bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 2826: Carbohydrate intake, glycemic load, and glycemic index and prostate cancer risk
Authors: Williams Christina D. , Whitley Brian , Hoyo Cathrine , Grant Delores , Iraggi Jared , Newman Kathryn , Gerber Leah , Taylor Loretta , Freedland Stephen 
Published: February 2011

Abstract
Background: The typical U.S. diet is characterized by high carbohydrate intake, and dietary carbohydrates can modulate insulin sensitivity depending on their glycemic effect. Glycemic load and glycemic index, which represent the quality and quantity of carbohydrate foods, and prostate cancer risk are poorly characterized. Objective: To examine the association between dietary carbohydrate intake, glycemic load, and glycemic index and risk of prostate cancer, and determine if these associations differ between Whites and Blacks. Methods: We analyzed data from an ongoing case-control study of White (N=109) and Black (N=143) veterans at the Durham VA Medical Center. Cases were 65 men with biopsy-confirmed prostate cancer. There were two groups of controls: biopsy-negative controls (N=89) and healthy (i.e. no biopsy indication) controls (N=98). All men had a PSA test done in the year prior to enrolling in the study. Demographic and lifestyle risk factors were collected using self-administered questionnaires. Diet information was obtained using the Harvard food frequency questionnaire. Odds ratios (OR) and corresponding 95% confidence intervals (95% CI) for prostate cancer risk were obtained using logistic regression analyses adjusted for age, race, and total energy. Results: Mean carbohydrate intake, glycemic load, and glycemic index were similar among cases and both groups of controls (all p-values &gt;0.05). We did not observe any statistically significant risk estimates for high (≥median) carbohydrate intake, glycemic load, or glycemic index. Compared to healthy controls, the ORs for prostate cancer risk associated with high carbohydrate intake, glycemic load, and glycemic index were 0.66 (95% CI 0.34-1.30), 0.57 (95% CI 0.22-1.49), and 1.18 (95% CI 0.61-2.02) respectively. Corresponding ORs when compared to biopsy-negative controls were 0.88 (95% CI 0.46-1.70), 0.69 (95% CI 0.29-1.64), and 0.83 (95% CI 0.43-1.59), respectively. The associations between carbohydrate intake, glycemic load, or glycemic index and risk of low-grade (gleason score &lt;7) as well as high-grade (gleason score ≥7) prostate cancer relative to healthy controls were null for all analyses. There was no evidence of effect modification by race in our analyses. Additional adjustment for fiber intake did not appreciably alter any of the ORs. Conclusion: Our findings in a small case-control study do not suggest that a high carbohydrate intake and/or high glycemic load increase the risk of prostate cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2826.
Abstract 2830: Energy balance and breast cancer risk among sisters pairs in the Breast Cancer Family Registry Study
Authors: Zhang Fang Fang , John Esther M. , West Dee W. , Knight Julia , Andrulis Irene , Buys Saundra , Daly Mary , Stearman Beth , Kaur Manleen , Vishwanatha Jamboor , Morabia Alfredo , Terry Mary Beth 
Published: February 2011

Abstract
Animal models have shown strong evidence that energy restriction inhibits mammary tumor development. Nevertheless, epidemiologic studies in humans generally do not support an association between energy intake and breast cancer risk. Failure to take into consideration the integrated effect of energy intake, physical activity and body size may obscure the true effect of energy intake on breast cancer risk. We analyzed the combined effects of energy intake, body size and physical activity on the risk of breast cancer among 4,564 women diagnosed with breast cancer between 1995 and 2006 and 3,411 of their unaffected sisters enrolled in the Breast Cancer Family Registry. Dietary data were collected using the food frequency questionnaire developed for the Hawaii-Los Angeles Multiethnic Cohort. Conditional logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). We observed an overall 50% increased risk of breast cancer among women in the highest quartile of energy intake compared to those in the lowest quartile (OR=1.5, 95% CI: 1.1-2.2, ptrend &lt; 0.01). The association with energy intake was limited to women with lower levels of strenuous physical activity (OR=1.9, 95% CI: 1.3-2.9 for &lt; 1.75 hours/week during the past three years), and was stronger among women with higher body mass index (BMI) (OR=2.2, 95% CI: 0.6-7.7 for BMI ≥ 30; OR=1.5, 95% CI: 0.6-3.7 for BMI 25-29; OR=1.3, 95% CI: 0.7-2.5 for BMI &lt; 25 kg/m2). Our results suggest that higher total energy intake in adulthood is associated with a 50% increase in breast cancer risk compared to sisters with lower energy intake in adulthood; these associations are stronger among less active and obese women.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2830.
Abstract 2831: Ornithine decarboxylase polymorphisms and risk of colorectal adenoma
Authors: Barry Elizabeth L. , Mott Leila A. , Sandler Robert S. , Ahnen Dennis J. , Baron John A. 
Published: February 2011

Abstract
Introduction: In a recent randomized trial the combination of difluoromethylornithine (DFMO) and the NSAID sulindac was remarkably effective in reducing the risk of colorectal adenoma recurrence. DFMO is a specific inhibitor of ornithine decarboxylase (ODC), which catalyzes the first step in polyamine synthesis. ODC and polyamines, which regulate cell growth and survival, have long been associated with colon carcinogenesis. In previous studies a SNP in the ODC promoter region was associated with risk of adenoma and response to aspirin treatment. The objective of this research was to perform a more comprehensive investigation of the association of adenoma risk with common genetic variation across the entire ODC gene, including potential upstream and downstream regulatory regions.
Methods: We investigated the association between genetic variation in the ODC gene and risk of adenoma recurrence among a cohort of 920 participants in the Aspirin/Folate Polyp Prevention Study. Using the Sequenom platform, we genotyped 29 SNPs within a 23kb region. Generalized linear regression was used to compute relative risks (RRs) and 95% confidence intervals (95% CIs) adjusted for age and gender. Interactions terms were used to test whether ODC genotype modified the protective effect of aspirin treatment.
Results: As gene frequencies for 26 of the 29 SNPs varied significantly by race/ethnicity, analyses were limited to whites only (86%). There were 7 SNPs associated with increased risk and 3 with decreased risk of adenoma recurrence (see table). In addition, at least three SNPs without any main effect modified the effect of aspirin treatment: rs1405948 (P for interaction=0.048), rs28362422 (P=0.043), and rs4669584 (P=0.050).
Conclusion: Our findings suggest that common genetic variation throughout the ODC gene and adjacent regulatory regions influence risk of adenoma recurrence as well as efficacy of aspirin treatment.Association of ODC polymorphisms with adenoma riskSNPRR95% CIP-valueModelMAFLocationrs23575511.231.06-1.440.008dominant0.345′ flankingrs23026141.371.08-1.740.009dominant0.04exon 2rs37526611.351.06-1.720.017dominant0.04intron 5rs10495001.381.08-1.750.009dominant0.04exon 12rs8181620.700.52-0.940.019recessive0.303′ flankingrs109296691.251.06-1.480.009dominant0.113′ flankingrs24634630.760.62-0.930.009recessive0.443′ flankingrs24304201.251.08-1.460.004dominant0.323′ flankingrs116949111.341.13-1.590.001dominant0.113′ flankingrs130009160.770.63-0.040.009recessive0.453′ flanking
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2831.
Abstract 2838: p53-R72P single nucleotide polymorphism is not associated with cancer risk, histopathologic features or clinical outcome in renal cell carcinoma in Caucasians
Authors: Hammerschmied Christine G. , Stoehr Robert , Walter Bernhard , Junker Kerstin , Moch Holger , Hinze Raoul , Hofstaedter Ferdinand , Hartmann Arndt 
Published: February 2011

Abstract
Aims:
At codon 72, the human p53 gene contains a single nucleotide polymorphism (SNP), where the sequence can either read CGC, which encodes the amino acid arginine (R), or CCC which codes for proline (P). This SNP, p53-R72P, was found to affect numerous carcinogenesis related cell functions, like apoptosis, cell cycle progression, DNA repair, growth arrest and transcriptional activation. P53-R72 was found to be more effective at protecting stressed cells from neoplastic development. Significant associations of this variant to cancer development were found in various cell types, e.g. breast, gastric and lung cancer. No data are available for renal cell carcinoma (RCC).
Methods:
DNA extracted from formalin-fixed, paraffin-embedded normal tissue of 334 caucasian renal tumor patients (among them 157 affected by clear cell, 54 by papillary, 70 by chromophobe carcinoma and 41 by benign oncocytoma) and 196 controls was examined by restriction fragment length polymorphism (RFLP) using primers for PCR and the restriction enzyme BSTUI. After digestion, the length of the resulting bands was estimated by gel electrophoresis. Genotype distribution of both groups was compared by two sided exact Chi2 test. We also tested for associations of any genotype to histologic subtype, stage, nuclear grade, age at diagnosis, tumor-related survival and gender. Survival analysis was performed using log rank statistics. For examination of the potential influence of the presence or absence of the C allele, analyses were repeated with a combined C/C+CG group vs. G/G.
Results:
Genotype distribution of RCC or benign oncocytoma carriers and controls did not differ significantly, and there was no correlation of genotype and age of onset. We did not observe a significant acceleration of a certain genotype relative to gender, age group, subtype, stage or nuclear grade. Both tumor-related survival and progression free survival were not affected by genotype. Similar results were obtained when the two C allele carrying groups were pooled for analysis.
Conclusions:
The p53 R72P polymorphism does not seem to affect the risk of developing RCC or benign oncocytoma, the course of the disease, or histopathologic features in Caucasians.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2838.
Abstract 2839: Effects of CDKN2A genetic polymorphisms on DNA methylation in head and neck cancer
Authors: Rios Leslimar , Aquino-Lopez Arianexys , Velez Germán L. , Rivera-Pena Bianca , Baez Adriana 
Published: February 2011

Abstract
Gene polymorphism has been found to be associated with the susceptibility to cancer or its severity as exemplified in the CDKN2A gene. CDKN2A regulates G1 arrest and plays an important role in head and neck cancer (HNSCC) carcinogenesis. Deregulated tumor expression of CDKN2A has previously been described in association with HNSCC clinical progression. Aberrant methylation of CDKN2A is common gene silencing mechanism in HNSCC. CDKN2A is polymorphic, with variant alleles G/A442, C/T 540, and C/G 500 associated with cancer. Previously we have shown that in the Puerto Rican population the G/A 442, GG variant is associated with an increased head and neck cancer risk (OR, 4.09). In the present study, we examined the CDKN2A G/A442, C/T 540 and C/G 500 polymorphisms using PCR-RFLP and the pattern of methylation of the CDKN2A gene by methylation-specific PCR or Methylight assay in 152 HNSCC. The allelic frequencies were compared to a control group of 69 age - matched healthy blood donors. CpG island methylation for CDKN2A was found in 45% HNSCCs. The G/A 442, GG variant was more common in tumors of the larynx (63%). A significant correlation between CDKN2A G/A442 and head and neck cancer was indicated (r = 0.24, P = 0.02). We found no association between CDKN2A gene hypermethylation and CDKN2A C/T 540 and C/G 500 polymorphisms, However, we confirmed that individuals carrying the AG variant in G/A 442 gene had a higher frequency of hypermethylation in HNSCCs. Our results suggest that G/A 442 polymorphisms of CDKN2A gene may affect the methylation status. Functional and bioinformatic studies to clarify these results are underway.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2839.
Abstract 2840: A functional nonsynonymous single nucleotide polymorphism in the migration and invasion inhibitory protein (MIIP) gene confers differential risk of breast cancer
Authors: Chen Kexin , Song Fangfang , Ji Ping , Zheng Hong , Song Fengju , Wang Yingmei , Hao Xishan , Wei Qingyi , Zhang Wei 
Published: February 2011

Abstract
The migration and invasion inhibitory protein (MIIP) gene encodes an inhibitor of cancer cell migration and invasion. Our previous studies using the colony formation assay have demonstrated that MIIP also inhibits tumorigenesis in breast cancer cells. Therefore, we hypothesized that genetic variations in MIIP may affect breast cancer development and prognosis. In this case-control study, we genotyped the MIIP single nucleotide polymorphism (SNP) rs2295283 (codon 167, A&gt;G, K&gt;E) from 1524 breast cancer patients and 1592 age-matched controls for its association with breast cancer risk. The SNP analysis was next performed on a validation set (736 cases and 760 controls). Colony formation and cell migration assays were then conducted to functionally interrogate the difference between the A and G variants. Compared with the AA genotype in both the test and validation sets, the combined AG+GG genotypes (167E) were associated with a significantly lower risk of breast cancer. Among the test set, the protective effect of the AG+GG genotypes was more evident among participants with a family history of cancer. Further case series analysis revealed that the GG genotype was less susceptible to breast cancer with tumor size &gt;2 cm and late clinical stage (II+III+IV). Colony formation assays showed that MIIP 167E (the G variant) was a more potent inhibitor of colony formation but not cell migration. These results suggest that MIIP K167E SNP may be a genetic predictor of breast cancer development and prognosis, as supported by differential abilities of the two isoforms in inhibiting breast cancer colony formation in vitro.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2840.
Abstract 2843: Caspase-8 gene SNPs in prostate cancer susceptibility: a replication study
Authors: Parry Marina , Elliott Graeme , Abo Ryan , Camp Nicola J. , Neal David E. , Donovan Jenny L. , Hamdy Freddie C. , Cox Angela 
Published: February 2011

Abstract
Introduction
A single nucleotide polymorphism (SNP) in the caspase-8 gene, (CASP8 D302H), has been reported to be involved in susceptibility to breast and pancreatic cancer, melanoma and glioma, but not colorectal or ovarian cancer. We previously have used a tagging-SNP approach to test the hypothesis that this SNP, or other variants in CASP8, were associated with prostate cancer, in 1009 cases, 987 men with normal serum prostate specific antigen (PSA) levels and 961 men with low serum PSA (&lt;0.5ng/ml). These subjects were drawn from those participating in the UK ProtecT (Prostate Testing for Cancer and Treatment) trial. Of the 15 tagging SNPs in caspase-8 that were genotyped, 7 showed some evidence of association with prostate cancer (P&lt;0.05). The aim of the present study was to attempt to replicate these results in an independent set of case and control subjects.
Methods
A further independent sample of men from the ProtecT trial formed the replication cohort for this study. Blood DNA samples were available for 1262 men with prostate cancer, 1258 men with normal serum PSA, and 609 men with low serum PSA. SNP genotyping was carried out by 5-prime nuclease PCR (TaqmanTM, Applied Biosystems). The association with prostate cancer was tested using logistic regression, controlling for sample set.
Results
Two SNPs with duplicate concordance rates of less than 98% were not included in the analysis. Genotype call rates for the remaining 5 SNPs were all greater than 95%, and genotype frequencies in control subjects were consistent with those expected under Hardy-Weinberg equilibrium. None of the 5 SNPs yielded significant evidence of association in the replication cohort, although some odds ratios were consistent between the two data sets. We combined the data from the test and replication cohorts to evaluate the overall evidence for association. The rare alleles of rs3769826 and rs6723097 conferred a reduced risk of prostate cancer with per-allele odds ratios (95% confidence interval) [OR(95%CI)] of 0.90 (0.82-0.98) and 0.88 (0.80-0.96), and P=0.013 and P=0.004 respectively. In addition, the deletion allele of the promoter indel rs3834129 conferred an increased risk of prostate cancer, with OR (95%CI) of 1.15 (1.05-1.27), P=0.003. While these results await further replication, it is interesting to note that the rare alleles of rs3769826 and rs6723097 are carried on European haplotypes that are associated with increased risk of breast cancer, suggesting the possibility of a different mode of action of caspase-8 in the two tumour types.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2843.
Abstract 2846: SNPs in apoptosis and cell cycle control related genes and brain tumor risk among children in Korea
Authors: Jeon Sujee , Han Sohee , Lee Kyoung-Mu , Park Ae Kyung , Ahn Hyo Seop , Shin Hee Young , Kang Hyoung Jin , Koo Hong Hoe , Seo Jong Jin , Choi Ji Eun , Kim Ho , Kang Daehee 
Published: February 2011

Abstract
Objective
In a hospital-based case-control study in Korea, we evaluated the association between polymorphisms in genes involved in apoptosis and cell cycle control and brain tumor risk among children.
Methods
Incident brain tumor cases (n=70) and non-cancer controls (n=254) were recruited from three teaching hospitals in Seoul between May 2003 and August 2006. Information on the characteristics of children and their parents were collected by trained interviewers using structured questionnaire. Tagging single-nucleotide polymorphisms (SNPs) were selected using a pairwise linkage-disequilibrium (LD) based algorithm (n=304) were genotyped for 43 cases and 153 controls in this study. Odds ratios (ORs) and 95% confidence intervals (CIs) for SNP genotypes were estimated using unconditional logistic regression adjusted for age and birth weight. The false discovery rate (FDR) was estimated to evaluate the probability of false positive associations; we considered FDR &lt;0.2 as noteworthy.
Results
Eleven tag SNPs in six genes, AICDA, LMO2, MYC, BCL2, BCL2A1, and CASP7 were significantly associated with childhood brain tumor (Ptrend&lt;0.05). Two SNPs (rs12306110 and rs3794318) in AICDA gene, encoding activation-induced cytidine deaminase, remained significant after adjusting of multiple tests. These SNPs were in tight LD. The most significant association with childhood brain tumor risk was for the rs12306110 (OR, 0.24; 95% CI, 0.11-0.51).
ConclusionOur results suggest that genetic polymorphisms in AICDA may be associated with the risk of brain tumor in childhood.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2846.
Abstract 2848: The DEC1 promoter polymorphism −249 T&gt;C reduces the risk of squamous cell carcinoma of the head and neck
Authors: Huang Yu-Jing , Niu Jiangong , Wang Li-E , Liu Zhensheng , Sturgis Erich M. , Wei Qingyi 
Published: February 2011

Abstract
The human DEC1 (deleted in esophageal cancer 1) gene is located on chromosome 9q, a region frequently deleted in various types of human cancers, including squamous cell carcinomas of the head and neck (SCCHN). Previous studies have shown that DEC1 expression was greatly reduced or absent in esophageal cancer, and its tumor suppressive ability was observed in both in vitro and in vivo assays. Therefore, we hypothesized that DEC1 might also play roles in the etiology of SCCHN. To assess the association between DEC1 polymorphisms and SCCHN risk, two independent promoter SNPs, −1628 G&gt;C (rs1591420) and −606 T&gt;C (rs4978620), the latter being in complete linkage disequilibrium with both −249 T&gt;C (rs2012775) and −122 (rs2012566), were genotyped in 1,111 non-Hispanic whites SCCHN patients and 1,130 age-and sex-matched cancer-free controls recruited at The University of Texas M. D. Anderson Cancer Center. The joint effect of DEC1 SNPs and the TP53 tumor suppressor gene codon 72 (Arg72Pro, rs1042522) polymorphism, which has been suggested to be associated with susceptibility to tobacco-related cancers, was also assessed. After adjustment for age, sex, and smoking and drinking status, a significantly protective effect on SCCHN risk was observed for the −606 T&gt;C (rs4978620) CC homozygotes (adjusted OR = 0.72, 95% CI= 0.52-0.98), compared with those carrying the −606 TT genotype. Stratification analyses showed that a decrease risk associated with the −606 CC genotype remained significant in the subgroups of never smokers, never drinkers, younger subjects (≤55 yr), patients with oropharyngeal cancer, and in the presence of the TP53Arg/Arg (rs1042522) genotype. By an in silico analysis, we identified that the −249 T&gt;C SNP would gain a transcription factor binding site. Indeed, further functional analysis showed that the T to C allelic change at the −249 site significantly enhanced transcriptional activity of the DEC1 promoter and the DNA-protein binding activity, supporting a tumor suppressor role of DEC1 in SCCHN. We conclude that the DEC1 promoter −249 T&gt;C (rs2012775) polymorphism is functional, modulating susceptibility to SCCHN among non-Hispanic whites. The association with oropharyngeal cancer among never smokers and never drinkers and with TP53 Arg/Arg genotype suggests that this polymorphism could modulate the human papillomavirus-induced carcinogenic process. (Supported by NIH grants R01CA131274 and R01ES011740)
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 2848.