bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 970: Effect of feeding a high fat, high simple carbohydrate diet on serum prostate specific antigen (PSA) in cynomolgus monkeys
Authors: Mubiru James N. , Garcia-Forey Magdalena , Bauer Cassondra , Shade Robert E. , Comuzzie Anthony G. , Rogers Jeffrey 
Published: February 2011

Abstract
Introduction
The prostate specific antigen (PSA) test is used for screening and monitoring of prostate cancer. However, PSA has clinical limitations as it is elevated in other pathological conditions other than prostate cancer. PSA is also influenced by other physiological and environmental variables like genetics and diet. The aim of this study was to investigate the effect of feeding a high fat, high simple carbohydrate (HFHSC) diet on serum PSA in a nonhuman primate species.
Methods
Fifteen cynomolgus monkeys (Macaca fascicularis) were fed an HFHSC diet for 4 months. Body weight and Dual energy X-ray absorptiometry (DEXA) measurements were done at 0, 8 and 16 weeks. Blood was also drawn from these animals and used to assay serum PSA and serum insulin levels.
Results 0 weeks Mean ± SD8 -weeks Mean ± SD16 weeks Mean ± SDP value (0-16) weeksBody weight (kg)5.48 ± 1.095.89 ± 1.355.99 ± 1.440.018Calorie intake (kcal/day)421.8 ± 115.20705.07 ± 101.52684.07 ± 102.361.7 × 10−8Tissue Fat (%)5.57 ± 3.817.29 ± 5.508.04 ± 6.70.155Region fat (%)5.33 ± 3.677 ± 5.237.7 ± 6.480.16Fat (g)289 ± 264.37412.07 ± 375.72467.6 ± 462.890.14Soft tissue mass (g)4860.53 ± 1105.735199.06 ± 1338.795269.33 ± 1435.430.0488Lean mass (g)4571.6 ± 968.114787 ±1125.334801.87 ± 1162.970.056Bone mineral content (g)228.44 ± 44.71234.71 ± 48.74236.85 ± 49.470.031PSA ng/ml0.70 ± 0.570.91 ± 0.460.96 ± 0.620.04Insulin µU/ml14.92 ± 12.1930.87 ± 26.1161.36 ± 66.290.014
Conclusions Feeding cynomolgus monkeys with an HFHSC diet for 4 months resulted in a significant increase in serum PSA levels. The mechanisms underlying this change in serum PSA is still under investigation, however, chronic hyper-insulinemia as indicated in this study might be one of the contributing factors.
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 970.
Abstract 974: Fellowships in Research and Science Teaching (FIRST): Innovative postdoctoral training for aspiring academic scientists
Authors: Knight Brandi B. , Taliaferro-Smith LaTonia , Eisen Arri , Eaton Douglas 
Published: February 2011

Abstract
Fellowships in Research and Science Teaching (FIRST) is a successful, three-year postdoctoral program at Emory University that combines traditional postdoctoral research training with mentored teaching instruction. Supported by the Institutional Research and Academic Career Development Award (IRACDA, K12) in the Division of Minority Opportunities in Research (MORE), FIRST encourages teaching experiences at minority serving institutions (MSIs) in the Atlanta University Center (Clark-Atlanta University, Morehouse College, and Spelman College). Fellows receive formalized instruction in pedagogy through a course entitled A Class within a Class, which provides training in innovative teaching techniques, use of technology in the classroom, course development and assessment, as well as peer-evaluation of lecture styles. Participation in the FIRST program creates a unique training experience that prepares fellows to become successful biomedical researchers as well as effective instructors. Despite having dual responsibilities during postdoctoral training, a study comparing 114 FIRST fellows to 500 traditional postdocs showed that FIRST fellows continue to publish in peer-reviewed journals at the same rate or above traditional postdoctoral fellows. In addition, FIRST fellows continue to pursue academic research careers and receive NIH grant funding. Along with the goals of the IRACDA programs, FIRST fellows have established research affiliations with Emory University and MSIs thus creating a collaborative network between research-intensive intuitions and under-represented minority liberal arts colleges.
NIH/NIGMS IRACDA Grant 5K12GM000680
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 974.
Abstract 979: Understanding the relationship between race and nicotine dependence
Authors: Wilson Shondelle M. , Thorpe Roland J. , Ford Jean G. , LaVeist Thomas A. 
Published: February 2011

Abstract
Background: Mounting evidence continues to demonstrate that nicotine dependence is a growing public health issue among current smokers. While duration of smoking, number of cigarettes smoked per day (CPD) and cessation attempts are common indicators of nicotine dependence, African Americans tend to smoke less cigarettes per day (CPD; 10 or less), initiate smoking at a later age and experience greater failed quit attempts, compared to whites, yet develop nicotine dependence. However, no previous study has examined the possibility that race differences in the social context which African Americans and non-Hispanic whites live may contribute to disparities and the persistence of nicotine dependence. Social class and immediate personal interactions occurs in various social contexts, including the living space, workplace, institutions or other physical environments. This project examines the contributions of demographic, behavioral and environmental factors as social contextual factors that contribute to smoking behavior and the persistence of nicotine dependence.
Objective: We examined race disparities in nicotine dependence among 761 African American and white current smokers living in similar social and environmental risk exposures and compared these estimates to 1461 black and white current smokers in a national sample of adults aged 20 and over.
Methods: Data was assessed from Exploring Health Disparities in Integrated Communities-Southwest Baltimore (EHDIC-SWB; 2003) and National Health and Nutritional Examination Survey (NHANES; 2001-2004) to determine if race disparities in nicotine dependence would be attenuated in EHDIC-SWB. Time to first cigarette was used to assess nicotine dependence. Logistic regression was used to assess the association between race and nicotine dependence, controlling for known confounders.
Results: In multivariate analysis, race differences in nicotine dependence were greater among African-Americans in a representative sample of US adults. African Americans in a national sample have a lower odds of nicotine dependence (OR = 0.8; 95% CI 0.46, 0.93) compared to whites. However, no race difference were detected among participants in the EHDIC-SWB study (0.87; 95% CI 0.62, 1.22).
Conclusions: Examination of social and environmental factors may reveal important insights into the nature of inequalities between black and white adults in health outcomes such as nicotine dependence. Our results highlight the importance of examining social contextual factors and suggest that the promotion of targeted interventions may reduce the prevalence of nicotine dependence among current smokers.
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 979.
Abstract 980: Intrathecal methotrexate induces focal cognitive deficits and alters CNS folate physiology in rats
Authors: Li Yan , Vijayanathan Veena , Gulinello Maria , Cole Peter D. 
Published: February 2011

Abstract
Background: In order to reduce the persistent neurologic toxicity of therapy for childhood acute lymphoblastic leukemia (ALL), many treatment protocols avoid cranial radiation, relying instead on intrathecal chemotherapy to prevent central nervous system relapses. Nevertheless a significant subset of survivors treated without radiation manifest persistent focal deficits in cognitive function. The folate antagonist methotrexate (MTX), a key component of prophylactic intrathecal therapy, is suspected to contribute to treatment-induced cognitive dysfunction. Our goal was to establish a rodent model to isolate the cognitive and neurotoxic effects of MTX after direct administration into cerebrospinal fluid (CSF).
Methods: Adult Long-Evans rats were given either intrathecal MTX 0.5mg/kg or artificial CSF via transcutaneous puncture at the level of the cisterna magna. Three days later, all rats subsequently underwent a battery of behavioral tests designed to assess cognitive domains frequently impaired among children treated for ALL, including spatial memory, visual memory, and motor coordination. Indicators of folate physiology (folate and homocysteine) in CSF and serum were measured using high performance liquid chromatography. Concentrations of interleukin-1β, IL-6, and tumor necrosis factor-α were measured in CSF to assess whether intrathecal MTX induces an inflammatory response.
Results: Intrathecal MTX administration reliably produced both visual and spatial memory deficits, without altering general activity or motor coordination. MTX administration was associated with a significant reduction in both CSF and serum folate concentrations, along with an increase in CSF homocysteine. At 24 hours post-injection of MTX, CSF folate decreased by 75% and CSF homocysteine was increased 4-fold, relative to baseline. Intrathecal injection of both MTX and artificial CSF was associated with a significant rise in CSF IL-6 within 6 hours, which then returned to baseline by 24h.
Conclusion: We have established an animal model in which intrathecal MTX induces cognitive dysfunction that mimics clinically observed toxicity, in association with a rapid fall in CSF folate and increase in CSF homocysteine. A non-specific, transient increase was seen in the proinflammatory cytokine IL-6 within CSF. This proinflammatory response does not appear sufficient to cause cognitive deficits, as it was observed among both groups of rats, while toxicity was demonstrated among only those who received MTX. This model will allow us both to further investigate the pathophysiology of treatment-induced cognitive dysfunction and to test protective interventions.
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 980.
Abstract 987: Researching policy proposals aimed at placing cancer on the global health agenda
Authors: Kawahara Norie 
Published: February 2011

Abstract
Deaths caused by cancer continue to increase around the world. People living in low- and middle-income countries are in greater danger than people living in high-income countries of succumbing to risks that can be relatively easily avoided by man-made interventions. These risks include smoking, unhealthy eating and lifestyle, lack of exercise, excessive intake of alcohol, and chronic infections such as HPV or hepatitis. The World Health Organization projects that if the challenges facing low- and middle-income countries are not addressed, by 2015 an estimated 5.7 million people will die annually in those countries, rising to 8.9 million by 2030. With limited medical resources, the priority challenges for the global health agenda remain focused on HIV/AIDS and malaria. Now, however, is the time to transform global health policies. The U.S. Commitment to Global Health clearly states that “Cancer Should Be Raised Onto the Global Health Agenda” and yet cancer remains to be recognized by the global health community as a priority issue. What is the positioning given to cancer on the global health agenda? What factors are preventing is inclusion in global health? What are the primary mechanisms that inform and decide the global health agenda? In contrast to infectious diseases, cancer slowly yet perniciously attacks the very roots of people's lives. This long time-frame means that we must consider a wide-range of factors, including economic, cultural and domestic and international policies. This policy-based research was implemented in the form of interviews with people from various sectors, encompassing various perspectives, including social determinants of health, health equity and solidarity and human rights. The results and analysis of this research are broken down into: (1) Top-down mechanisms, (2) Bottom-up mechanisms, and (3) the formation of new values through an IT network that functions to meld (1) and (2) and promote them in tandem. The results will be used to present the challenges and outlook for raising cancer onto the global health agenda. In order to ensure the global advancement of cancer research, in accordance with the principles and theory enshrined in the Universal Declaration of Human Rights, which stipulates that all people have the right to enjoy the benefits of science and technology, an urgent prerequisite is to promote strategic analysis with the objective of including cancer in the United Nations Millennium Development Goals (MDGs). Achieving the inclusion of cancer in the MDGs would significantly raise the profile of cancer in the global health agenda.
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 987.
Abstract LB-101: A novel role of semaphorin4a (sema4a) in genotoxin-induced DNA damage response in human lung fibroblasts
Authors: Bae Dongsoon , Chun Gina , Patierno Steven R. , Ceryak Susan M. 
Published: February 2011

Abstract
Dysregulation of DNA repair signaling after genotoxin exposure contributes to genomic instability and carcinogenesis. Hexavalent chromium [Cr(VI)] is a genotoxin of occupational and environmental concern. Protein tyrosine phosphatase (PTP) inhibitors (i.e., sodium orthovanadate (SOV)) activate key survival pathways. We reported that SOV enhances clonogenic survival after Cr(VI) exposure by overriding Cr-induced growth arrest in human lung fibroblasts (HLFs). PTP inhibition with SOV increased expression of DNA damage/repair genes as determined by microarray analysis. Kinetic analysis of DNA double-strand breaks (DSBs) by comet assay showed equal DSB formation 15 min after Cr(VI) exposure in the absence and presence of SOV. However, PTP inhibition significantly decreased DSBs 0.5-24 hr after Cr(VI) treatment. Aim of the present study was to determine the molecular mechanism(s) by which PTP inhibition affects DNA damage response during genotoxic stress. Gene expression was examined by DNA Damage Signaling Pathway PCR Array after 1 μM Cr(VI) treatment for 24 hr in the absence or presence of SOV. The PTP inhibitor reversed Cr-mediated changes in expression of several unique genes. Interestingly, the sema4a gene, known to be involved in T cell activation and endothelial cell proliferation and migration, was strongly induced by co-treatment of SOV and Cr(VI). Gene expression correlated with increased sema4a protein expression after co-treatment of SOV and Cr(VI). A potential role of sema4a in Cr-induced DNA DSB formation/repair in the absence or presence of SOV was assessed after sema4a siRNA transfection. Silencing of sema4a did not alter the effect of SOV on Cr-induced DSBs. However, sema4a silencing completely blocked Cr-induced DSBs 4 hr after exposure. These results suggest a novel role of sema4a in DNA DSB formation/repair in normal HLFs. Taken together, these data shed light on the emerging role of semaphorins as mediators of cell survival as well as potential therapeutic targets in carcinogenesis.
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 LB-101.
Abstract LB-104: Differences in repair of DNA cross-links between lymphocytes and tumor cells from colon cancer patients
Authors: Herrera Mercedes , Dominguez Gemma , Garcia Jose M. , Peña Cristina , Jimenez Carmen , Silva Javier , Garcia Vanesa , Gomez Irene , Diaz Raquel , Martin Paloma , Bonilla Felix 
Published: February 2011

Abstract
The more common approach to comet assay studies with cancer patients involves indirect measurement of the effect of antineoplastic drug or radiation regimen by assessing DNA damage in surrogate cells, such as peripheral blood lymphocytes of cancer patients, to predict how tumor cells may be affected. The aim of the present study was to compare the capability of different cells isolated from a series of 23 colon cancer patients to repair the damage induced by a cancer drug. We adapted the in vitro comet repair assay for nucleotide excision repair to measure the ability of lymphocytes and normal and tumor epithelial colon cells to remove DNA cross-links induced by oxaliplatin. The excision repair rate was measured quantitatively by the tail parameters: tail DNA, tail length, extent tail moment, and olive tail moment. Kruskal-Wallis analysis revealed significant differences in recognition and excision activity between different cell types (P &lt; 0.001) for all the comet parameters studied. Hence, colon cells showed higher recognition and excision activity than lymphocytes and tumor cells displayed the highest repair capability. We found no significant correlation between the repair activity of tumor colon cells and lymphocytes in any of the comet parameters considered. Our data support the view that lymphocyte repair activity is not predictive of the repair ability of the tumor and that lymphocytes cannot act as surrogate cells.
Note: This abstract was not presented at the AACR 101st Annual Meeting 2010 because the presenter was unable to attend.
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 LB-104.
Abstract LB-106: Inhibition of glycolysis with 2-deoxyglucose inhibits spontaneous metastasis in murine osteosarcoma
Authors: Thamm Douglas H. , Lori Janet , Sottnik Joseph L. 
Published: February 2011

Abstract
We recently reported on a re-analysis of previously published gene expression data from a large set of primary solid and metastatic tumors originating from different tissues using the latest available tools for normalization, identification of differentially expressed genes and pathway analysis (Ptitsyn A., et al, BMC Bioinformatics 2008;9 Suppl: S8). Analysis of multiple independent datasets indicated significantly reduced oxidative phosphorylation in metastases compared to primary solid tumors, implying a potential enhancement of the Warburg phenotype in metastatic progression. We thus sought to determine if inhibition of anaerobic glycolysis with the competitive inhibitor 2-deoxy-D-glucose (2-DG) would reverse this metastatic bioenergetic phenotype in highly metastatic cancer cells. We evaluated the effects of 2-DG on DLM8 osteosarcoma cell migration and Matrigel invasion via Boyden chamber assays, and modulation of in vitro production of matrix metalloproteases, VEGF, and cathepsin L were evaluated by gelatin zymography, ELISA and western analysis respectively. The effects of 2-DG administration in vivo was evaluated in an orthotopic, spontaneously metastatic, luciferase-transfected postsurgical model of murine osteosarcoma utilizing DLM8, which is syngeneic to C3H mice. DLM8 cells were implanted into the distal tibias of C3H mice, followed by amputation of the affected limb 16 days later. 2-DG or saline were administered postoperatively (500 mg/kg IP 3x/week, n=5 per group) until sacrifice. Presence of metastasis was evaluated using biweekly bioluminescence imaging and metastasis-free interval calculated using the Kaplan-Meier method. Concentrations of 2-DG associated with minimal antiproliferative activity dramatically inhibited DLM8 cell migration and invasion. There was a dose-dependent decrease in cathepsin L expression upon 2-DG exposure, and VEGF production was inhibited at high 2-DG concentrations, but there were no repeatable changes in MMP activity within the concentration range associated with inhibition of migration and invasion. Postoperative administration of 2-DG significantly delayed DLM8 metastasis (median metastasis-free interval 8 vs 34 days, p = 0.049). In conclusion, glycolysis inhibition with 2-DG is associated with an inhibition of osteosarcoma migration, invasion and in vivo metastasis, at concentrations associated with minimal antiproliferative activity.
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 LB-106.
Abstract LB-110: CDK4 activation is a key step in ELF alteration and haploinsufficeny of cdk4 prevents HCC formation in elf+/− mice
Authors: Baek Hye Jung , Pishvaian Michael J. , Cho Kwan Ho , Mishra Bibhuti , Reddy E. Premkumar , Mishra Lopa , Kim Sang Soo 
Published: February 2011

Abstract
Transforming growth factor (TGF-) is an important regulator of cell growth and the loss of TGF- signaling occurs early in carcinogenesis. Embryonic liver fodrin (ELF), an interaction protein of Smads, is involved in TGF- signaling. Significantly, elf+/− mice spontaneously developed the hepatocellular cancer (HCC) and lots of human HCC exhibited decreased or absent ELF expression. Here, we investigated how alteration of ELF led the deregulation of cell cycle progression and eventually formed the HCC. Up regulation of ELF expression led the decreased phosphorylation of Rb protein with the remarkable reduction of CDK4 than other CDKs and cyclins. Then, inhibition and downregulation of CDK4 by inhibitor and siRNA rescued the abnormality of G1/S transition and over-activation of Rb phosphorylation caused by infection of ELF shRNA in SNU475 HCC cell line. We further demonstrated the biochemical communications using immunoprecipitation that ELF interacted CDK4, and Smad3 in competitive way and TGF-ß-dependent manner. In addition, haploinsufficieny of cdk4 in elf+/− mice displayed the dramatic decrement of HCC formation than elf+/− mice with decreased Ki-67 and c-myc expressed hepatocyte in liver tissue. Thus, in response to ELF deficiency, the activation of CDK4 contributes to the phosphorylation of Rb protein, which leading to facilitated G1/S transition. Our data highlight CDK4 as an attractive target for pharmacologic inhibition and importance of elf+/− model to demonstrate pre-clinical efficacy in the treatment of HCC with ELF alteration.
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 LB-110.