bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 5654: Novel changes in colonic epithelial junctional complexes precede onset of colitis in response to Citrobacter rodentium infection
Authors: Ahmed Ishfaq , Chandrakesan Parthasarathy , Umar Shahid 
Published: February 2011

Abstract
Activation of β-catenin is recognized as a critical early factor in tumorigenesis. Citrobacter rodentium (CR) induces transmissible murine colonic hyperplasia (TMCH) and variable degrees of inflammation and necrosis depending upon the genetic background. Utilizing the CR-induced hyperplasia and/or inflammation in C3H/HeNHsd (C3H) inbred mice, we observed a dual phase wherein initially, an increase in proliferation at days 5 and 7 was followed by development of colitis at day 9 of TMCH. When sequential changes in proteins involved in adherens and tight junctions were analyzed in isolated colonic crypts, increasing levels of β-catenin, ZO-1, ZO-2 and claudin-2 were measured in TritonX100-soluble fraction at days 5 and 7 of TMCH, while E-cadherin and claudin-5 were mainly present in TritonX100-insoluble (cytoskeletal) pool. Interestingly, the cytoskeletal pools exhibited extensive degradation of β-catenin/E-cadherin/ZO-1 and ZO-2 but not of claudin-5 at days 5 and 7 of TMCH and preceded active colitis at day 9. Immunohistochemically, almost complete loss of membrane-bound β-catenin/E-cadherin and ZO-2 was recorded between 9 and 11 days post-infection. However, changes in permeability, as measured by increases in serum FITC-dextran levels, increased significantly at days 5 and 7 and peaked between day 9 and 11 post-infection paralleling bacterial dissemination to spleen and liver at these time points. Mechanistically, β-catenin translocated to the nucleus, interacted with increasing levels of T-cell factor-4 and upregulated downstream targets, cyclinD1 and c-myc thereby promoting crypt hyperplasia at days 5 and 7 of TMCH. When CR-infected mice were placed on: 6% pectin (source of colonic butyrate), 4% curcumin and 4% bael extract diets for 9 days starting 2 days post-CR infection, all three dietary interventions: i) reduced the morbidity and mortality of CR-infected C3H mice, ii) restored the junctional labeling of β-catenin/E-cadherin and ZO-2, iii) blocked increases in colonic permeability thereby preventing bacterial dissemination to distant organs and finally, iv) promoted β-catenin-independent increases in colonic crypt proliferation as was revealed by increased Ki-67 labeling. Thus, i) fragmentation of β-catenin/E-cadherin/ZO-1 and ZO-2 precedes loss of barrier function and onset of colitis and, ii) epithelial hyperproliferation in response to dietary interventions may facilitate epithelial recovery following inflammatory insult but may also promote mucosal priming for neoplasia. TMCH model therefore provides an excellent tool to separate the anti-inflammatory effects of dietary ingredients from pro-proliferatory functions in vivo.
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 5654.
Abstract 5662: RBAC, a modified form of Arabinoxylan from rice bran, impairs prostate cancer cell line proliferation, adhesion, and invasion in vitro
Authors: Brush Thomas P. , Trinh Sandra , Brawner Christopher M. , Ali Karriem H. , Hauke Ralph J. , Elkahwaji Johny E. 
Published: February 2011

Abstract
Introduction and objective: Prostate cancer (CaP) remains a major concern of public health in the United States. Standard treatment already in clinical use has a high curability rate in patients diagnosed with localized and androgen-dependent CaP; however, the progression to hormone refractory CaP is associated with disease relapse and poor prognosis. Hence, it is important to discover a novel strategy to prevent progression of disease whilst minimizing toxicity. One such promising approach is the dietary administration of certain natural compounds such as RBAC, a rice bran carbohydrate extract hydrolyzed by Shiitake mushroom enzymes. Several experimental studies have shown that RBAC in vitro increases both susceptibility and sensitivity of many human malignant cells to undergo apoptosis and to respond to chemotherapeutic drugs. Furthermore, RBAC immunomodulates natural killer (NK) cells in vitro and in vivo and enhances plasma cytokine production and anti-tumor activity in an in vivo mouse model. The aim of this study was to investigate the direct anti-tumor activity of RBAC on CaP cell lines and its impact on cell proliferation, adhesion, and invasion.
Methods: A panel of stromal and epithelial cell lines was used [Mesenchymal Stromal Cells (MSC) and CaP epithelial cell lines (PC3 and LNCaP)]. Cell lines were cultured in appropriate media supplemented with 10% FBS in a 5% CO2 incubator. Cells were treated for 24, 48, and 72h with different doses of RBAC (0-1000 µg/ml). The cell proliferation, adhesion, and invasion assays were determined by Trypan blue and AlamarBlue® proliferation assays, Cytotracker™ adhesion assay, and CytoSelect™ invasion assay, respectively.
Results: RBAC significantly decreased the epithelial cell proliferation of MSC, and CaP human malignant cell lines (PC3 and LNCaP) (p&lt;0.05). The inhibition occurred in a dose-dependent manner and was more pronounced at high doses of RBAC (1000 µg/ml). Also, that same dose of RBAC impaired the MSC-PC3 cell adhesion and PC3 cell invasion in vitro.
Conclusions: These data suggest that RBAC exhibits an anti-proliferative and pro-apoptotic effects on CaP cell lines in vitro and might have therapeutic potential in advanced human CaP.
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 5662.
Abstract 5727: B vitamins and reduced risk of lung cancer among 900 cases and 1800 controls from the EPIC cohort study
Authors: Brennan Paul J. , Johansson Mattias , Relton Caroline , Vollset Stein Emil , Midttun Oivind , Nygard Ottar , Ueland Per Mange , Vineis Paolo ,   on behalf of the EPIC cohort study.
Published: February 2011

Abstract
Background: B-vitamins including folate help to ensure DNA integrity and the regulation of gene expression and may be associated with subsequent reduced cancer risk. One previous cohort study among smokers identified a substantial protective effect for vitamin B6 on lung cancer.
Methods: The EPIC study population included 385,747 participants from 23 centres in ten countries who completed a dietary questionnaire and provided a blood sample at recruitment between 1992 and 2000. 899 lung cancer cases were identified by 2006, with an average follow-up of 5 years, and matched to 1,770 controls for country, sex, date of birth and time of blood collection. Circulating concentrations were measured for four specific B-vitamins (B2, B6, folate and B12) as well as methionine, homocysteine and cotinine.
Results: After adjusting for matching variables and cotinine, a substantial decreasing risk for lung cancer was seen for increasing levels of B6 (relative risk of 4th vs 1st quartile [RR] = 0·44, with 95% confidence interval [CI] 0·33-0·60; p for trend [ptrend]&lt;0·000001), as well as for methionine (RR=0·52, CI 0·39-0·69; ptrend&lt;0·000001). Similar and consistent decreases in risk were observed for never, former and current smokers, indicating that results were not due to a smoking associated artifact. The magnitude of risk was also constant with increasing length of follow-up, indicating the effects were not explained by pre-clinical disease. A decrease in risk was also seen for folate, (RR=0·68, CI 0·51-0·90; ptrend=0·001), although this was apparent only for former and current smokers. When participants were classified by median levels of both methionine and B6, having above median levels of both resulted in a substantial decrease in lung cancer risk overall (RR=0·41, CI 0·31-0·54), as well as separately among never (RR=0·36, CI 0·18-0·71), former (RR=0·51, CI 0·34-0·76), and current smokers (RR=0·42 CI 0·27-0·65).
Interpretation: Higher serum levels of both vitamin B6 and methionine were associated with a substantial decrease in lung cancer risk on average 5 years later, indicating that they, or strongly related dietary factors, have an important effect on future lung cancer development. Increased knowledge of protective factors for lung cancer over and above tobacco cessation could make a significant contribution to disease prevention, particularly in former and never 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 5727.
Abstract 68: Nampt regulates fatty acid synthesis, ER homeostasis, and survival in prostate cancer
Authors: Ryan Sarah , Kridel Steven 
Published: February 2011

Abstract
Nicotinamide adenine dinucleotide (NAD) is crucial for the survival of living organisms. This coenzyme functions in both redox metabolism and as a substrate for several proteins, notably Sirtuin deacetylases and poly-(ADP ribose) polymerases, which control stress response and apoptosis in cancer. The rate limiting step of NAD biosynthesis is catalyzed by Nicotinamide phosphoribosyl transferase (Nampt). Recent evidence suggests Nampt may play a role in cancer by regulating survival. The Nampt inhibitor FK866 is in phase II clinical trials against a variety of solid malignancies, however no studies have focused on the role of NAD in prostate cancer (PCa). Because tumor cells have a high requirement for NAD and PCa has increased fatty acid synthesis, we hypothesized that Nampt is important for PCa cell survival and metabolism. Our studies demonstrate that Nampt activity is required for the survival of prostate tumor cells (PC-3, LNCaP, and DU145), but not normal prostate epithelial cells, as determined by treatment with FK866. Exogenous NAD rescued cell death, indicating FK866 is a specific inhibitor of Nampt. To test whether PCa cells can rely on de novo NAD synthesis, we treated cell lines with FK866 and added back nicotinic acid, the substrate for the de novo pathway. Only DU145 cell survival was rescued by nicotinic acid demonstrating that NAD biosynthesis pathways are heterogeneous in PCa. Furthermore, expression of Nicotinic acid phosphoribosyl transferase (Naprt1), the rate-limiting step of the de novo pathway, correlated with the rescue by nicotinic acid in DU145 cells. Additionally, Nampt inhibition activated endoplasmic reticulum (ER) stress and autophagy in a pro-survival manner in all cell lines. Interestingly, FK866 also dramatically reduced fatty acid synthesis in PC-3 and DU145 cells, independent of fatty acid synthase levels. However, LNCaP cells showed no decrease in 14C-acetate incorporation. Robust phosphorylation of ACC occured in DU145 and PC-3 cells upon treatment with FK866, and this effect was rescued by adding back NAD. This correlated with reduced ATP levels and activation (phosphorylation) of AMPK at T172. LNCaP cells had a less dramatic depletion of ATP and no changes in AMPK or ACC phosphorylation, indicating a potential mechanism of fatty acid synthesis shutdown. However, lipid synthesis (as measured by incorporation of 14C-choline) was reduced in all 3 cell lines, albeit to a lesser extent in LNCaP cells. Overall, these findings demonstrate a novel role for Nampt in PCa, and highlight the contribution of NAD to ER homeostasis, fatty acid synthesis, and survival. Targeting NAD biosynthesis could be a novel approach to disrupting PCa cell survival and lipid synthesis.
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 68.
Abstract 76: Mitochondrial filamentation
Authors: Gosalvez Mario 
Published: February 2011

Abstract
A number of molecular targets have been scrutinized in cancer research therapeutics. I will call briefly your attention to mitochondrial fillamentation. This is a molecular target important for the development of cancer reversal techniques and the possible use of cancer as a therapeutic agency when all the cancers will be cured for the duration of life.
My group signaled recently that when mitochondria are isolated with low thermal, mechanical, and chemical stress many of them appear with short micro filaments, of 25, 10, and 5 nanometers of diameter radially anchored in the mitochondrial external membrane, with or without cones of anchorage or veils of condensation.
These probably more physiological mitochondria are partially or almost totally uncoupled from oxidative phosphorylation (1). In darkness, anoxia and in the presence of bicarbonate, fillamented mitochondria are able to produce oxygen at a rate superior to their oxygen uptake. Oscillations of the oxygen concentration are observed when recording these mitochondrial preparations for long periods of time. Also these mitochondria seem to be able to compartmentalize some enzymes of the glycolytic pathway. Fillamented mitochondria are abundant at rest and in young animals. In cancer cells, senility, or high activity their number and extent of fillamentation decrease.
My agents for cancer reversal possibly increase mitochondrial fillamentation, while some chemical carcinogens decrease it, even at doses lower than those needed for their mutagenic effects. This is inferred from their effects on oxygen production by fillamented mitochondria (1, 2).
These novel aspects of mitochondria, to which I call your attention, deserve further investigation by the cancer and mitochondria research community (1, 2, 3)
(1) M Gosálvez Gosálvez. Producción de Oxígeno por Mitocondrias Filamentadas. Importancia para el Cáncer y la Neurodegeración. Anales de la Real Nacional Academia de Medicina, CXV, 3°, 747-756, 1998. Madrid. Spain
(2) M Gosálvez Gosálvez. Reversión del Cáncer y Filamentación Mitocondrial. Anales de la Real Nacional Academia de Medicina. CXVII, 4°, 825-834, 2000, Madrid. Spain.
(3) Mario Gosálvez y Gosálvez. “The Zipper Mechanism”. Madrid. 1982.
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 76.
Abstract 964: Chlormethiazole, an inhibitor of CYP2E1, prevented chemical carcinogen-initiated and alcohol-promoted hepatic carcinongenesis in rats.
Authors: Ye Qinyuan , Chavez Pollyanna R.G. , Lian Fuzhi , Wang Yan , Hu Kang-Quan , Ling Wenhua , Seitz Helmut K. , Wang Xiang-Dong 
Published: February 2011

Abstract
Chronic and excessive alcohol ingestion, a known risk factor of liver cancer, has been shown to upregulate hepatic cytochrome P450 2E1 (CYP2E1), which is associated with the production of reactive oxygen species and carcinogenic acetaldehyde, the activation of procarcinogens as well as the enhanced catabolism of retinoid. Further, treatment with the CYP2E1 inhibitors, including chlormethiazole (CMZ), have been shown to protect against alcohol-induced liver injury. In order to determine whether treatment with CYP2E1 inhibitor protects against diethylnitrosamine (DEN)-initiated, alcohol-promoted carcinogenesis in the liver, we fed rats (n=6) with either an ethanol liquid diet (Lieber-DeCarli diet) or a non-ethanol liquid diet with isocaloric maltodextrin, with or without CMZ (100 mg/kg BW), for a short-term (1 month) and a long-term (10 months). DEN was given as an initiator for hepatic carcinogenesis by i.p. injection of 20 mg DEN/kg BW. Hepatocarcinogenesis was assessed by examining the placental glutathione-s-transferase (p-GST) immunostaining of altered hepatic foci (AHF) and hepatic tumors lesions. Hepatocyte proliferation was assessed by immunohistochemistry for proliferating cellular nuclear antigen and Ki67, as well as cyclin D1. Hepatic expression of TNF-α and activation of NF-κB and CYP2E1 were assessed by either RT-PCR or Western blotting analysis. Hepatic retinol and retinoic acid were analyzed by reverse-phase HPLC. Results showed that CMZ treatment significantly inhibited ethanol-induced AHF formation, CYP2E1 expression and activity, TNF-α mRNA expression, NF-κB activation and hepatocyte proliferation after a 1-month period. After 10-months of treatment, hepatic nodular regenerative hyperplasia, and hepatocellular adenoma and carcinoma were detected in the ethanol-fed rats, but not in the rest of rat groups with the same dose of DEN treatment, including non-ethanol fed rats and ethanol-fed rats with CMZ treatment. In addition, the CMZ treatment prevented alcohol-reduced retinol and retinoic acid in the livers of rats after 1- and 10-months of treatment. These data demonstrate that CYP2E1 inhibitor can counter the tumor-promoting action of ethanol by restoring normal hepatic levels of retinoic acid. In considering the efficacy and complex biological functions of retinoids in human cancer prevention, intervention using CYP2E1 inhibitors that target alcohol-induced CYP2E1, could provide complementary or synergistic protective effects against alcohol-related cancer risk.
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 964.
Abstract 978: Secondhand tobacco smoke in bars and restaurants in Guatemala: Before and after indoor smoking ban evaluation
Authors: Arvizu Mariel , Hernandez Juan Carlos , Barnoya Joaquin , Navas-Acien Ana 
Published: February 2011

Abstract
Since February 2009 Guatemala has implemented a smoke-free law that includes bars and restaurants. In this study, we sought to assess air nicotine levels in bars and restaurants 6 months after the implementation of the law (post-law) and to compare them with levels found in 2007 (pre-law). Exposure was estimated by passive sampling of vapor-phase nicotine using a filter badge. Filters were placed for 7 working days in 10 bars and 11 restaurants randomly selected in Guatemala City. In total, 50 monitors were placed (for quality control, 10% were duplicate and blank). Filters were checked once to verify the correct placement, count the number of persons and smokers if there were any. Nicotine was measured by gas-chromatography and the time weighted average concentration in µg/m3 was estimated. Median (interquantile range, IQR) air nicotine levels are presented and compared using Mann-Whitney rank test. In addition, 32 employees answered a survey about air quality and opinions about secondhand smoke. The survey results were also compared with pre-law survey results using a chi-square statistic. Before the law, detectable levels of nicotine were found in all bars and restaurants. Median nicotine levels were 4.57 (IQR 1.71-6.44) μg/m3 in bars and 0.58 (IQR 0.43-0.7) μg/m3 in restaurants. After the law, nicotine was detected in all bars and most (76%) restaurants. Median nicotine levels were 0.59 (IQR 0.17-0.80) μg/m3 in bars and 0.06 (IQR 0.01-0.09) μg/m3 in restaurants. These levels were significantly lower compared to those found before the law (p=0.003 and p=0.05; respectively). The nicotine reduction was similar in bars (87%) and restaurants (89%). Employees’ support for a smoke-free workplace rose significantly after the law was implemented (from 32% to 81%, p&lt;0.001). In conclusion, six months after the law went into effect, nicotine levels were significantly decreased in bars and restaurants and workers support for the law was high. Given that no other tobacco control law has been implemented in Guatemala, our results can be attributed to the smoke-free law. However, in order to be effective in reducing lung cancer incidence a smoke-free law should be strictly enforced. Our data should prove useful to exert pressure upon the Guatemalan government to more strictly enforce the law.
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 978.
Abstract 989: Reliability of a modified version of the Health Belief Model Scale-C for cervical cancer screening behaviors in lesbians
Authors: Tracy Kathleen , Dawson Rebecca S. , Tang Ying 
Published: February 2011

Abstract
Background: Cervical cancer incidence and mortality rates have decreased significantly during the last 60 years as a result of wide spread cervical cancer screening, yet certain subgroups of women continue to be at elevated risk due to lack of screening; lesbians are one such group. To better understand the association between health beliefs and cervical cancer screening behaviors in lesbians, we adapted the Champion Health Belief Model Scale from its original focus on breast cancer screening to a focus on cervical cancer and screening via Papanicolaou (Pap) test.
Purpose: The purpose of this pilot study was to assess the reliability and validity of our adapted version of the Health Belief Model Scale (HBMS) using an internet-based survey. Analysis included descriptive statistics of demographic data and internal consistency reliability estimates using Cronbach's alpha coefficients.
Methods: HBMS items for perceived susceptibility, perceived seriousness, perceived benefits, and perceived barriers subscales were modified from their original form to reference cervical cancer (rather than breast cancer) and Pap testing (rather than mammography). In addition, we constructed a knowledge scale based on a series of true/false questions regarding risk factors for cervical cancer and recommendations for cervical cancer screening.
Results: Complete data were available for 218 self-identified lesbian volunteers ranging in age from 18 to 68. Cronbach's internal consistency reliability coefficients were calculated for each subscale from our adaptation of the HBMS. Coefficients ranged from .75 to .91. Coefficients were similar to those reported previously.
Conclusion: Our adaptation of the HMBS for assessing health beliefs regarding cervical cancer screening was determined to be reliable and valid. The HBMS-C has the potential to be a useful tool in ongoing studies of the associations between health beliefs and cervical cancer screening behaviors.Reliability coefficients for HBMS-CSubscaleAlphaSusceptibility.91Seriousness.88Benefits.79Barriers.81Knowledge.75
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 989.