bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract B112: Metabolic syndrome and risk of colon adenomas
Authors: Ortiz-Martinez Ana P. , Thompson Cheryl L. , Berger Nathan , Li Li 
Published: May 2012

Abstract
Background: The metabolic syndrome (MetSyn) is characterized by central obesity, impaired glucose tolerance, hypertension, hypertriglyceridemia and low-density lipoprotein cholesterol, that may lead to cardiovascular disease and type 2 diabetes mellitus. This syndrome has also been associated with risk of colorectal neoplasia. Even though colon adenomas are the main precursor lesions for colorectal cancer, few studies have examined the relationship between MetSyn and adenomatous polyps. Thus, we aimed to determine the association between the MetSyn and adenomatous polyps in a population of adults in the United States.
Methods: In an ongoing screening colonoscopy-based study, we have prospectively collected data (lifestyle risk factors and fasting blood samples) from 323 incident polyp cases (26.2%) and 910 (73.8%) controls at the University Hospitals of Cleveland; as part of the Case Transdisciplinary Research in Cancer and Energetics (TREC) Colon Polyps Study. Information on relevant covariates was collected through a computer-assisted interview. Height, weight, waist and hip measurements, as well as blood collection was obtained just prior to their colonoscopy by a research nurse. The MetSyn was determined by the use of both the criteria of the American Heart Association/National Heart, Lung, and Blood institute (AHA/NHLBI) revised definition of the NCEP-ATP III report and the criteria of the International Diabetes Federation (IDF). Descriptive statistics and unconditional logistic regression models were used to assess the association between the MetSyn and likelihood of being diagnosed with adenomatous polyps, with each of the two MetSyn definitions.
Results: Our study population included 469 women (38%) and 764 men (62%). The mean age of participants was 55.4±8.9 years, 473 (38%) of participants classified themselves as African American and 760 (62%) as Caucasian. For both criteria used, the prevalence of the MetSyn was higher in cases (NCEP-ATPIII=48.3%, IDF=58.4%) than controls (NCEP-ATPIII=41.2%, IDF=49.9%) (p&lt;0.05). After adjusting for age, race, cigarette consumption, NSAID use and family history of colorectal cancer, persons with MetSyn according to the IDF criteria, were 41% more likely to have polyps (OR=1.41, 95% CI= 1.07–1.86, p=0.0140) as compared to those without the MetSyn. Analysis using the ATP-III criteria showed that persons with MetSyn were 24% more likely to have polyps (OR=1.24, 95% CI=0.95–1.63), although this association was not statistically significant (p=0.1149).
Conclusions: The MetSyn appears to be an independent risk factor of polyps; particularly when the IDF criteria are used. These results suggest that patients with the MetSyn are potentially at increased risk for colorectal cancer. Thus, colorectal cancer screening should be emphasized in patients with the MetSyn, and individuals at high risk of colon cancer should be encouraged to reduce their MetSyn factors.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B112.
Abstract B113: Determinants of serum sex hormone binding globulin and testosterone in overweight and weight-reduced premenopausal women
Authors: Azrad Maria , Gower Barbara A. , Hunter Gary R. , Nagy Tim R. 
Published: May 2012

Abstract
Introduction: Epidemiological studies have linked androgens and low sex hormone binding globulin (SHBG) with increased risk for breast cancer in premenopausal women. Obesity and the metabolic complications associated with increased adiposity have been shown to mediate both of these factors. The purpose of this study was to determine whether weight reduction through caloric restriction (CR), CR + aerobic exercise (CR+AE) or CR + resistance training (CR+RT) modifies serum total testosterone, bioavailable testosterone and SHBG.
Methods: Participants were 138 healthy, over weight (BMI 27–79) premenopausal women not taking oral contraceptives randomized to CR, CR+AE or CR+RT in order to achieve normal body weight (BMI&lt;25).
Results: All three groups significantly reduced BMI from baseline to follow-up. There was no significant difference in adjusted mean BMI among the groups following weight loss. All three groups significantly increased SHBG (p&lt;0.0001) and significantly decreased bioavailable testosterone (p&lt;0.0001) from baseline to follow up. With all participants combined there was significant decrease in total testosterone as well as in the CR group (p≤0.05 for both). There was no difference in adjusted mean total testosterone, bioavailable testosterone and SHBG concentrations among the three groups following weight loss. Multiple linear regression models revealed that 64% of the variance in baseline SHBG was explained by age, intra-abdominal fat, bioavailable testosterone, insulin, and high density lipoprotein (HDL). After adjusting for baseline SHBG, 81% of the variance was explained by age, free testosterone and HDL in the weight reduced state. Twenty-three percent of the variance in baseline total testosterone was explained by age, estradiol, norepinephrine, low density lipoprotein (LDL) and leptin. After adjusting for baseline total testosterone, 58% of the variance was explained by age, estradiol and leptin in the weight reduced state.
Conclusions: Testosterone, bioavailable testosterone and SHBG are highly influenced by obesity and can be modified through weight loss. Weight loss through CR or in combination with exercise achieves similar effects on testosterone and SHBG concentrations. The determinants of serum total testosterone and SHBG are different in the overweight and weight reduced state.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B113.
Abstract B117: Association of endogenous sex hormone levels with breast cancer risk factors in premenopausal Japanese women
Authors: Nagata Chisato , Nakamura Kozue , Wada Keiko , Hayashi Makoto , Takeda Noriyuki , Yasuda Keigo 
Published: May 2012

Abstract
We assessed associations between blood levels of estrogen and androgen and breast cancer risk factors in premenopausal Japanese women. A total of 551 premenopausal women who reported having regular menstrual cycles less than 40 days long were included in the present study. Women were not included if they were using oral contraceptives or hormone therapy, or if they had cancer, diabetes mellitus, chronic hepatitis, or thyroid disease. Information on potential breast cancer risk factors including body size, physical activity, and reproductive factors were obtained using a self-administered questionnaire. The phase of menstrual cycle at blood donation, categorized in early follicular, late follicular, peri-ovulatory, midluteal, or other luteal, was used for adjustment together with age. Estradiol level was significantly inversely associated with body mass index (BMI), while testosterone and DHEAS levels were significantly positively associated with BMI; the geometric mean of estradiol in women with BMI at or above 24 kg/m2 was about 25% lower than that in women with BMI below 18 kg/m2. The geometric means of testosterone and DHEAS were 31% and 24% higher, respectively, in women in the high BMI group. Nulliparous women had significantly higher testosterone levels than parous women. Breastfeeding was associated with decreased levels of testosterone and DHEAS. Physical activity, age at menarche, number of births, and age at first birth were not significantly associated with these hormone levels. A reduced breast cancer risk of obese premenopausal women may be due, in part, to a decreased estradiol level.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B117.
Abstract B118: Modifiable correlates of low testosterone in U.S. men
Authors: Corinne Joshu E. , Platz Elizabeth A. 
Published: May 2012

Abstract
Background: In some studies, men with low total, free, or SHBG-adjusted testosterone possibly had a higher risk of cancer death. Because testosterone replacement therapy for men with clinically low testosterone has an uncertain risk versus benefit ratio, identifying modifiable factors that influence testosterone level and that are public health targets is needed. Obesity (lower testosterone) and cigarette smoking (higher testosterone) are two behavioral factors that are recognized to influence testosterone levels; given the great magnitude of the adverse effects of cigarette smoking, it is not a prevention strategy. Thus, in this study we investigated obesity as well as dietary and lifestyle factors in association with low total and free testosterone.
Methods: The Third National Health and Nutrition Examination Survey (NHANES III), conducted 1988–1994, was a cross-sectional study of the U.S. civilian non-institutionalized population. Subjects participated in an interview, underwent a physical examination, and provided a blood specimen. Serum was available for 1470 men who participated in the morning session of Phase I (1988–1991) and were ≥20 years old. Testosterone and sex hormone binding globulin (SHBG) were measured by competitive electrochemiluminescence immunoassay. Free testosterone was estimated by mass action. We excluded men whose testosterone level was ≤2nd percentile because these men may have had congenital hypogonadism. We defined low total and free testosterone as ≤ 3.0 ng/mL and ≤ 0.07 ng/mL, respectively. We estimated the associations of the modifiable factors with low total and free testosterone using logistic regression adjusting for age and race/ethnicity.
Results: Measures of overall and central adiposity were positively associated with low total and free testosterone. After mutual adjustment, men with high waist circumference (ethnic specific cutpoints; vs. low) were 2.59 (95% CI: 1.12–6.00) times more likely to have low total testosterone and 2.65 (95% CI: 1.44–4.89) times more likely to have low free testosterone, whereas body mass index and percent body fat did not remain statistically significantly associated. Independent of waist circumference, percent of calories from protein, fruit and vegetable intake, alcoholic beverage consumption, and physical activity were not statistically significantly associated with low total and free testosterone. These results were similar in men who did not have comorbidities at time of blood draw and in non-smokers.
Discussion: Cross-sectionally, high waist circumference was the most consistent correlate of low total and free testosterone. These findings suggest that avoiding or reducing central adiposity may be one way to prevent clinically low androgen levels. Given that men with low androgens may have a higher risk of cancer death, our results may have import for cancer prevention and/or survival.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B118.
Abstract B12: Racial disparities in breast cancer treatment delay and type in three North Carolina counties
Authors: Vines Anissa I. , Nie Yonghong , Amos Keith 
Published: May 2012

Abstract
Objective: The purpose of this study was to explore racial disparities in delays in treatment and type of treatment received among breast cancer patients in three North Carolina counties represented in the Carolina Community Network to Reduce Cancer Health Disparities (CCN). The CCN is a regional community-based cancer network that aims to reduce prostate, breast and colorectal cancer disparities among adult African Americans in North Carolina.
Methods: North Carolina Central Cancer Registry data on black and white women diagnosed with breast cancer in Orange, Edgecombe, and Nash counties between 2000 and 2005 (n=1205) were used to obtained information on treatment and tumor status. Using standard guidelines for breast cancer care, delay in first course of treatment, type of treatment received, and tumor receptor status were assessed.
Results: Although within the recommended guidelines, treatment delay was longer for black breast cancer patients in comparison to white patients, regardless of stage at diagnosis. Treatment delay was highest for black patients in Edgecombe, a county with the highest proportion of blacks overall. Majority of stage I and II breast cancer patients received surgery and tended to elect for breast conservation surgery over mastectomy. Estrogen and Progesterone receptor negative breast cancers were more common in blacks than whites across the three counties, especially in Edgecombe County.
Conclusions: Our findings suggest treatment standards are not equivalently met among black and white women. Findings warrant further research into the identified treatment delays and tumor type differences to improve survival for black women, especially those in Edgecombe County. These preliminary results suggest that patients in Edgecombe County may have a higher prevalence of the hormone receptor negative phenotype of breast cancer. This more aggressive type of breast cancer may be attributing to the higher mortality rates in comparison to the other two counties.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B12.
Abstract B120: Metastatic differentiated thyroid cancer: Could we preview (and prevent) when the metastasis will develop? A recent experience from Brazilian Institute
Authors: Miasaki Fabíola Y. , Mesa Cleo O. , Paes Aline , Nakatani Viviane Y. , de Carvalho Gisah A. , Graf Hans 
Published: May 2012

Abstract
Since the new data about molecular signature of undifferentiated thyroid cancer suggest that they can develop from differentiated thyroid cancers (mainly those with BRAF mutations). The aim of this study was to identify clinical risk factors to metastasis development after the diagnosis and/or undifferentiation in non-medullary thyroid cancers. For this purpose, we follow up all 125 patients with non-medullary thyroid carcinomas who have been seen in our institution in the last 2 years. The data were collected and analyzed. From these patients, we identify 15 patients with distant metastasis: only one with anaplastic thyroid cancer. Between the differentiated thyroid carcinomas, 11 were female and 3 were male (3.1:1 ratio). Although the majority of differentiated thyroid carcinomas have a good prognosis, distant metastasis was found in the initial diagnosis in 9 of 14 patients (64.3%) with differentiated thyroid carcinomas. No correlation between type of tumor (follicular or papillary) and metastasis development was observed. All of them had received radioiodine therapy until clinical stabilization or the maximum dose allowed (638.57mCi ± 281.43). All the metastasis from differentiated thyroid carcinomas had uptake iodine. Although the majority of patients could not be considered cured, classic undifferentiation was not detected in these patients. The patient with anaplastic thyroid cancer had died in the first year of follow-up. Only one patient had died because COPD complications and all the others were still alive. Interestingly, 64.3% of patients had 9 or more years of survival until the present moment. Because we had few patients who developed metastasis after the diagnosis, we cannot valuate the meaning of our findings. However, since the majority of distant metastasis are present from the very beginning, it seems that the correct and precocious diagnosis of thyroid nodules and/or goiter prevent thyroid cancer progression.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B120.
Abstract B122: Multi-SNP analysis of one-carbon metabolism genes and prostate cancer outcomes
Authors: Zeigler-Johnson Charnita M. , Chang Bao-Li , Panossian Saarene , Spangler Elaine , Malkowicz S. Bruce , Rebbeck Timothy 
Published: May 2012

Abstract
Introduction: There is little known about the epigenetics of prostate severity. One-carbon metabolism genes in conjunction with folate and B-vitamins influence DNA repair mechanisms and methylation patterns. Better understanding of the relationship of gene activity that may potentially be altered by nutrient intake can provide new strategies for decreasing the prevalence of advanced prostate cancer. The goal of this project is to determine the association of one-carbon cycle genes in relation to prostate cancer outcomes.
Materials and Methods: We studied prostate cancer patients with one-carbon genotypes (604 European American, 92 African American.) The genes of interest included CBS, MTHFD1, MTHFR, MTRR, MTR, SHMT1, TYMS, SLC19A1 and TCN2. Data were analyzed with race stratification. Odds ratios (OR) were calculated by logistic regression models adjusted for age and percent African ancestry (African-Americans only.) These models were used to examine case-case associations analyzing tumor stage, grade and aggressiveness (high stage and high grade combined) and age at onset. Cox regression models were used to calculate hazard ratios (HR) for the incidence of biochemical failure after treatment. Multi-SNP associations were conducted in European American cases only using risk scores derived from the per allele ORs from a combination of 6 SNPs (MTHFD1 R653Q, MTHFR A222V, MTRR L333V, MTR D919G, SHMT L474F, TCN R259P) and 9 SNPs (the 6 mentioned previously plus CBS 68bp Ins, SLC19A1 61bpDel and Tyms 3UTRdel6.)
Results: Genotypes involved in one-carbon metabolism differed significantly by race. Among African-American cases, a significant protective association was found for SLC19A1 61bpDel for aggressive disease (OR=0.1, 95% CI=0.01–0.9, additive model.) Associations with biochemical failure in European Americans were observed for recessive carriage of MTR D919G (HR=2.8, 95% CI=1.1–7.3) and MTRR K350R (HR=4.3, OR=1.1–16.3, additive model.) In the multi-SNP model, biochemical failure was associated with the risk scores of 9 SNPs (HR=0.77, 95% CI=0.61–0.94.) No additional associations were observed for other clinical characteristics of prostate cancer.
Conclusions: These results suggest that one-carbon metabolism genotypes in combination may be associated with prostate cancer in specific subgroups. Multi-SNP models may provide more information than single SNP analyses for studying complex genetic pathways. Additional research of gene interactions and effects of nutrient intake may provide clues about prevention and treatment of prostate cancer, especially in groups at high risk for poor outcomes.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B122.
Abstract B123: Sequence variants in inflammatory genes, plasma antioxidants, and prostate cancer risk
Authors: Zhang Jianjun , Dhakal Ishwori , Greene Graham , Lang Nicholas , Kadlubar Fred 
Published: May 2012

Abstract
Background: Presence of xenotropic murine leukemia virus-related virus and chronic inflammation in prostate tumor tissue suggests that inflammation plays a role in prostate cancer etiology. This study thus investigated whether variants in genes involved in inflammation influence alone or interact with plasma antioxidants to influence prostate cancer risk in a population-based case-control study in Central Arkansas.
Methods: Cases (n=193) were men, ages 40–80 years, diagnosed with prostate cancer in three major hospitals in 1998–2003, and controls (n=197) were matched to cases by age, race, and county of residence.
Results: After adjustment for confounders, polymorphisms in COX2 (rs689466) and IL-8 (rs4073) were not significantly associated with prostate cancer risk. However, significant interactions were observed between these genetic variants and plasma antioxidants on the risk of this malignancy. The protective effect of the mutant allele of the COX polymorphism was more pronounced among subjects with high plasma levels of β-cryptoxanthin, lycopene, β-carotene, or selenium (≥median) [e.g., OR (95% CI): 0.37 (0.15–0.86) (AG/GG vs. AA) for β-cryptoxanthin]. Conversely, the promoting effect of the variant allele of the IL-8 polymorphism was more remarkable in subjects with low plasma levels of Lutein/zeaxanthin, β-cryptoxanthin, and β-carotene (&lt;median) [e.g., OR (95% CI): 2.44 (1.08–5.75) (AT/TT vs. AA) for β-carotene].
Conclusions: We found that genetic variants in inflammatory genes interact with plasma antioxidants to modulate the risk of prostate cancer. The results obtained from our study need to be replicated in large epidemiologic studies.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B123.
Abstract B124: Genetic variants in sex hormone production, energy regulation and vitamin C and D uptake influence risk of non-Hodgkin's lymphoma
Authors: Skibola Christine F. , Conde Lucia , Halperin Eran , Agana Luz , Holly Elizabeth A. , Riby Jacques , Smith Martyn T. , Bracci Paige M. 
Published: May 2012

Abstract
Infectious and autoimmune diseases associated with B-cell lymphomas involve inflammation, chronic activation and proliferation of lymphocytes. Since most lymphomas develop in the absence of any known chronic antigenic stimulation, genetic polymorphisms may provide alternative means to exert proinflammatory responses that fuel lymphoproliferation and promote B-cell growth and survival that contribute to lymphoma risk. We have previously reported associations between non-Hodgkin lymphoma (NHL) risk and genetic polymorphisms in pathways involving sex hormone synthesis/metabolism, energy regulation, and uptake and metabolism of dietary nutrients. To further corroborate the relevance of these pathways and to identify additional risk loci, we used data from our recent genome-wide association study of NHL (748 cases, 811 controls) and conducted focused candidate gene/pathway analyses.
A number of SNPs in the estrogen related genes, ESR1, CYP17A1, CYP19A1, and HSD17B2, influenced risk of diffuse large B-cell lymphoma (DLBCL) or follicular lymphoma (FL) in men and women. ESR1 encodes estrogen receptor 1 (ER) and regulates estrogen production by direct modulation of the CYP19A1 promoter. CYP17A1, CYP19A1 and HSD17B2 produce important enzymes involved in estrogen and testosterone synthesis. Estrogen and testosterone exert dose-dependent biphasic immunomodulatory effects. Thus, SNPs in these genes may mediate sex hormone levels and influence B-cell survival and growth characteristics, and possibly the potential for B-cells with pre-neoplastic lesions to undergo transformation.
Several SNPs in LEP and/or LEPR, involved in energy regulation, were associated with risk of FL and DLBCL. Leptin, the LEP gene product, is a proinflammatory adipokine that once bound to its receptor (LEPR) exerts immune-mediated responses including pro-survival signals to B-cells. SNPs in the vitamin C (SLC23A2) and vitamin D (VDR) receptor genes were associated with FL risk. Vitamin C is an antioxidant that may play a key role in preventing oxidative-stress related DNA damage and genotoxicity to B-cells. Vitamin D inhibits proliferation and induces lymphocyte differentiation. An inverse association with lymphoma risk and UV exposure supports a role for low vitamin D in lymphomagenesis. These studies provide further evidence for the important roles of sex hormones, leptin, and vitamins C and D in the etiology of lymphoma.
Citation Information: Cancer Prev Res 2010;3(1 Suppl):B124.