study, the metabolic syndrome was associated with decreased prostate cancer incidence. The authors hypothesize that this finding reflects a decrease in bioavailable (free and albumin-bound) testosterone with the metabolic syndrome and a concomitant reduction in prostate cancer risk.

Humans↗

Genetic polymorphisms of interleukin-1B (IL-1B), IL-6, IL-8, and IL-10 and risk of prostate cancer.

Chronic intraprostatic inflammation is suspected to play a role in the pathogenesis of prostate cancer. Polymorphisms in cytokine genes can influence inflammation and immune response and may be related to the risk of prostate cancer. Four common single nucleotide polymorphisms (SNPs) in the genes encoding interleukin-1B (IL-1B), IL-6, and IL-8 were assessed in 503 prostate cancer cases and 652 controls, and three SNPs in IL-10 were assessed in an additional 817 prostate cancer cases and 1,190 controls (for a total of 1,320 prostate cancer cases and 1,255 controls). Cases and controls were selected from the on-going Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial and were frequency matched on age, ethnicity, time-period since initial screening, and date of blood draw. Single-locus analyses were conducted using conditional logistic regression. In addition, we did a haplotype analysis for the three IL-10 SNPs tested. Overall, no associations were detected between the seven polymorphisms in the four cytokine genes examined in this study and prostate cancer risk. Further stratifying by use of nonsteroidal anti-inflammatory drugs did not modify the associations. Findings were similar for early or advanced prostate cancers. Similarly, we observed no association between the major IL-10 haplotypes and the risk of prostate cancer. At least seven common polymorphisms in genes of inflammatory cytokines IL-1B, IL-6, IL-8, and IL-10 do not seem to play a role in the risk of prostate cancer.

Aged↗

Metabolic factors associated with benign prostatic hyperplasia.

CONTEXT: Benign prostatic hyperplasia poses a significant public health problem, but its etiology remains unclear. Obesity and associated abnormalities in glucose homeostasis may play a role in benign prostatic hyperplasia development by influencing prostate growth. OBJECTIVE: The objective of this study was to determine whether obesity, fasting plasma glucose concentration, and diabetes are associated with radiologically determined prostate enlargement, an objective measure of benign prostatic hyperplasia. DESIGN: This study was a cross-sectional analysis with robust variance estimates to account for multiple measures over time in the same individuals. SETTING: This prospective cohort study was composed of community volunteers. PATIENTS: Patients studied were 422 adult men enrolled in The Baltimore Longitudinal Study of Aging. MAIN OUTCOME MEASUREMENTS: Total prostate volume as determined by pelvic magnetic resonance imaging was measured. RESULTS: Among 422 participants, 91 (21.6%) had prostate enlargement (defined as total prostate volume >/= 40 cc) at first visit. Compared with men of normal weight [body mass index (BMI) < 25 kg/m(2)], the age-adjusted odds ratio (OR) for prostate enlargement for overweight men (BMI, 25-29.9 kg/m(2)) was 1.41 (95% CI, 0.84-2.37), for obese men (BMI, 30-34 kg/m(2)) was 1.27 (95% CI, 0.68-2.39), and for severely obese men (BMI >/= 35 kg/m(2)) was 3.52 (95% CI, 1.45-8.56) (P = 0.01). Men with elevated fasting glucose (>110 mg/dl) were more likely to have an enlarged prostate than men with normal fasting glucose (</=110 mg/dl) (OR, 2.98; 95% CI, 1.70-5.23), as were men with a diagnosis of diabetes (OR, 2.25; 95% CI, 1.23-4.11). CONCLUSIONS: Obesity, elevated fasting plasma glucose, and diabetes are risk factors for benign prostatic hyperplasia.

Adult↗

C-reactive protein levels and subsequent cancer outcomes: results from a prospective cohort study.

Chronic inflammation has been implicated in the pathogenesis of many common chronic diseases, including cancer. C-reactive protein (CRP) concentration is a non-specific serum marker of inflammation, and higher levels have been observed among individuals who go on to develop cardiovascular disease. Nested case-control studies were conducted within the CLUE II study, a community-based cohort, to examine the association between CRP concentrations and subsequent development of colorectal or prostate cancer. CRP concentrations were higher among individuals who went on to develop colon cancer, but not rectal or prostate cancer, compared with controls. The association between CRP concentrations and development of colon cancer is consistent with other evidence suggesting a role of inflammation and cancer. Preventive interventions that decrease systemic chronic inflammation have the potential to reduce certain types of cancer as well as cardiovascular disease. However, the potential benefits of anti-inflammatory chemopreventive agents must be weighed against their adverse effects before widespread use is recommended.

C-Reactive Protein↗

C47T polymorphism in manganese superoxide dismutase (MnSOD), antioxidant intake and survival.

INTRODUCTION AND OBJECTIVE: Manganese superoxide dismutase (MnSOD), an enzyme that catalyzes superoxide radical quenching, is hypothesized to protect against premature aging. A C47T transition in the MnSOD gene may affect the enzyme's distribution to the mitochondrion, a site of high oxidative stress. We examined the association between this polymorphism and survival. METHODS: Individuals who donated a blood sample to the CLUE I and II campaigns in 1974 and 1989, respectively, and completed a food frequency questionnaire in 1989 (N=6151) were included in the analysis. Hazard ratios (HR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards models. Mortality follow-up extended from 1989 to 2002. RESULTS: MnSOD genotype distributions were 27% CC (wildtype homozygotes), 50% CT (heterozygotes) and 23% TT (variant homozygotes). TT and CT genotypes compared to the CC genotype were not associated with all-cause or cardiovascular disease mortality. A slight, but non-statistically significant higher risk of cancer mortality was observed for the CT (HR=1.13, 95% CI: 0.86-1.49) and TT (HR=1.24, 95% CI: 0.90-1.70) genotypes compared to CC genotype (p-trend=0.19). CONCLUSION: We did not observe an association between the C47T polymorphism in the MnSOD gene and survival. These null associations were not modified by fruit and vegetable intake, cigarette smoking status, or body mass index.

Age Factors↗

Are findings from studies of obesity and prostate cancer really in conflict?

Recent studies on the association between obesity and prostate cancer appear to be in conflict. A recent prospective cohort study reported that the incidence of prostate cancer was lower among obese men under the age of 60 years and among those men with a family history of prostate cancer. Similarly, a case-control study found obesity was inversely associated with prostate cancer risk in men aged 40-64 years. However, several prospective cohort studies found that obese men are more likely to die from prostate cancer than non-obese men. Finally, two recent studies found that among men with prostate cancer, obese men were more likely to have a biochemical progression after surgery. We postulate that by closely examining the comparison groups used in these studies, these findings may, in fact, be in agreement. Specifically, this paradox within the literature may result from the possibility that obesity influences the development of aggressive (i.e., higher stage, higher grade, recurrence, death) and non-aggressive disease differently. We suggest that obesity may reduce the risk of non-aggressive disease but simultaneously increase the risk of aggressive disease. Finally, additional methodological issues are discussed that investigators need to be aware of to be able to draw inferences across studies of obesity and prostate cancer outcomes.

Disease Progression↗

What can geography tell us about prostate cancer?

One of the most striking characteristics of prostate cancer is the degree of geographic variation in its patterns of occurrence and progression; this variation is apparent at local, national, and international levels. Although geographic theory, methods, and data are increasingly utilized for public health research, epidemiologic research in prostate cancer etiology and progression has not taken full advantage of the spatial sciences as partner disciplines. This article reviews the known factors influencing the biology and epidemiology of prostate cancer and some of the ways in which findings to date have benefited from geography. A model is presented for geographically integrated research in prostate cancer, with discussion of how spatially referenced data and methods could enhance approaches to answering remaining questions in prostate cancer.

Demography↗

Missing stage and grade in Maryland prostate cancer surveillance data, 1992-1997.

BACKGROUND: Missing data in cancer surveillance records are common; however, little information exists on the types of cases most likely to have missing data, or how missing data influence research or policy. Two clinical elements often missing in surveillance data are histologic grade and stage of disease. Missing data are either not clinically ascertained or not successfully abstracted. METHODS: Prostate cancer cases (N=22,217) reported to the Maryland Cancer Registry during 1992-1997 were geocoded by residence and analyzed. Multi-level logistic regression was used to examine case attributes and area-level demographic, economic, and health services characteristics predictive of either missing stage or grade. A scanning statistic was used to explore geographic clustering of high and low rates of missing stage and grade within the state, before and after adjustment for significant variables from multi-level models. RESULTS: Older age, black race, missing grade, and higher county-level median income increased the likelihood of missing stage, whereas more recent year of diagnosis, higher blockgroup-level median income, and county-level rurality decreased the likelihood. Older age, missing or later stage, higher blockgroup-level median income, and more urologists per case in one's county of residence increased the likelihood of missing tumor grade, and more recent year of diagnosis, higher county-level median income, and rurality decreased the likelihood. Adjustment reduced statistically significant clusters of missing stage from six to two, and clusters of missing grade from three to zero. CONCLUSIONS: Results suggest systematic influences on missing stage and grade, which could be investigated with case-control follow-back studies.

Adolescent↗

Obesity, serum prostate specific antigen and prostate size: implications for prostate cancer detection.

PURPOSE: Obesity has been associated with lower serum testosterone, theoretically resulting in decreased PSA production. Obesity has also been associated with prostatic enlargement, making the detection of existent cancer more difficult. Together these findings would result in an apparent protective effect of obesity on prostate cancer risk due to technical detection issues unrelated to cancer biology. We examined the association between BMI, and PSA and prostate weight in a cohort of men undergoing RP. MATERIALS AND METHODS: We evaluated the association of BMI with prostate weight and PSA using linear regression, adjusting for patient age at RP, year of RP, race, and pathological stage and grade in 1,414 men treated with RP between 1988 and 2004 at the 5 equal access medical centers that comprise the Shared Equal Access Regional Cancer Hospital Database. RESULTS: On multivariate analysis increasing BMI was associated with increasing prostate weight but only in men younger than 63 years and not in men 63 years or older (p-trend <0.001 and 0.44, respectively). In men younger than 63 years mean multivariate adjusted prostate weight +/- SE in those with a BMI of less than 25 vs 30 to 34.9 kg/m was 33.8 +/- 1.4 vs 41.4 +/- 1.6 gm. There was no significant association between BMI and preoperative PSA (p-trend = 0.70). CONCLUSIONS: In a cohort of men undergoing RP obesity was associated with larger prostate size but only in younger men. There was no association between BMI and PSA. Assuming equal PSA, the degree of prostatic enlargement observed in younger obese men in this study would be expected to result in a modest decrease in the odds of detecting prostate cancer in a contemporary series of PSA screened men due to the decreased sensitivity of cancer detection related to larger prostate size. Obesity may appear protective for prostate cancer in younger men due to technical issues unrelated to cancer biology.

Humans↗

Sexually transmitted infections and prostatic inflammation/cell damage as measured by serum prostate specific antigen concentration.

PURPOSE: Although inflammation and cell damage due to STIs are hypothesized to contribute to the later development of prostate disease, few clinical studies have been done to investigate the extent to which sexually transmitted agents infect and induce an inflammatory immune response in the prostate. We indirectly investigated this question by measuring serum PSA, a possible marker of prostatic inflammation and cell damage, in men with documented STIs. MATERIALS AND METHODS: Archived serum specimens from young men with laboratory confirmed exudative STIs, including gonorrhea, chlamydia and trichomonosis, and young men with no STI diagnoses were identified in 2 prospective studies of patients at Baltimore City STI clinics, that is 84 in the STI Transmission and Acquisition Study, and 61 in the Mucosal Immunity Study. Serum specimens from visits before, during and after STI diagnoses in men with at least 1 exudative STI diagnosis and from all visits in men with no STI diagnoses were tested for total PSA concentration. RESULTS: After combining the studies patients with STIs were more likely to have a 40% or greater increase in PSA than patients with no STI diagnoses (32% vs 2%, p <0.01). CONCLUSIONS: These findings suggest that STIs may contribute to prostatic inflammation and cell damage in a subset of infected men. Further studies are warranted to replicate study findings and determine host and infection characteristics associated with large PSA increases.

Adolescent↗

Concordance rates and modifiable risk factors for lower urinary tract symptoms in twins.

INTRODUCTION: Lower urinary tract symptoms, which are common in older men, are thought to be determined genetically and by modifiable environmental risk factors. We examined the contribution of these 2 etiologic components in a cohort of U.S. twins. METHODS: In 1998, a questionnaire that assessed lower urinary tract symptoms, weight, height, alcohol consumption, cigarette smoking, and physical activity was sent out to members of the National Academy of Science-National Research Council Twins Registry. We analyzed 1,723 complete twin pairs with information on lower urinary tract symptoms and zygosity and who did not have a previous diagnosis of prostate cancer. We calculated concordance rates of categories of the International Prostate Symptom Score in monozygotic (MZ) and dizygotic (DZ) twins. Generalized estimating equations were used to calculate the odds ratio of having high-moderate/severe lower urinary tract symptoms. RESULTS: Concordance rates were higher in MZ than in DZ twins with concordance rate ratios of 2.2 and 6.9 depending on the specificity of definition of symptoms. Genetic factors contributed 72% to the risk of high-moderate/severe lower urinary tract symptoms. Taking into account correlated individuals, we observed high odds of lower urinary tract symptoms in obese men compared with lean men (odds ratio = 1.91; 95% confidence interval = 1.16-3.15 comparing first versus fourth quartile). Cigarette smoking was not associated with lower urinary tract symptoms, but alcohol consumption was positively associated. Men who were more physically active tended to have lower odds of lower urinary tract symptoms compared with less active men (0.62; 0.36-1.08). CONCLUSION: The findings indicate a strong genetic component of lower urinary tract symptoms, but also support previous studies that modifiable environmental risk factors are associated with this condition.

Aged↗