bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 3615: Does selenium supplementation increase serum glucose levels in men at high risk for prostate cancer.
Authors: Algotar Amit M. , Hsu C H. , Stratton Steven P. 
Published: August 2014

Abstract
Background: Current literature regarding the effect of selenium supplementation on risk of diabetes is inconclusive. Hence a longitudinal study was conducted to investigate the effect of selenium supplementation on serum glucose levels in elderly men.
Methods: Data were obtained from 699 men participating in a randomized, double-blind, placebo-controlled Phase 3 clinical trial investigating the effect of two doses of selenium (200 and 400 μg/day) compared to placebo on incidence of prostate cancer. Subjects were followed every six months for up to five years. Serum glucose levels were obtained every six months. Mixed effects regression models were used to assess if rate of change of serum glucose levels was significantly different in the selenium supplemented groups as compared to placebo. Sensitivity analyses were performed to assess the robustness of findings and to minimize the possibility of residual bias due to fasting status.
Results: Of the total 2893 glucose measurements, 734 were carried out when the subject had been fasting for ≥ 8 hours. The changes in serum glucose levels during the course of the trial were not statistically significantly different as compared to placebo for the selenium 200 μg/day (p = 0.88) or selenium 400 μg/day (p = 0.45) treatment groups. Sensitivity analyses demonstrated comparable results for models using the total population and models restricted to subjects with only fasting glucose data.
Conclusion: These results do not support a relationship between selenium supplementation and risk of diabetes. Hence recommendations regarding selenium supplementation based on increased risk of diabetes seem premature.
Citation Format: Amit M. Algotar, C H. Hsu, Steven P. Stratton. Does selenium supplementation increase serum glucose levels in men at high risk for prostate cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3615. doi:10.1158/1538-7445.AM2013-3615
Abstract 3617: Fat intake after prostate cancer diagnosis and risk of lethal prostate cancer and total mortality.
Authors: Kenfield Stacey A. , Richman Erin L. , Sesso Howard D. , Ma Jing , Stampfer Meir J. , Chavarro Jorge E. 
Published: August 2014

Abstract
Context and Objective: Although prostate cancer is the 2nd leading cause of cancer death in the US, few studies have evaluated the effect of diet after diagnosis on prostate cancer progression and all-cause mortality. We examined fat intake after prostate cancer diagnosis in relation to risk of lethal prostate cancer and all-cause mortality. Methods: This was a prospective study of 1,019 men diagnosed with prostate cancer between 1982 and 2000 in the Physicians’ Health Study. Men completed a dietary food frequency questionnaire a median of 5.1 years after diagnosis. We examined post-diagnostic intake of saturated, monounsaturated, polyunsaturated, and trans fats, as well as animal and vegetable fats. Cases were confirmed by medical record review. The main outcomes were lethal prostate cancer, defined as prostate cancer-specific death or metastasis to bone, and all-cause mortality. Multivariate Cox proportional hazards regression was used to estimate the relative risk of lethal prostate cancer and all-cause mortality. Models were adjusted for age at diagnosis, time since diagnosis, clinical T-stage, Gleason Score, prostate cancer treatment, BMI, smoking status, intake of alcohol and protein, total calories, and other fats. Results: We observed 87 lethal prostate cancer events and 395 total deaths over a median follow-up after diagnosis of 13.9 years. There was a suggestion of a positive relation between saturated fat intake and lethal prostate cancer that failed to reach statistical significance. The hazard ratio (HR) for lethal prostate cancer associated with a 5% increase in energy from saturated fat was 1.97 (0.89, 4.36; p=0.10). In addition, saturated fat intake after diagnosis was associated with increased risk of all-cause mortality (HR per 5% energy: 1.49; 95%CI: 1.02, 2.16; p=0.04) while vegetable fat was associated with reduced risk of all-cause mortality (HR per 10% energy: 0.63; 95%CI; 0.46, 0.88; p=0.007). Conclusions: Among men diagnosed with prostate cancer, replacing calories from carbohydrates with saturated fat after diagnosis may increase risk of all-cause mortality, while replacing calories from carbohydrates with vegetable fat may reduce risk of all-cause mortality.
Citation Format: Stacey A. Kenfield, Erin L. Richman, Howard D. Sesso, Jing Ma, Meir J. Stampfer, Jorge E. Chavarro. Fat intake after prostate cancer diagnosis and risk of lethal prostate cancer and total mortality. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3617. doi:10.1158/1538-7445.AM2013-3617
Abstract 3623: Association between helicobacter pylori infection and lung cancer: a meta-analysis.
Authors: Wu Na , Xu Bin , Li Yafei 
Published: August 2014

Abstract
Lung cancer is still the leading death cause of cancers. Helicobacter pylori (Hp) is one of the most common bacteria infecting human. In the past decade, some investigators endeavored to clarify the possible association of lung carcinoma risk with Hp infection, with conflicting results. Whether Hp infection is a risk factor for lung cancer remains largely uncertain. We performed a meta-analysis on the association between Hp infection and lung cancer. Medline, OVID, EMBASE and Chinese Biomedical Literature database (CBM) database were comprehensively searched for the relevant literatures until September 2012. Meta-analysis was performed using the program Review Manager 6.2. Heterogeneity was also explored. Seven case-control studies with a total of 1011 cases and 1040 controls met the inclusion criteria and were included in the meta-analysis. Hp infection was detected seropositivity for antibodies against Hp using ELISA in all 7 studies. Our meta-analysis showed that patients with lung cancer have a significantly higher rate of seropositivity for antibodies against Hp than controls, with an odds ratio of 3.15 (95% CI, 1.49-6.67). This meta-analysis suggests there may be a potential effect of Hp infection on the risk of lung cancer. This warrants further large and well-designed studies for thorough investigation.
Citation Format: Na Wu, Bin Xu, Yafei Li. Association between helicobacter pylori infection and lung cancer: a meta-analysis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3623. doi:10.1158/1538-7445.AM2013-3623
Abstract 3624: Genetic variation in SIRT1 affects susceptibility of lung squamous cell carcinomas in former uranium miners from the Colorado plateau.
Authors: Leng Shuguang , Picchi Maria A. , Liu Yushi , Lin Yong , Stidley Christine A. , Gilliland Frank D. , Jacobson Marty R. , Belinsky Steven A. 
Published: August 2014

Abstract
Epidemiological studies of underground miners suggest that occupational exposure to radon causes lung cancer with squamous cell carcinoma (SCC) as the predominant histological type. However, the genetic determinants for susceptibility of radon-induced SCC in miners are unclear. Double-strand breaks (DSBs) induced by radioactive radon daughters are repaired primarily by non-homologous end joining (NHEJ) that is accompanied by the dynamic changes in surrounding chromatin, including nucleosome repositioning and histone modifications. Thus, a molecular epidemiological study was conducted to assess whether genetic variation in 16 genes involved in NHEJ and related histone modification affected susceptibility for SCC in radon-exposed former miners (267 SCC cases and 383 controls) from the Colorado plateau. A global association between genetic variation in the haplotype block where SIRT1 resides and the risk for SCC in miners (P=0.003) was identified. Haplotype alleles tagged by the A allele of SIRT1 rs7097008 were associated with increased risk for SCC (Odds Ratio = 1.69, P = 8.2×10−5) and greater survival in SCC cases (Hazard Ratio = 0.79, P = 0.03) in miners. Functional validation of rs7097008 demonstrated that the A allele was associated with reduced gene expression in bronchial epithelial cells and compromised DNA repair capacity in peripheral lymphocytes. Together, these findings substantiate genetic variation in SIRT1 as a risk modifier for developing SCC in miners and suggested that SIRT1 may also play a tumor suppressor role in radon-induced cancer in miners.
Citation Format: Shuguang Leng, Maria A. Picchi, Yushi Liu, Yong Lin, Christine A. Stidley, Frank D. Gilliland, Marty R. Jacobson, Steven A. Belinsky. Genetic variation in SIRT1 affects susceptibility of lung squamous cell carcinomas in former uranium miners from the Colorado plateau. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3624. doi:10.1158/1538-7445.AM2013-3624
Abstract 3636: Systems biology approach links genetic, epigenetic, and transcriptomic features to tamoxifen sensitivity.
Authors: Gamazon Eric R. , Weng Liming , Im Hae Kyung , Zhang Xiaotong , Ziliak Dana M. , Huang R. Stephanie 
Published: August 2014

Abstract
Utilizing existing genome-wide genotype, transcriptome and microRNA (miRNA) datasets, we developed an integrative approach to evaluate the role of genetic-epigenetic regulatory networks in human complex traits. In this study, we focused on cellular sensitivity to tamoxifen, a commonly prescribed breast cancer medication as a phenotype of interest. A sequential multi-dimensional model was constructed to first identify genes/miRNAs whose expression levels are correlated with tamoxifen sensitivity. This in turn facilitated the identification of SNPs associated with potential functionally relevant genomic features. Finally, associations between these selected SNPs and cellular sensitivity to tamoxifen were evaluated. A permutation-based false discovery rate (FDR) procedure showed that association findings from our approach have much lower FDRs when compared to those obtained through a traditional single-step genome-wide association study (GWAS) between SNP and drug sensitivity. Our model identified 50 unique SNPs associated with 30 miRNAs and 34 gene expression levels, all of which associated with cellular sensitivity to tamoxifen phenotypes in HapMap YRI samples. Among them, several miRNAs and genes have been previously implicated to play a role in tamoxifen sensitivity; most are novel. Functional studies on select miRNAs/genes are currently underway in both the HapMap samples and breast cancer cell lines.
Citation Format: Eric R. Gamazon, Liming Weng, Hae Kyung Im, Xiaotong Zhang, Dana M. Ziliak, R. Stephanie Huang. Systems biology approach links genetic, epigenetic, and transcriptomic features to tamoxifen sensitivity. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3636. doi:10.1158/1538-7445.AM2013-3636
Abstract 364: Exercise slows tumor progression and normalizes tumor vasculature in murine models of breast cancer.
Authors: Betof Allison S. , Jones Lee W. , Dewhirst Mark W. 
Published: August 2014

Abstract
The effect of endurance exercise to improve post-ischemia perfusion of normal tissues is established but whether such effects extend to hypoxic solid tumors is largely uninvestigated. Thus, we evaluated the hypothesis that exercise slows tumor growth and improves the structure and function of tumor blood vessels, resulting in decreased hypoxia and increased effectiveness of cyclophosphamide chemotherapy. To investigate the effects of exercise on tumor microenvironment, we utilized voluntary wheel running after tumor cell implantation in two orthotopic models of murine breast cancer: ER(-) 4T1 breast tumor cells in BALB/c mice and ER(+) E0771 breast tumor cells in C57Bl/6 mice. Endurance exercise significantly increased microvessel density (CD31, p&lt;0.003), vessel maturity (co-localization of NG2 and desmin with CD31, p&lt;0.003), and perfusion (ADCperf, p&lt;0.05), which resulted in significant reductions in intratumoral hypoxia (EF5, p&lt;0.002). This was associated with significant inhibition of tumor growth (p&lt;0.004), and increased apoptosis compared with sedentary controls (cleaved caspase-3, p&lt;0.05). Next, given that hypoxia is a major cause of chemoresistance, we tested whether exercise-induced improvements in perfusion and reduction of hypoxia could improve the efficacy of conventional chemotherapy. The combination of exercise plus cyclophosphamide was associated with significantly prolonged growth delay compared with exercise or chemotherapy alone (p&lt;0.01). In this work, we provide the first conclusive evidence that exercise may do more than decrease symptoms and improve quality of life for cancer patients. Our data suggest that exercise may be an effective adjunct therapy to reduce tumor hypoxia leading to enhanced efficacy of anticancer therapy.
Funding: ASB is supported by DOD BC093532. LWJ is supported by NIH CA143254, CA142566, CA138634, CA133895 and funds from George and Susan Beischer. MWD is supported by NIH CA40355.
Citation Format: Allison S. Betof, Lee W. Jones, Mark W. Dewhirst. Exercise slows tumor progression and normalizes tumor vasculature in murine models of breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 364. doi:10.1158/1538-7445.AM2013-364
Abstract 3648: Unraveling phenotype heterogeneity in prostate cancer susceptibility in Finland utilizing covariate-based analysis.
Authors: Cropp Cheryl D. , Simpson Claire L. , Wahlfors Tiina , George Asha , Jones MaryPat S. , Harper Ursula , Ponciano-Jackson Damaris , Tammela Teuvo , Schleutker Johanna , Bailey-Wilson Joan E. 
Published: August 2014

Abstract
Prostate cancer is the most common male cancer in developed countries. Previously, we reported a genome-wide linkage scan in 69 Finnish Hereditary Prostate Cancer (HPC) families, which replicated the HPC9 locus on 17q21-q22 and a locus on 2q37. We used ordered subset analysis (OSA) to detect other loci linked to HPC in subsets of families to detect other loci linked to HPC incorporating mean family age of onset as a trait-related covariate to address genetic heterogeneity. The overall mean age of onset across the families was 66.2±8.8 years while the range of individual onset ages ranged from 46-98 years and age of onset varies within families. The highest OSA LOD score was 2.876 (ΔLOD p=0.02) on 15q26.2-q26.3 in a subset of 40 families ascending by age at onset, suggesting that a subset of early age at onset families may be segregating a risk allele(s) at this locus. No other ΔLOD scores were significant after permutation testing. To better capture the effect of age on the linkage signals, we used LODPAL to perform a model-free linkage analysis in affected relative pairs, while adjusting for the age of each individual family member as a single covariate. Preliminary results revealed strong evidence of linkage to HPC on chromosome 15q (LOD=4.9, 132cM) and 8q (LOD=3.1, 157cM). Future analyses are planned which will use age of onset, PSA levels and other clinical characteristics to prioritize regions which may harbor genetic variants of large effect on PRCA.
Citation Format: Cheryl D. Cropp, Claire L. Simpson, Tiina Wahlfors, Asha George, MaryPat S. Jones, Ursula Harper, Damaris Ponciano-Jackson, Teuvo Tammela, Johanna Schleutker, Joan E. Bailey-Wilson. Unraveling phenotype heterogeneity in prostate cancer susceptibility in Finland utilizing covariate-based analysis. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3648. doi:10.1158/1538-7445.AM2013-3648
Abstract 3651: Parity-related molecular signatures and breast cancer heterogeneity.
Authors: Rotunno Melissa , Sun Xuezheng , Figueroa Jonine , Sherman Mark , Garcia-Closas Montserrat , Meltzer Paul , Williams Tyisha , Smith Schneider Sallie , Jerry Joseph , Yang Rose , Troester Melissa 
Published: August 2014

Abstract
Background. Parity is an established protective factor for ER-positive but not ER-negative breast cancer and it may increase the risk of triple-negative (negative for ER, PR, and HER2) tumors. Characterizing parity-related gene expression patterns in normal breast and breast tumor tissues may improve our understanding of the biological mechanisms underlying the subtype-specific associations between parity and breast cancer risk. Method. Gene expression changes associated with parity were identified in microarray data (4x44 K Agilent) from breast tissue of 74 non-diseased reduction mammoplasty (RM) patients. This parity signature, together with published parity signatures, were compared by GSEA method with gene expression (4x44 K Agilent and Illumina arrays) from both normal (N=150) and tumor (N=208) tissues of breast cancer patients from the Polish Breast Cancer Study (PBCS), overall and by tumor ER status. Results. We identified 908 genes significantly up-regulated by parity status (parous vs. nulliparous, FDR = 0.047), including genes in inflammatory pathways. Parity-related signatures identified by us and by previously published studies were significantly enriched in normal and tumor tissue of parous PBCS patients, specifically in ER-positive tumors (FWER&lt;0.1). Conclusions. Our analysis identified a novel parity-related gene signature in normal breast tissue from healthy women, which is also detected in normal and tumor tissues in breast cancer patients with ER-positive tumors. The lack of parity-associated signatures in ER-negative tumors may reflect the disruption of parity-associated pathways (pro-inflammatory) in ER-negative tumors.
Citation Format: Melissa Rotunno, Xuezheng Sun, Jonine Figueroa, Mark Sherman, Montserrat Garcia-Closas, Paul Meltzer, Tyisha Williams, Sallie Smith Schneider, Joseph Jerry, Rose Yang, Melissa Troester. Parity-related molecular signatures and breast cancer heterogeneity. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3651. doi:10.1158/1538-7445.AM2013-3651
Abstract 3655: c-JunNH2-teminal kinase 1 plays a crucial role in vitamin D-mediated cancer cellmaturation through interacting with vitamin D receptor.
Authors: Shi Qi , Bi Xiuli , Fang Wenfeng , Hu Dong , Chen Zhiguo , Dong Huali , Yang Wancai , Yang Wancai 
Published: August 2014

Abstract
Vitamin D is chemopreventive against colorectal carcinogenesis in vivo and in vitro. The protective effects of vitamin D against colonic carcinogenesis are most probably mediated through the vitamin D receptor (VDR). When bound to the hormonally active form of vitamin D, 1,25(OH)2-D3, VDR transactivates genes that inhibit proliferation, or promote differentiation and apoptosis. Previous studies showed that stress-activated protein kinase JNKs (c-Jun NH2-terminal kinases) and p38 cooperated to activate VDR and increase vitamin D3-dependent growth inhibition in breast cancer cells. To determine whether vitamin D-mediated maturation is associated with JNK1 and VDR in colorectal cancer cells, we treated the human colon cancer cell HT29 with 1,25(OH)2-D3, and found that 1,25(OH)2-D3 significantly inhibited cell proliferation and induced apoptosis, which was associated with induction of phosphorylated JNK1 (p-JNK1) and p21,p27, which was also associated with increased the expression of PARP and cleaved Caspase 3. In the JNK1 knockout mouse model in which tumor spontaneously formed in intestinal tract, we found that VDR was significantly reduced or not expressed in mouse intestinal epithelial cells, compared to those in the wild-type mice. Further, we found that VDR transcriptional activity was lower in JNK1-/- mouse embryonic fibroblast cells (MEFs), assayed by transfection with VDR-element-Luc reporter. When the JNK1-/- MEFs were treated with calcitriol, the induced of VDR transcriptional activity was also attenuated, compared to that in JNK1+/+ MEFs. Moreover, increasing expression of activated JNK1 by transfection with pcDNA3-Flag-MKK7 (activated JNK1) in HT29 colon cancer cells, VDR-element-Luc was significantly increased, and VDR expression levels were also increased. Finally, we co-transfected HEK239 cells with pcDNA3-HA-VDR and pcDNA3-Flag-MKK7 plasmids and conducted co-immunoprecipitation assay, we found that VDR was physically binding to JNK1. Taken together, JNK1 interacted with VDR and affected VDR at transcriptional and translational levels. Thus, the status of JNK1 may play a critical role in vitamin D-medicated cancer prevention through modulating vitamin D receptor. Whether JNK1 affects VDR polymorphisms and then influences cancer prevention efficacy of vitamin D is under further investigation.
*Supported by National Natural Science Foundation Of China (81272251)
Citation Format: Qi Shi, Xiuli Bi, Wenfeng Fang, Dong Hu, Zhiguo Chen, Huali Dong, Wancai Yang, Wancai Yang. c-JunNH2-teminal kinase 1 plays a crucial role in vitamin D-mediated cancer cellmaturation through interacting with vitamin D receptor. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 3655. doi:10.1158/1538-7445.AM2013-3655