bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1966: Plasmonic gold nanostars: A potential agent for molecular imaging and cancer therapy
Authors: Yuan Hsiangkuo , Khoury Christopher , Wilson Christy , Grant Gerald , Vo-Dinh Tuan 
Published: August 2012

Abstract
Gold nanoparticles offer great potential for bioapplication due to their biocompatibility, chemical stability, and plasmon tunability. Due to the increased demand in custom-designed bioapplication, tailoring nanoparticle's plasmon for a specific application remains an active area of research. Plasmonic gold nanostars, with their sharp tips and small cores, yield unique optical properties in the near infrared region favorable for biological applications. We present a high-yield biocompatible synthesis of gold nanostars, whose geometry is adjustable such that the plasmon band can be tuned into the near-infrared “tissue diagnostic window”. Nanostars offer several interesting plasmon properties including intense surface-enhanced Raman scattering (SERS) for ultrasensitive detection, strong two-photon photoluminescence (TPL) for real-time particle tracking, and efficient photothermal transduction for hyperthermic therapy. Here, we demonstrate nanostars tracking and photothermal ablation both in vitro and in vivo. Using SKBR3 breast cancer cells incubated with bare nanostars, photothermal ablation was observed within 5 minutes of irradiation (980 nm CW laser, 15 W/cm2). On a mouse preinfused systemically with PEGylated nanostars for 2 days, extravasation of nanostars was observed and localized photothermal ablation was demonstrated on a dorsal window chamber within 10 minutes of irradiation (785 nm CW laser, 1.1 W/cm2). These preliminary results have illustrated the theranostic potential of gold nanostars for the use in molecular imaging and cancer therapy.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1966. doi:1538-7445.AM2012-1966
Abstract 197: Epigenetic regulation of miRNA expression in osteosarcoma
Authors: Skarn Magne , Namlos Heidi M. , Ahmed Deeqa , Lind Guro E. , Meza-Zepeda Leonardo A. , Myklebost Ola 
Published: August 2012

Abstract
Epigenetic and genetic alterations of microRNAs (miRNAs) are frequently seen in cancer, and are responsible for the deregulation of differentiation and proliferation programs. The levels of transcription of miRNAs have been directly linked to epigenetic silencing, i.e. hypermethylation of CpG islands in tumors. Osteosarcoma is the most common primary malignant bone tumor and shows complex genomic aberrations. Using Illumina's Infinium technology we have profiled global promoter methylation of the EuroBoNeT osteosarcoma cell line panel (eurobonet.eu), in addition to a small panel of normal samples (osteoblast primary cultures and normal bone). A list of miRNAs that could be associated to a promoter CpG island was generated by identifying miRNAs that are encoded within transcripts of protein-coding host genes, or within 10 kb from a CpG island. Using an integrative approach, we have analyzed miRNA expression patterns together with DNA methylation data. Interestingly, hypermethylation of the upstream promoter seems to strongly suppress miRNA expression, and a high inverse correlation was observed between the degree of DNA methylation and expression of 17 miRNAs. The identified miRNAs were associated with hypermethylation in a high proportion of the osteosarcoma cell lines and hypomethylation in normal samples, suggesting that their transcription is regulated by promoter methylation, and that their silencing may play a role in osteosarcoma biology. To study this further, a subset of the cell lines was treated with a DNA demethylation agent. The relative expression levels of 8 miRNAs were found to increase upon treatment, as determined by quantitative RT-PCR. Thus, the transcription of these miRNAs seems to be regulated by epigenetic mechanisms. The methylation status of CpG islands associated with the most interesting miRNAs was then analyzed in more detail using methylation-specific PCR and direct bisulphite sequencing. We are currently expanding these investigations to a large tumor set where we will use quantitative methylation-specific PCR as a tool to determine the methylation status. Based on our findings, methylation of CpG islands seems to play a crucial role in controlling miRNA expression in osteosarcomas. This reveals new possibilities for activation of tumor-suppressing miRNAs by epigenetic treatment of osteosarcomas.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 197. doi:1538-7445.AM2012-197
Abstract 198: Identification of differentially expressed microRNAs and other non-coding RNAs in ependymomas
Authors: Costa Fabricio F. , Bischof Jared M. , Vanin Elio F. , Lulla Rishi R. , Sredni Simone T. , Rajaram Veena , Wang Min , Renaud Gabriel , Passetti Fabio , Tomita Tadanori , Goldman Stewart , Bonaldo Maria F. , Soares Marcelo B. 
Published: August 2012

Abstract
Ependymomas are tumors that present great challenges in treatment despite the advances in neurosurgical techniques and adjuvant therapy. In order to identify possible molecular markers that could improve clinical management and better treatment, we have profiled ependymomas for the expression of microRNAs (miRNAs) and other non-coding RNAs (ncRNAs). miRNAs are ncRNAs that can block mRNA translation and affect mRNA stability. Several lines of evidence have recently shown that up or down-regulation of miRNAs correlate with many human cancers indicating that they can function as classical tumor suppressors and/or oncogenes. In this study, we have evaluated with the use of TaqMan Low Density Arrays (TLDAs) and RNA-Seq the expression profiles of non-coding RNAs in ependymoma samples and normal brain tissue. We analyzed the miRNA expression profile of 34 ependymoma samples using paraffin tissue compared to 6 normal brain control samples enriched for ependymal cells. miRNA expression profiles were correlated with clinico-pathological parameters, morphological features and the location of the tumor in the brain. We have been able to classify the tumors based on the miRNA expression profile and to identify miRNAs that are differentilly expressed in ependymomas when compared to normal samples. For example, miR-135a, miR-594 and miR-34a were identified as over-expressed and miR-485-5p and miR-383 as down-regulated (p&lt;0.01; FDR&lt;0.05). We have also identified and are currently confirming some of the targets for these miRNAs. Finally, we have utilized high-throughput Whole Transcriptome (WT) analyses with the SOLiD system to identify other differentially expressed miRNAs and long ncRNAs in ependymomas. The transcriptome of 3 ependymomas and 2 controls were sequenced, thus generating approximately 5 Gb of data. In conclusion, using different strategies, we have been able to identify ncRNAs that are differentially expressed in ependymomas compared to normal ependymal tissue, some of which are of clinical importance. Financial Support: Children's Memorial Research Center, The Falk Brain Tumor Foundation and The Maeve McNicholas Memorial Foundation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 198. doi:1538-7445.AM2012-198
Abstract 1989: The effect of resveratrol combined with DFMO or DenSpm on MCF-7 breast cancer cells and MCF-10a non-cancerous cells
Authors: Benassi Isabella , Smith Riley M. , White KateLyn , Dennis Shanna , Nelson Niki , Feirer Russ 
Published: August 2012

Abstract
Resveratrol, (3,5,49-trihydroxy-trans-stilbene), was first reported to act as a chemo-preventative anticancer compound in mice by Jang et al. in 1997. Resveratrol has been shown to induce apoptosis and reduce both cell viability and mitotic index in many cancer cell lines, including MCF-7. The current work extends these studies to determine its effects on glucose utilization and enzymes involved in polyamine metabolism. Glucose uptake was found to be reduced in MCF-7 cells treated with resveratrol. Work in other labs has shown resveratrol to sensitize cancer cells to other chemotherapeutic compounds. In the present study, the effects of combinations of resveratrol with compounds that affect polyamine metabolism, DFMO (difluoromethylornithine) and DenSpm (N1, N11-diethylnorspermine), were tested. Both DFMO and DenSpm were found to reduce cell proliferation and mitotic index in MCF-7 cell lines and more importantly, a synergistic effect was observed when these compounds were used in combination with resveratrol. In this investigation resveratrol was also found to induce apoptosis and reduce cell viability, mitotic index, and glucose uptake in non-cancerous, transformed mammary epithelial cells (MCF-10a). Similar findings have been reported with other non-cancerous cells including intestinal smooth muscle cells (Garcia et al., 2011). The combination of resveratrol and DFMO also reduced glucose uptake, proliferation, and mitotic index in this non-cancerous cell line (MCF-10a). These compounds were found to affect the expression of ODC (ornithine decarboxylase) and SSAT (spermidine/spermine acetyl transferase), enzymes involved in polyamine metabolism, and other proteins involved in cell cycle regulation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1989. doi:1538-7445.AM2012-1989
Abstract 1993: Fishing for artemisinin-interacting proteins from human nasopharyngeal cancer cells
Authors: Eichhorn Tolga , Schloissnig Siegfried , Lehmann Wolf-Dieter , Mertens Rolf , Krauth-Siegel Luise , Efferth Thomas 
Published: August 2012

Abstract
Determining cellular target molecules of drugs by chemical proteomic techniques is complex and tedious. Most approaches rely on activity-based probe profiling and compound-centric chemical proteomics. The antimalarial artemisinin also exerts profound anti-cancer activity, but the mechanisms of action are incompletely understood. In the present study, we have identified artemisinin-interacting target proteins from human nasopharyngeal carcinoma cell line CNE1. Thereby, our approach overcomes usual problems in traditional fishing procedures, because the drug was attached to a polystyrene surface without further chemical modification. Using mass spectrometry we have identified 20 proteins which effect cell cycle arrest, apoptosis, inhibition of angiogenesis, disruption of cell migration, and modulation of nuclear receptor responsiveness. One protein out of the twenty was further investigated in vitro for direct ligand binding. Furthermore, a blind-docking based approach confirmed experimentally identified proteins and suggested further interacting proteins. Theoretically predicted interaction partners may serve as a starting point to complete the whole set of proteins binding artemisinin. In our investigations, we have comprised artemisinins role in cancer treatment in a greater shape through a systematic biological strategy and thus, are able to show novel insights into its mode of action.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1993. doi:1538-7445.AM2012-1993
Abstract 1995: Huachansu inhibits proliferation of non-hodgkin lymphoma cells by induction of apoptosis
Authors: Efuet Ekem T. , Cohen Lorenzo , Yang Peiying 
Published: August 2012

Abstract
Huachansu, a hot water extract of venom or the skin glands of Bufo gargarizans or B. melanostictus, has been used in the treatment of various cancers in Asia and in China. Despite extensive use in the treatment of various solid tumors such as pancreatic, hepatocellular, non-small-cell lung carcinomas, its effect on the growth of malignancies of hematopoietic and non-hematopoietic origin, particularly lymphomas, is limited. Here we investigated the anti-proliferative effect and molecular mechanisms of Huachansu in non-Hodgkin lymphoma Raji, Ramos, BJAB and Namalwa cells. These cells were treated with Huachansu (0 to 50 αl/ml) for 72 hrs and cell proliferation was assessed by WST-1 assay. The molecular mechanism associated with Huachansu's anti-proliferative effect was examined by western blotting, cell cycle and apoptosis as determined by PI and Annexin V staining. Huachansu inhibited proliferation of all four lymphoma cell lines tested with IC50 ranging from 6.7 αl/ml to 17.1 αl/ml. At a low concentration of 25 αl/ml, Huachansu triggered a sub G1 arrest in both Raji and Ramos cells, indicative of cell death while also causing a marked increase of early to late apoptotic cell death in both cell lines. Intriguingly, the expression of MCL-1 proteins was markedly reduced by Huachansu at 12.5 αl/ml in Raji cells, while completely blocked at 25 αl/ml in Ramos cells. At 50 αl/ml, Huachansu decreased total Akt more robustly in Ramos compared to Rajis cells, with no significant reduction in the levels of survivin. Huachansu (25 αl/ml) inhibited the expression of pRB proteins in Raji cells and substantially increased the levels of caspase-3 in Ramos (12.5 αl/ml) in a concentration dependent manner, indicative of apoptosis. Given that bufalin is one of the major bioactive components of Huachansu, we tested its effect on the proliferation of Ramos cells. Bufalin (125 ng/ml) indeed suppressed the proliferation of Ramos cells. The effect of both Huachansu and bufalin on transcriptome of Ramos cells is currently being investigated and will be reported. Collectively, our data suggest that Huachansu is effective in inducing cell death and apoptosis, in part, by upregulatiing caspase-3 activity and inhibiting the phosphorylation of RB protein in lymphomas. Considering that the concentration of Huachansu needed to inhibit cell proliferation by 50% was similar to the dose of Huachansu routinely used in the clinics in China, our preliminary data suggests that Huachansu has a great potential to be developed as an anticancer agent for non-Hodgkin lymphoma and warrant further investigation. This study is supported in part by Gabrielle's Angel Foundation.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 1995. doi:1538-7445.AM2012-1995
Abstract 2007: Differential roles of BCL-XL and BCL-2 in protecting mitochondria against oxidative stress in CML cells
Authors: Zhang Hui , Lu Weiqin , Liu Terrence , Chen Gang , Chen Zhao , Trachootham Dunyaporn , Arlinghaus Ralph B. , Huang Peng 
Published: August 2012

Abstract
Previous studies have identified that BCR-ABL elevates cellular reactive oxygen species (ROS) through mitochondria and NAD(P)H oxidase (NOX). However, it is still unknown how BCR-ABL over-expressed cells can maintain such altered redox status, while escaping from the persistent oxidative stress-induced cell damage or apoptosis. Therefore elucidation of the mechanisms by which CML cells cope with oxidative stress will provide important insights into the molecular events leading to leukemia development and drug resistance. The major goals of this study are to investigate the role of BCR-ABL-regulated downstream cell survival factors in providing an adaptive mechanism which allows CML cells to survive in the presence of cellular oxidative stress, and to evaluate the potential therapeutic implications. Several experimental models were used to test the cellular redox status and relative sensitivity of oxidative stress-induced cell death in our study, including BCR-ABL inducible cell lines, BCR-ABL stably transformed cell lines and BCR-ABL-expressing CML blast crisis cells with different BCL-XL/BCL-2 patterns. Additionally, we established an artificial CML cell model with heterogenic BCL-XL/BCL-2 expression to assess the correlation between cell survival factor genetic background and cell sensitivity to Imatinib and oxidative stress. In this study, BCL-XL has been identified as the major survival factors responsive to BCR-ABL-promoted cellular oxidative stress and plays a dominant role in regulating the threshold of oxidative stress-induced apoptosis. The cell survival factors BCL-XL and BCL-2 differentially protect mitochondrial integrity under oxidative stress. BCL-XL is an essential survival factor in maintaining viability of the cells with the excessive ROS while BCL-2 seems to play a relatively minor role. In addition, combination of redox-modulating reagent α-phenethyl isothiocyanate (PEITC) with BCL-XL/BCL2 inhibitor ABT737 or suppression of BCL-XL expression by BCR-ABL inhibitor Gleevec dramatically sensitizes CML cell to ROS stress-induced apoptosis. These data together suggest that elevation of BCL-XL is important for the development of CML, and that redox-directed therapy may merit further clinical investigations in CML treatment.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2007. doi:1538-7445.AM2012-2007
Abstract 2023: The role of RASSF1A in FasL expression and function
Authors: Perera Janaki , Burger Jordyn , Aznavoorian-Cheshire Sadie , Pratt Joanne C. 
Published: August 2012

Abstract
RASSF1A is a tumor suppressor protein that is epigenetically silenced in a variety of tumor cells, including those of lymphocytic origin. Several previous studies have identified a role for RASSF1A in death receptor-dependent apoptosis in abnormal cells of epithelial origin downstream of tumor necrosis factor receptor 1 (TNF-R1) engagement; however relatively little is known about a possible role for Rassf1A in lymphocytic cells. Interaction of Fas ligand (FasL) on activated T lymphocytes with the Fas receptor on other immune cells plays a major role in down-modulating immune responses through activation-induced cell death (AICD). Apoptosis of T cells that have undergone clonal expansion in response to antigenic stimulation through the TCR is a key regulatory feature of the adaptive immune response that prevents the accumulation of excessive lymphocytes once the antigen has been cleared. We have examined the effect of RASSF1A overexpression on FasL transcriptional activation and function in the Jurkat human T cell line. We have demonstrated that over-expression of RASSF1A induced a significant increase in FasL promoter (FasLp) activity. Similar-fold increases in transcriptional activity were observed when the distal NFAT binding site (3X NFAT plus minimal promoter) within FasLp was used in co-transfection reporter assays; however, other transcription reporters (AP1, NFkB) were unaffected. Experiments with mutant Jurkat cell lines indicate that early signaling mediators, including tyrosine kinases and PLCγ, are critical in the RASSF1A-induced enhancement of FasL production. Poly (ADP-ribose) polymerase (PARP) cleavage is mediated by caspases, and is indicative of apoptosis. Supernatants from anti-CD3 stimulated Jurkat cells that stably overexpress RASSF1A show an increased ability to induce cleavage of PARP in apoptosis-sensitive J16 target cells when compared to anti-CD3 stimulated vector-transfected cells. Taken together, these results indicate that RASSF1A plays a role in expression of soluble FasL leading to increased apoptosis-inducing activity by these lymphocytic cells. The loss of this activity could contribute to outgrowth of malignant clones of lymphocytic origin in which RASSF1A is silenced.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2023. doi:1538-7445.AM2012-2023
Abstract 203: Hotair, a long non-coding RNA, exhibits pro-oncogenic activity in pancreatic cancer
Authors: Kim Kyounghyun , Safe Stephen 
Published: August 2012

Abstract
HOTAIR is a long intervening non-coding RNA (lincRNA) that represses specific gene transcription by interaction with the Polycomb Repressive Complex 2 (PRC2) that trimethylates histone H3 lysine 27, leading to reprograming of chromatin states. HOTAIR is a poor prognostic indicator for survival of breast, colon and liver cancer patients and is highly associated with cancer invasion and metastasis. In this study, we show that HOTAIR is more highly expressed in pancreatic tumors than normal tissue and is strongly correlated not only with cell invasiveness but also cell proliferation and death. Overexpression of HOTAIR increased cell invasion in pancreatic cancer cells expressing low levels of HOTAIR and this was previously observed in other cancer cell lines. However, unlike previous reports, HOTAIR knockdown in Panc1 and L3.6pL pancreatic cancer cells that overexpress this lincRNA decreased cell proliferation, altered cell cycle progression, and induced apoptosis, demonstrating an expanded function for HOTAIR in pancreatic cancer cells compared to other cancer cell lines. Results of gene profiling studies after HOTAIR knockdown showed that there was minimal overlap between HOTAIR-regulated genes in pancreatic vs. breast cancer cells and HOTAIR uniquely suppressed several interferon-related genes and genes related to cell cycle progression in pancreatic cancer cells. Consistently, Gene Set Enrichment Analysis (GSEA) shows that HOTAIR regulates gene sets relevant to cell proliferation using HOTAIR Knockdown gene profiling data and pancreatic patient gene expression data. Analysis of selected genes suppressed by HOTAIR in Panc1 and L3.6 pL cells showed by knockdown of EZH2 and chromatin immunoprecipitation assays that HOTAIR-mediated gene repression was both PRC-2-dependent and -independent. HOTAIR knockdown in L3.6pL cells also inhibited tumor growth in mouse xenograft model, further demonstrating the pro-oncogenic function of HOTAIR in pancreatic cancer. These results indicated that HOTAIR is a potential molecular target for inhibiting pancreatic cancer cell invasion, metastasis and proliferation for inducing cell death.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 203. doi:1538-7445.AM2012-203