bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1822: Decision making and cancer clinical trial participation among African Americans
Authors: Nguyen Van T. , Wujcik Debra , Wolff Steven 
Published: June 2012

Abstract
INTRODUCTION: Although the disparity in clinical trial participation is well documented, the main reason why African Americans and the medically underserved do not participate in cancer clinical trials (CCT) has not been agreed upon. It is apparent that new policies and initiatives are required to ensure minority access to CCT and applicability of subsequent results from CCT.
METHODS: In-depth interviews were conducted to explore issues of fear and mistrust in CCT participation. Participants were asked questions regarding their perceptions of cancer, research, cancer clinical trials; attitudes toward participation in clinical trials; and the effect of trust in decision-making. Afterward, participants completed a survey, a modification of the Wake Forest Physician Trust Scale to assess trust in medical research study. One field expert and one medical student independently reviewed the tapes, transcripts, and surveys from the interviews for themes, trends, and congruence. Saturation was achieved at eight interviews.
RESULTS: Eight African Americans, 7 female and 1 male, participated. Three themes emerged related to decision making and CCT participation: 1) Motivation to participate comes from believing what they were doing would help those coming after them; 2) Trusted sources for CCT information include the research team, primary care providers, and trusted individuals; 3) Final decision making, based on all of the advice and information given, would be theirs to make.
CONCLUSION: Potential African American participants in CCT have many trusted sources to turn to and receive advice regarding their decision to participate or not. However, they will listen to the CCT research team and their primary care providers, especially if what they perceive is a trusting and open relationship is established. Given that these potential participants are the ones who make the final decisions, just as much of an effort should be placed on making sure that they have all of the information that they want, whether these conversations are with researchers or primary care providers who know about CCT. An emphasis on how potential African American participants can contribute to CCT and positively affect the lives of other African Americans with the same diagnoses should also be made. Results from this study and a previous study will form the basis for an intervention study.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1822. doi:10.1158/1538-7445.AM2011-1822
Abstract 1825: Sustained aerobic exercise alone does not counteract the tumor-promoting effects of a westernized diet on prostate cancer progression in vivo
Authors: Vandersluis Avi D. , Venier Natalie A. , Kiss Alex , Colquhoun Alexandra J. , Fleshner Neil E. , Klotz Laurence H. , Venkateswaran Vasundara 
Published: June 2012

Abstract
Introduction: The influence of lifestyle behaviors on prostate cancer (PCa) is well established. Our lab has previously reported that diets high in both fat and carbohydrates – the “Westernized” diet – promote PCa tumor growth in vivo. Numerous studies have also found an inverse relationship between exercise and PCa progression. However, the exact relationships between diet, exercise and PCa, as well as their underlying mechanisms, are unclear. Herein we aim to investigate the effect of sustained aerobic exercise on PCa tumor growth in animals fed a “Westernized” diet or a normal diet.
Methods: Athymic nude mice (n=46) were inoculated subcutaneously with LNCaP cells. Mice were fed ad libitum with either a high-fat/high-carbohydrate diet (HFHC) or a standard normal diet (Normal), and randomized into exercising (Ex) and non-exercising groups (No-Ex). Exercise was undertaken 3 days per week (3 × 15 mins; 2-min breaks between cycles; 2.0-7.0 m/min) for 8 weeks, using a forced exercise wheel. Body weights, tumor volumes, and food consumption were recorded tri-weekly. Comparisons between groups over time were performed using RANOVA Type 3 Tests of Fixed Effects.
Results: There were no significant differences in body weight between the groups over time. The HFHC-Ex group (n=10) had the highest rate of tumor growth compared to all other groups (p&lt;=0.0007). No significant differences were observed between the rate of tumor growth of the HFHC-No Ex group (n=11) and the Normal-No Ex group (n=12) or between the Normal-No Ex group and the Normal-Ex group (n=10). However, the rate of tumor growth of the Normal-Ex group was reduced compared to the HFHC-No Ex group (p&lt;=0.0008). Food consumption analysis revealed significant differences (p&lt;=0.012) in energy consumption (kcal) between each of the groups over time. Mice in HFHC-Ex group consumed the most energy compared to all other groups followed by HFHC-No Ex&gt;Normal-Ex&gt;Normal-No Ex groups.
Conclusions: The results indicate that exercise stimulated an increase in food consumption. In mice fed a tumor-promoting “Westernized diet,” this enhanced the rate of tumor growth. However, in mice placed on a normal diet, this increase in energy consumption did not correspond with increased tumor growth over time, emphasizing the importance of both exercise and healthy diet in the progression of PCa. Further studies to examine the relationship between diet and exercise with respect to PCa progression are currently underway.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1825. doi:10.1158/1538-7445.AM2011-1825
Abstract 1839: Improving colorectal cancer screening rates in minority and underserved populations: A tailored community approach
Authors: Darwish-Yassine May 
Published: June 2012

Abstract
Disparities in colorectal cancer screening rates continue to be observed across population groups in Michigan. In 2008, screening rates were below the general population for each of the minority population groups except Asian Americans (63.7% + 15.0%); rates were exceptionally low for Hispanics (46.5% + 15.4%) and Arab Americans (45.6% + 21.9%).
Four special projects were conducted that focused on increasing awareness of colorectal cancer (CRC) screening in Michigan's underserved populations. We present a summary of each project methodology and highlight the outcomes of each intervention type as it relates to awareness of colorectal cancer risk and behavioral changes within the selected populations.
Generally, community-wide interventions, particularly those using media, seek to increase preventive behaviors within a community by targeting a large part of the population in a defined area. The evaluations presented in this report were designed to include all community members 50 years of age or older living in the campaign geographical area and did not necessarily target individuals who were touched by every type of intervention offered. This was primarily due to the timeline and resources surrounding the interventions. However, our evaluation results show signs of improvement in CRC awareness within the study communities, and suggest that tailored and culturally-appropriate approaches are effective in health promotion at the community level.
Reducing disparities in cancer outcomes undoubtedly requires repeated and sustained efforts for achieving optimal outcomes.

Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1839. doi:10.1158/1538-7445.AM2011-1839
Abstract 1848: Decursin derivatives with increased in vivo stability suppress androgen receptor signaling and prostate cancer cell growth: Structure-bioactivity relationship
Authors: Zhang Yong , Shaik Ahmad , Chai Yubo , Li Li , Zhang Jinhui , Zhang Wei , Xing Chengguo , Kim Sung-Hoon , Lü Junxuan , Jiang Cheng 
Published: June 2012

Abstract
Androgen receptor (AR) signaling is crucial for the genesis and progression of prostate cancer (PCa). Targeting AR signaling remains an attractive approach for PCa chemoprevention and therapy. Our previous studies suggest that decursin, which is isolated from the Korean medicinal herb Angelica gigas Nakai, has novel anti-androgen attributes in comparison to that of AR antagonist drug bicalutamide (Casodex) and stronger anti-proliferative and pro-apoptotic activities in cell culture models. However, decursin quickly de-esterifies to decursinol in vivo, which lacks the anti-androgen and anti-proliferative activities. We report here that a novel prototype derivative (decursinol thiocarbamate, DTC) shows in vivo stability in single dose pharmacokinetic studies, with no detection of decursinol. Molecular docking with the wild type AR ligand binding domain (LBD) suggested that its AR-binding energy is inferior to DHT, but higher than decursin. Mechanistically DTC retains all the desirable properties of decursin, including inhibiting AR nuclear translocation, decreasing cellular AR protein abundance by promoting its 26S proteasomal-mediated degradation and lacking agonist activity. Dose-response comparisons showed that DTC was half as potent as decursin to inhibit AR signaling and androgen sensitive LNCaP PCa cell growth. In animal studies with mice, daily i.p. injection of DTC (2 mg per mouse) decreased AR transcriptional targets such as probasin and NKX3.1 in the mouse prostates. Chemical deposits on the surface of liver and other organs were observed suggesting poor solubility. Additional derivatives aimed to improved solubility had been synthesized and are being investigated for structure-activity relationship. Overall, the data suggest that DTC is a prototype stable decursin derivative retaining the novel AR antagonist activity for PCa chemoprevention or treatment.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1848. doi:10.1158/1538-7445.AM2011-1848
Abstract 1849: Chemopreventive efficacy of naproxen, sulindac, and their nitric oxide-derivatives in the hydroxylbutyl(butyl)nitrosamine induced model of urinary bladder cancer
Authors: Grubbs Clinton J. , Boring Daniel , Steele Vernon E. , Verney Zoe M. , Lu Yian , You Ming , Lubet Ronald A. 
Published: June 2012

Abstract
A variety of studies were performed with naproxen (a standard NSAID with a good cardiovascular profile), sulindac, and their nitric oxide (NO)-derivatives. In Fisher 344 rats, OH-BBN (2x/week for 8 weeks by gavage) induced invasive urinary bladder cancers. When treatment was initiated one week following the final dose of OH-BBN, both naproxen (400 ppm) and sulindac (400 ppm) were highly effective preventive agents at these human equivalent doses. The NO-derivatives of each compound (NO-naproxen, 550 ppm and NO-sulindac, 520 ppm) were similarly effective. When the dose of naproxen was decreased from 400 ppm to 75 ppm a strong preventive effect was still observed. This activity was observed even when treatment with naproxen was started 12 weeks after the last OH-BBN treatment; microcarcinomas already existed at this time. In an attempt to make a more direct comparison between the human and rat data, animals were treated with 40 mg/kg BW/day of naproxen by gavage. Similar to the dietary dose of 400 ppm, the agent was highly effective; however, gavaging the rats permitted more direct comparison of the pharmacokinetics observed in the rat with known results in humans. In contrast to the naproxen data, reducing the dose of sulindac from 400 to 150 ppm, a dose comparable to the human dose employed by Meyskens, et al. (Cancer Prevention Res. 1:32-38, 2008), resulted in only limited activity. Finally, the effects of naproxen and NO-naproxen on modulation of gene expression in the livers of treated rats were determined. Limited, but similar, gene expression changes induced by both agents were observed. Interestingly, neither agent induced the antioxidant response element genes [e.g., GST Pi, quinone oxidoreductase, aldo keto reductase A37 (aflatoxicol)] that one might have expected to be highly induced by free NO. Supported by the NCI contract number HHSN261200433001C.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1849. doi:10.1158/1538-7445.AM2011-1849
Abstract 2151: Characterization of a novel anti-apoptotic signaling pathway downstream of FGFR4 in rhabdomyosarcoma
Authors: Wachtel Marco , Schaefer Beat 
Published: June 2012

Abstract
FGFR4 is highly overexpressed in Rhabdomyosarcoma tumors and contains activating mutations in eight percent of the cases. These data strongly suggest that FGFR4 plays an important role in the tumorigenesis of this cancer type. However, the molecular mechanisms behind the benefit of active FGFR4 for Rhabdomyosarcoma cells are largely unknown.
Here, we describe a survival pathway activated by FGFR4 in Rhabdomyosarcoma cells. Active FGFR4 is able to block apoptosis induced by inhibition of other central signaling pathways with small molecule inhibitors, such as the IGF1R pathway with AEW541 and PI3K-controlled pathways with BEZ235. Using different biochemical and genetic approaches, we could locate the apoptotic block upstream of the pro-apoptotic BH3-only proteins bmf and bim. To further elucidate the mechanism of this prosurvival signaling, we then performed proteomic studies to define the complete interactome of FGFR4 in Rhabdomyosarcoma cells. These analyses revealed a strong interaction of FGFR4 with PLCγ, linking FGFR signaling to PKCs. Indeed, activation of PKCs strongly inhibits AEW541/BEZ253-induced apoptosis, suggesting that PKCs are central for FGFR4-activated survival signaling. In contrast, the classical survival pathways via Akt and Erk are not or only marginally involved in the rescue mechanism.
Treatment approaches targeting the IGF1R/PI3K axis in Rhabdomyosarcoma are under intensive investigation. Our data suggest that rescue mechanisms via FGFR4 and PKCs should be taken into account when applying such treatment strategies. A combination of IGF1R- and FGFR4/PKC-inhibitors therefore might be superior compared to single treatments.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2151. doi:10.1158/1538-7445.AM2011-2151
Abstract 2160: Critical BRCA1 role as a transcriptional regulator in prostate cancer DNA damage response
Authors: De Luca Paola , Moiola Cristian , Zalazar Florencia , Gueron Geraldine , Cotignola Javier , Vazquez Elba , Gardner Kevin , De Siervi Adriana 
Published: June 2012

Abstract
Loss or mutation of the BRCA1 gene is associated with nearly 5% of all breast cancers. Since many cases of sporadic cancers that also show decreased BRCA1 expression are often associated with higher grade tumors, significant interest has developed in defining mechanisms of BRCA1 regulation at the level of transcription. BRCA1 plays numerous roles in regulating genome integrity. It interacts with crucial proteins and is considered a gene-specific transcriptional co-regulator; however, BRCA1's role in the transcriptional response to DNA damage is poorly understood. In this study we show that BRCA1 plays a central role in the transcriptional response to genotoxic stress in prostate cancer. Using BRCA1-depleted or BRCA1-overexpressing human prostate cancer cell lines, we found that BRCA1 mediates apoptosis, cell cycle arrest and decreased viability in response to doxorubicin treatment. Furthermore, xenograft studies using human prostate carcinoma PC3 cells demonstrate that BRCA1 depletion results in increased tumor growth. In addition, genome-wide screens using the combined application of chromatin immunoprecipitation and microarray technology (ChIP-chip) reveals that BRCA1 is highly enriched at the promoters of greater than 1300 genes. Gene Ontology (GO) analysis of this “BRCA1 ChIP signature” reveals a significant enrichment in genes that function in cell cycle regulation and the response to DNA damage including “M phase”’ and “Mitotic checkpoint” terms, suggesting a specific role for BRCA1 in controlling mitotic events following genotoxic stress. We have validated multiple members of this BRCA1 ChIP signature including: BLM, FEN1, DDB2, H3F3B, BRCA2, CCNB2, MAD2L1, GADD153 and ATM. Further focused analysis reveals that BRCA1 occupancy at the ATM promoter increases its transcription and H2AX phosphorylation. Notably, following doxorubicin exposure, BRCA1 is released from the ATM promoter and redistributed to other genes like GADD153 where it induces expression, apoptosis and cell cycle arrest. RNAi depletion of GADD153 blocks BRCA1-dependent apoptosis and cell cycle arrest in response to doxorubicin, suggesting that GADD153 is required for BRCA1 mediated drug sensitivity. These findings define a novel mechanism through which BRCA1 influences cell fate decisions in response to genotoxic insult through direct transcriptional control of genes, including GADD153 and ATM. Thus, tumors with absent or reduced expression of BRCA1 are likely to show a marked resistance to chemotherapy for prostate cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2160. doi:10.1158/1538-7445.AM2011-2160
Abstract 2175: Role of p38 MAPK in regulating Cripto-1 expression and signaling in human embryonal carcinoma cells
Authors: Held Natalie , Rangel Cristina , Castro Nadia , Gonzales Monica , Nagaoka Tadahiro , Karasawa Hideaki , Salomon David S. , Bianco Caterina 
Published: June 2012

Abstract
Cripto-1 (CR-1) is a cell-membrane protein that is overexpressed in several different types of human carcinomas. We have previously shown that TGFβ1 and Activins can enhance CR-1 expression while BMP2 and BMP4 can inhibit CR-1 expression in NTERA-2 embryonal carcinoma cells and in LS174T colon cancer cells. Nevertheless, there is still a very incomplete picture as to the nature of the epigenetic, transcriptional and hormonal factors that might be involved in regulating Cripto-1 expression under different conditions. Previous studies have demonstrated that activation of p38 MAPK can regulate expression of Nodal, a Cripto-1 ligand, during early embryogenesis and is necessary for the specification of mouse cardiomyocytes from embryonic stem cells, which depends upon a Nodal-dependent signaling pathway involving Cripto-1. We therefore evaluated if activation of p38 MAPK might be involved in regulating Cripto-1 expression and Cripto-1 dependent signaling in human embryonal carcinoma cells. In undifferentiated NTERA-2 and NCCIT embryonal carcinoma cells two p38 MAPK inhibitors PD169316 and SB20358 completely inhibited the basal levels of CR-1 mRNA and protein expression in both cell lines. A JNK inhibitor SP600125 had only minor effects on CR-1 mRNA and protein expression whereas the p44/42 MAPK inhibitor U0126 showed no effect. Transfection of specific siRNA against p38 MAPK was also able to significantly interfere with CR-1 mRNA and protein expression in NTERA2 and NCCIT embryonal carcinoma cells. In contrast, knockdown of p44/42 MAPK or JNK with specific siRNA did not significantly affect CR-1 expression in embryonal carcinoma cells. We therefore evaluated whether CR-1 might trigger activation of p38 MAPK in embryonal carcinoma cells and in mouse mammary epithelial cells. Recombinant CR-1 protein was found to stimulate in a delayed fashion (after 50-60 minutes) p38 MAPK phosphorylation in mouse mammary epithelial cells and in embryonal carcinoma cells suggesting a feed-forward activation loop. Whether p38 MAPK functions in undifferentiated embryonal carcinoma cells to regulate CR-1 expression and/or signaling involving regulation of invasion, migration and epithelial to mesenchymal transition in human embryonal carcinoma cells and in mouse mammary epithelial cells is under investigation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2175. doi:10.1158/1538-7445.AM2011-2175
Abstract 2182: IGFBP-6 in nasopharyngeal carcinoma is a candidate tumor suppressor gene by regulating the expression of EGR-1
Authors: Kuo Yuan-Sung , Lin Chin-Tarng , Wu Han-Chung 
Published: June 2012

Abstract
Nasopharyngeal carcinoma (NPC) is one of the common cancers in South-Eastern Asia, particularly southern China, Singapore and Taiwan. It has been proposed to be closely associated with Epstein-Barr virus (EBV), but other researches also show that EBV can enhance the NPC proliferation but not related with initiation or promotion of NPC carcinogenesis. The aim of this study was to identify the pivotal genes that may be altered during NPC progression. Using cDNA microarray analysis, we compared the expression of 18 genes between NPC and normal nasomucosal cells. Q-RT-PCR analysis found the expression of IBFBP-6 in NPC cell lines and immunolocalization of IGFBP-6 in NPC cells and biopsy specimens to be very weak. To explore the effects of IGFBP-6 on NPC tumor growth, we constructed inducible plasmids containing full-length IGFBP-6 cDNA (pBIG2i-IGFBP-6) and established pBIG2i-IGFBP-6-transfected NPC stable cell lines (NPC-TW01-pBIG2i-IGFBP-6). We then performed in vitro and in vivo functional analysis of the IGFBP-6 in these cell lines. Over-expression of IGFBP-6 significantly suppressed the proliferation, invasion and metastatic activity of NPC cells and increased their apoptosis. We found the EGR-1, caspase-1 and TSP-1 genes to be markedly up-regulated when NPC-TW01-pBIG2i-IGFBP-6 was treated with doxycycline. Knocking down EGR-1 with EGR-1 siRNA resulted in a decrease in expression of caspase-1, TSP-1 and EGR-1 but not the expression of IGFBP-6. However, in knockdown cells the unchanged expression of IGFBP-6 did not inhibit the migration of NPC cells. Chromatin immunoprecipitation and luciferase reporter assay experiments showed that IGFBP-6 bound the EGR-1 promoter regions and activated EGR-1 promoter. We conclude that IGFBP-6 can regulate the progression of NPC by regulating the expression of EGR-1. These results suggest that IGFBP-6 could be used as a new target for NPC therapy.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 2182. doi:10.1158/1538-7445.AM2011-2182