bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 196: A real-time PCR based long noncoding RNA profiler for cancer research
Authors: Wu Fangting , Mo Yin-Yuan 
Published: August 2012

Abstract
Long non-coding RNAs (lncRNAs) are non-protein coding transcripts longer than 200 nucleotides, which are abundantly expressed in human and mouse. A recent study indicates that there are at least 16,000 ncRNAs among which over 3,000 are lncRNAs. In particular, accumulating evidence suggests that dysregulation of lncRNAs is associated with many types of human diseases, highlighting their potential as biomarkers and therapeutic targets. However, studies on lncRNA are still at a very early stage and our understanding of lncRNA function is very limited. Thus, investigation of the expression patterns of lncRNAs is a crucial step to understanding of their roles in normal physiological process as well as disease conditions such as cancer. To this end, we developed a qPCR based disease-related human lncRNA profiler, which allows for the quantification of differential expression of 83 individual lncRNAs among various experimental RNA samples. All 83 lncRNAs chosen for the array are based on publications and the majority of them are associated with cancer. To determine the utility of this lncRNA profiler, we profiled their expression in breast cancer specimens compared to matched normal tissue and identified several lncRNAs are dysregulated, suggesting that lncRNAs may function as oncogenes or tumor suppressors. In addition to those that have already been reported in the literature, we also identified dysregulation of a few lncRNAs not yet in the literature. Furthermore, gene expression profiling with this lncRNA profiler in a series of breast cell lines such as MCF10A, MCF7 and MDA-MB-231 cells identified differential expression patterns unique to each cell line, which may provide a basis for future analysis of these differentially expressed lncRNAs. Finally, we identified several lncRNAs that are induced by p53 in HCT-116 and MCF-7 cells. Experiments are underway to further characterize these p53 inducible lncRNAs. Together, these results suggest that this lncRNA profiler is a valuable research tool for cancer research. The features of this profiler are easy, convenient, sensitive and specific. Accordingly, it serves the first step toward the understanding of the role of lncRNAs in cancer.
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 196. doi:1538-7445.AM2012-196
Abstract 1960: Nanosponges as suitable platforms for targeted chemotherapy
Authors: Harth Eva M. , Hariri Ghazal , Stevens David M. , Spears Benjamin R. 
Published: August 2012

Abstract
We will report on the treatment efficacy of a degradable nanosponge drug delivery system. Degradable targeted nanosponges have been developed that are tailored in size and cross-linking density as supramolecular 3-D nano-networks. The organic polyester backbone can be functionalized in convenient ‘click’ chemistries with targeting peptides, dyes and cell penetrating units with particles that are fully soluble in organic solvents but retain their cross-linked architecture like a macromolecule. Furthermore, we found that the tailoring of the cross-linking density of the particles are correlated to the degradation and release properties of the particles to govern a fast, medium and slow linear release of the encapsulated drugs. Drugs can be encapsulated after the nanoparticle is formed and specifically hydrophobic drugs, for example chemotherapeutics, can be encapsulated with high efficiencies. The encapsulation into particle was found to be advantageous towards the solubility of the drug itself and resulted in vivo studies that showed a 3-5 time higher efficacy of the drug in targeted tumor regression studies. Similar efficacies are observed in glioma and lung cancer. We will report on novel combination therapies and efforts towards the delivery of a broad range of therapeutics in non-small lung cancer.
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 1960. doi:1538-7445.AM2012-1960
Abstract 1977: Higher doses of BAMLET may be required to induce cell death in HPV16-infected cancer cells
Authors: Barman Provaboti , Azambuja Katherine Marie De , Toyama Joy A. , Chua Kristofer Magat , Elashoff David , Wiley Dorothy 
Published: August 2012

Abstract
Introduction: Recent experiments showed that BAMLET (Bovine Alpha lactalbumin Made LEthal to Tumor cells), biochemically equivalent to HAMLET, administered at doses shown to induce volume reduction and clearance of cutaneous wart in humans was insufficient to clear DMBA-induced skin papillomas in C57/Bl6 mice expressing HPV16 E7 transgene on a K14 promoter. Gustufsson et al., reported &gt;75% subjects and 96% of warts reduced lesion volume when 0.7 mM HAMLET solution was topically administered. Thus, BAMLET's limited effect on papilloma reduction led to an in vitro dose-response experiment evaluating exponentially increasing doses of BAMLET on HPV16-infected CaSki cells, a well described cancer cell line. Five doses were selected versus normal saline controls and the cell viability was evaluated at 4, 24 and 72 hours using trypan blue exclusion assay. Methods: Caski cells were cultured in 6-well plates, 2 x 105 cells/well were initialized and allowed to grow to confluence. The initiating dose was based on published data as the exposure dose for our initial mouse studies. Exponential extrapolations of the baseline dose were evaluated: BAMLET administered at 0, 17.5µM (1.0-fold), 31.1µM (1.8-fold), 55.3µM (3.2-fold), 98.4µM (5.6-fold) and 175.0µM (10-fold) at time 0 and allowed to grow. At 4, 24, and 72 hours, cells were typsinized, pelleted, and resuspended in 1 ml PBS. A 10µL aliquot of Trypan-blue (0.4% v/v) was mixed with 10 µL of resuspended cells and incubated for 3 minutes. Duplicate specimens were evaluated under microscopy (10X) using a hemocytometer. Viable (white) and non-viable (blue) cells were counted and the average prevalence of viable cells was estimated for each dose. Results: For 0, 17.5µM, 31.1µM and 55.3µM doses, viability at 4, 24, and 72 hours were closely approximated: 74-92%, 81-91% and 67-88%, respectively. However, at 98.4µM and 175.0µM doses, a significant reduction in viability was observed in a time-dependent manner. Specifically, 95% vs. 91%, 68% vs. 0% and 6% vs. 2% viability were each observed at 4, 24 and 72 hours for these doses, respectively. Conclusions: These data suggest that the sensitivity of HPV16 infected cells to BAMLET may differ significantly from low-risk viruses that often cause cutaneous warts. While these data sheds light on the ineffectiveness of BAMLET in our ongoing animal experiment, they should be similarly considered in trials of BAMLET in humans where more pathogenic HPVs are the causal agent.
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 1977. doi:1538-7445.AM2012-1977
Abstract 1979: Sweet wormwood-derived artesunate causes cell cycle arrest in ovarian cancer cell lines
Authors: Greenshields Anna , Hoskin David 
Published: August 2012

Abstract
Introduction: Artesunate is a semi-synthetic derivative of artemisinin, a natural compound from the herb sweet wormwood (Artemisia annua L). Artemisinin has been used for centuries in traditional Chinese medicine while artesunate has recently been used as an anti-malarial drug. Artesunate is also cytotoxic to human cancer cells. Since the use of artesunate as an anti-malarial agent is associated with few adverse effects, artesunate may represent a less toxic alternative to conventional chemotherapy. This study investigates the effects of artesunate on ovarian cancer cell lines and the mechanism(s) underlying its activity. Methods and Results: Artesunate had a time- and dose-dependent growth inhibitory effect on all ovarian carcinoma cell lines examined (SKOV3, OVCAR3, IG-OV-1, HEY) using an MTT assay. Further examination of artesunate-treated SKOV3 and HEY cells using Oregon Green-488 and Annexin-V-FLUOS/propidium iodide staining indicated that artesunate had a strong anti-proliferative effect but was not cytotoxic towards the ovarian cancer cells. Cell cycle arrest occurred in the G1 and G2 phases of the cell cycle, and western blot analysis showed artesunate-induced changes in the expression and phosphorylation of a range of cell cycle proteins including the retinoblastoma protein, p21, and cyclin B1. Pretreatment with holotransferrin increased artesunate's anti-proliferative activity. Conclusions: These data show that artesunate possess a strong anti-proliferative activity in ovarian cancer cell cultures and therefore warrants further investigation as a possible treatment for ovarian cancer. Research supported by NSERC.
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 1979. doi:1538-7445.AM2012-1979
Abstract 1982: Turmeric oil inhibits hepatocellular carcinoma through abolishing EpCAM expression
Authors: Li Yan , Dunki-Jacobs Erik , Li Suping , Martin Robert C.G 
Published: August 2012

Abstract
Background: In previous study, we found that turmeric oil, a volatile oil from turmeric, can prevent hepatocellular carcinoma (HCC) in an orthotopic HCC mouse model. Epithelial cell adhesion molecule (EpCAM), a marker of cancer stem cells (CSC), is correlated with HCC initiation, progression, and prognosis. Our resent data showed that turmeric oil can decrease EpCAM expression in esophageal cancer and HCC cell lines. Since the role of EpCAM in HCC carcinogenesis is becoming clarified, it is likely that turmeric oil prevents HCC through EpCAM signaling. Aim: To investigate the mechanism of turmeric oil for HCC prevention. Method: EpCAM expression in the specimens from HCC patients (n=25) was evaluated by immunohistochemical staining. Red fluorescent protein (RFP)-labeled H4IIE cells were inoculated into liver lobe of ACI rats. The rat HCC tumor tissues from RFP-H4IIE cell inoculation were evaluated for the subpopulation cells, which co-expressed RFP and EpCAM. The HCC rats by H4IIE cell inoculation were treated with turmeric oil (100mg/kg, i.p, every 2 days) for 2 weeks. The H4IIE cells treated with turmeric oil as well as with EpCAM siRNA, and then inoculated at 106 into the right flank of nude BALB/c mice for 1 week. Three HCC cell lines from human (HepG-2), mouse (hepal-6), and rat (H4IIE) cells, were treated with turmeric oil to evaluate the cell viability EpCAM expression, and β-catenin in vitro. Results: In human samples, a strong EpCAM expression was found HCC tissues, while EpCAM was barely detected in the healthy controls. In HCC animal models, RFP+ EpCAM+ cells were detected in the formed tumor tissue and in circulation. The incidence of HCC by H4IIE cells inoculation was significantly decreased in rats treated with turmeric oil. Abolishing of EpCAM by turmeric oil caused the H4IIE cells unable to form tumor in nude mice. In cell culture study, turmeric oil significantly decreased EpCAM expression in all three HCC cell lines. Turmeric oil caused relocalization of β-catenin, a component in Wnt/β-catenin pathway, in nuclear and cytosol (Figure 1). Conclusion: 1) EpCAM-positive HCC cells contribute to HCC initiation in animal models; 2) The inhibition of HCC by turmeric oil is through decreasing EpCAM expression; 3). The regulation of EpCAM expression by turmeric oil is associated with Wnt/β-catenin pathway.
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 1982. doi:1538-7445.AM2012-1982
Abstract 1983: Thymoquinone induces cell killing in glioblastoma cells through generation of DNA damage and cell cycle arrest
Authors: Racoma Ira O. , Snapka Robert M. , Wani Altaf A. 
Published: August 2012

Abstract
Glioblastoma (GBM) is the most aggressive and common type of brain tumor in humans. Surgical resection followed by radiation and chemotherapy is the current standard treatment; however, due to the upregulation of several survival pathways, tumor recurrence is quite common with a median survival of 12 to 15 months. Therefore, there is an urgent need for more effective therapeutic strategies for the treatment of glioblastoma. Naturally occurring phytochemicals have steadily received much scientific attention, owing to the fact that many of these compounds have potent action against tumors. Thymoquinone (TQ) is the bioactive compound of the volatile oil extracted from the black seed, Nigella sativa. TQ has shown anti-oxidant, anti-inflammatory and anti-neoplastic actions with a selective cytotoxicity for human cancer cells compared to several normal cells. Here, we show that TQ is able to dose-dependently inhibit colony formation in three distinct glioblastoma cell lines (T98, U87 and Gli36), with the highly tumorigenic Gli36 being the most sensitive to the anti-proliferative effects of TQ. We also show that TQ induces persistent γ-H2AX activation, a marker of DNA double strand breaks, in a time- and dose-dependent manner. TQ also causes G2/M cell cycle arrest in GBM cells to a degree that correlates with the cells’ relative clonogenic sensitivity. Moreover, co-treatment with TQ and N-acetyl cysteine, a simple thiol nucleophile and antioxidant, prevented cell death, DNA double strand breaks, and cell cycle arrest. Taken together, our findings demonstrate that TQ is a potent inhibitor of GBM cell proliferation and growth, and that this effect may be mediated by generation of reactive oxygen species.
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 1983. doi:1538-7445.AM2012-1983
Abstract 1986: GBM cell migration and proliferation is inhibited by crude Rosa canina plant extracts
Authors: Idassi Ombeni , Cagle Patrice , Goktepe Ipek , Martin Patrick M. 
Published: August 2012

Abstract
Glioblastoma multiforme (GBM) are aggressive and malignant tumors that develop in the brain. These tumors are characterized by increased rates of proliferation and invasive migration as well as angiogenesis. To date few therapeutic options exist for the treatment and management of GBMs, therefore we decided to investigate the anti-oncogenic properties of extracts from the rosehip plant. Rosehip extracts have been used for centuries as alternative therapies. Currently, rosehip extracts are being used as over the counter supplements and recent studies demonstrate that it has an anti-tumor effect. Therefore, we tested the anti-migratory and antiproliferative capacity of extracts from the rosehip (Rosa canina) plant in GBM cell lines. Three human GBM cell lines, U-251 MG, U-1242MG and A-172, were treated with rosehip extracts (1 mg/mL - 25ng/mL) and demonstrated a decrease in cell proliferation. The rosehip extract-mediated decrease in cell proliferation was equal to the decrease of cell proliferation observed when U0126 (10µM), a know inhibitor of GBM cell proliferation was utilized. Utilizing a fluorescent-based labeling strategy (Live-Dead Assay), we examined whether rosehip extracts prevented cell proliferation by initiating apoptosis. Pretreatment of the GBM cells with rosehip extracts (1 mg/mL - 25ng/mL) induced the inhibition of cell proliferation without promoting apoptosis; whereas, cells treated with staurosporine (1 µM), a known inducer of apoptosis, showed an increase in cell apoptosis. Additional studies demonstrated that rosehip extracts prevent GBM cell proliferation by decreasing the active state of MAPK and AKT. Furthermore, rosehip extract-treated GBM cells also prevent cell migration by regulating actin remodeling. Taken together, these data suggest that rosehip extracts inhibit cell proliferation via a cytostatic mechanism that does not by induce apoptosis while also serving as a migration inhibiting agent. These data suggest that, rosehip extracts may serve as an alternative, or supplement, to current therapeutic regimens for GBMs.
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 1986. doi:1538-7445.AM2012-1986
Abstract 1997: Resveratrol modifies the activity and expression of antioxidant enzymes in somatic cancer cells
Authors: Khan Md. Asaduzzaman , Chen Han-chun , Wan Xin-xing , Xu Ai-hua , Zhang Dian-zheng 
Published: August 2012

Abstract
Background & Objectives: Resveratrol has been reported as a potent anti-cancer compound, but it's mode of action is not completely understood. In this study, we investigated the effects of resveratrol treatment on the activity and expression of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPX) in three somatic cancer cell lines: PC-3 (prostate cancer), MCF-7 (breast cancer) and HepG2 (hepatocellular cancer). Methods: The cells were treated with different concentration (0-200 μM) of resveratrol for 24, 48 and 72 hours.Cell growth was studied by cell counting; cell homogenate was taken for the measurement of enzyme activities; proteins were isolated for western blotting to measure the genetic expression. Results: Resveratrol showed dose-dependent growth inhibitory activity in all cells. It was significantly effective against PC-3 and HepG2 even in 10 μM, and 25 μM concentration, but not in MCF-7 cells. However 50 μM showed significant growth inhibitory effect in MCF-7, and also in HEK293T (human embryonic kidney cell line as control) cells. 25 μM was identified as most effective dosage against PC-3 and HepG2 cells, without affecting HEK293T cells. Treatment of 25 μM for 48 hours increased the activity of SOD enzymes by 3-4 folds in PC-3; 2-3 folds in HepG2; 1.5-1.8 folds in MCF-7; and 1.2-1.5 folds in HEK293T cells. Resveratrol treatment also significantly increased the activity of CAT in HepG2, moderately in MCF-7, but non-significantly in PC-3 and HEK293T cells. However, the treatment of resveratrol showed no significant change in GPX activity in any cell line. Western blotting also revealed the increased expression of SOD2 in PC-3, and HepG2 cells at 25 μM resveratrol treatment. CAT expression was moderate, but no change in GPX1 expression was found in the tested cancer cells. Conclusions: The results of this study could confirm the dose dependent growth inhibitory potential of resveratrol; however, the dose of resveratrol in treatment of the cancer cells should be limited, as higher dose (Δ50 μM) has also been found dangerous for normal cells (HEK293T). Resveratrol at low dose (25 μM) potentially increases the activity and expression of SOD enzyme in cancer cells while inhibiting cell growth. Moderate increase of CAT activity and expression is also observed, but no significant change in GPX activity and expression in cell lines used in this study. These findings may contribute to understanding the mechanisms of resveratrol action in treatment of cancer. The work was supported by the National Basic Research Program of China (No. 2011CB910700-704)
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 1997. doi:1538-7445.AM2012-1997
Abstract 2001: Caffeic acid phenethyl ester inhibits growth of human lung adenocarcinoma cells with an epidermal growth factor receptor T790M mutation susceptible property
Authors: Huang Wen-Chien 
Published: August 2012

Abstract
Purpose: Target therapeutics targeting epidermal growth factor receptor (EGFR) effectively kills non-small cell lung cancer cells along with a high proportion acquires T790M mutation of EGFR, an amino acid alteration likely causing drug resistance. Caffeic acid phenethyl ester (CAPE), a naturally occurring small molecule isolated from honeybee propolis, is known to possess preferential bioactivity against lung cancer cells. Materials and Methods: In this study, we evaluated the effect of CAPE on A549 (EGFR wild-type) and H1975 (EGFR T790M mutation) human lung adenocarcinoma cells by using assays as follows: MTS for viability, DNA histogram for hypoploidy and cell cycle analysis, DiOC6(3) staining for mitochondrial transmembrane potential, and Western blotting for caspase-3 cleavage Results: We found that CAPE inhibited the growth of lung adenocarcinoma H1975 cells with an extent greater than A549 (IC50 approximate 5 versus 10 mg/mL) after 24 - 48 h treatment. This differential growth inhibition was accompanied by much higher percentages of sub-G1 (7.5 folds) and G2/M arrest (2.6 folds) in H1975 cells. No significant difference could be seen for changes in mitochondrial transmembrane potential and caspase-3 cleavage, indicating a mitochondria-independent and caspase-3-inependent pathway involved. Conclusion: It suggests that CAPE may have potential to be developed as a small-molecule therapeutics against lung adenocarcinoma cells harboring wild-type epidermal growth factor receptor and, more effectively, the T790M-mutated clone.
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 2001. doi:1538-7445.AM2012-2001