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Total 151 results found since Jan 2013.
Abstract A83: Lentiviral shRNA-mediated knockdown of eosinophilic Galectin-10/Charcot-Leyden crystals: A novel approach to cancer immunotherapy
Conclusion: The creation of galectin-10 knockdown eosinophils provides a useful model for investigating eosinophilic galectin-10's ability to modulate T cell access and homing to tumors, and a putative role, similar to Treg galectin-10, in regulating tumoral T lymphocytic proliferation can certainly be envisioned. The consideration of galectin-10 knockdown eosinophils as a singular approach to cancer immunotherapy, or in combination with other anti-cancer therapies such as adoptive T cell therapies, or therapeutic cancer vaccines, is intriguing.Note: This abstract was not presented at the conference.Citation Format: Christ...
Source: Cancer Epidemiology Biomarkers and Prevention - September 30, 2015 Category: Cancer & Oncology Authors: Clarke, C. A., Lee, C. M., Laniyan, I., Furbert-Harris, P. Tags: Other Topics in Cell, Molecular, and Tumor Biology: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A05: Identification of RASA1 as a novel melanoma tumor suppressor gene
In this study, we addressed functional roles of RASA1 in melanoma tumorigenesis. Ectopic expression of wild-type RASA1 in human melanoma cell lines SKMEL28 and WM983C (with BRAF V600E) decreased, while RASA1 Y472H mutant enhanced soft agar colony formation, tumor growth, and Ras activity. The RASA1 L481F mutant lost its tumor suppressive activity. The siRNA- or shRNA-mediated knockdown of RASA1 promoted soft agar colony formation, tumor growth, and RAS activation in human melanoma cell lines IGR1 and KML1 (with BRAFV600E). Mechanistically, RASA1 required RasGAP activity to suppress colony formation and showed higher activi...
Source: Cancer Research - July 16, 2015 Category: Cancer & Oncology Authors: Sung, H., Kanchi, K. L., Messina, J., Lee, J.-H., Ding, L., Wilson, R. K., Weber, J. S., Kim, M. Tags: Advances in Melanoma Biology Source Type: research
Abstract A26: Protein phosphatase 4 (PP4) as a potential therapeutic target gene for BRAF wild type melanoma
Protein phosphatase 4 (PP4) participates in cell cycle progression and regulation of centrosome maturation. Gene expression of PP4 is elevated in cancerous tissues of various origins and its overexpression in pancreatic cancer is of prognostic importance. Microarray analysis from primary and metastatic melanoma tissues (N=89) showed that PP4 mRNA expression was up-regulated in metastatic melanoma as compared to primary melanoma of any thickness (relative expression: 1.12 ±0.14, p intestine> skin and subcutaneous tissue. Human melanoma cell lines also demonstrate PP4 gene expression with variable levels. We hypothesized th...
Source: Cancer Research - July 16, 2015 Category: Cancer & Oncology Authors: Essner, R., Gong, K. W., Kaufman, D., Chen, H., Ginther, C., Dering, J., Euw, E. v., Chmielowski, B., Finn, R., Slamon, D. Tags: Advances in Melanoma Biology Source Type: research
Abstract B32: Responses of direct in vivo melanoma xenograft cells to targeted therapeutics
The purpose of this study was to investigate the mechanism of resistance of a melanoma cell line generated from a direct in vivo xenograft (DIVX) model. Although BRAF and MKK1/2 inhibitors have produced positive clinical responses in melanoma patients with BRAF-V600 mutations, between 25-50% of patients show intrinsic resistance. Deciphering the mechanisms of intrinsic resistance will be critical for developing future treatment strategies. MB947P cells were established from a direct in vivo xenograft of a resected metastatic melanoma and exhibited innate resistance to apoptosis induced by MKK1/2 inhibitor (AZD6244/selumeti...
Source: Cancer Research - July 16, 2015 Category: Cancer & Oncology Authors: Basken, J., Fujita, M., Ahn, N. Tags: Principles of Response and Resistance to Therapy Source Type: research
Abstract B26: PI3K class I and mTOR regulate distinct steps in Met dependent tumorigenesis
The Receptor Tyrosine Kinase (RTK) Met, overexpressed or mutated in cancer, plays a major role in cancer progression and represents an attractive target for cancer therapy. Although several Met inhibitors are in clinical trials, resistance may occur as experienced in the clinic with other RTKs. Thus, a need for alternative / complementary therapy may be required to target Met driven tumors efficiently.The aim of this study was to investigate whether PI3K plays a role in Met oncogenic activity, in view of designing appropriate therapy.The study was performed on two cell models suitable to study Met driven NIH3T3 cells expre...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Hervieu, A., Kermorgant, S. Tags: PI3K-mTOR Activation in Human Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B27: Superoxide anion O2.-mediated activation of mTORC2 by estrogen receptor in breast cancer cells: Role of acetylation dependent inhibition of MnSOD
Conclusion: Our finding unravel a new role of MnSOD as important control switch through which ER might affect its downstream non genomic signaling cascades in a redox dependent manner particularly potentiation of mTOR signaling complex 2. We present data in support of MnSOD being responsible for previously reported ER dependent superoxide anion O2.- potentiation in breast cancer cells following E2 exposure. We showed that MnSOD interacts with ER alpha which in turn is associated with its diminished SIRT 3 dependent deacetylation, leading to its inhibition and superoxide anion O2.- build up and consequent activation of mTOR...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Lone, M. U. d., Kanchan, R. K., Tripathi, C., Baghel, K. S., Tiwari, B., Bhadauria, S. Tags: PI3K-mTOR Activation in Human Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A30: A genome-wide siRNA screen in mammalian cells for regulators of S6 phosphorylation
To identify the cellular components that participate in the regulation of mTOR complex 1 (mTORC1), the amino acid-dependent, rapamycin-inhibitable complex, we carried out a genome-wide RNAi depletion screen. We employed a rabbit monoclonal antibody specific for RPS6 [Ser235P/Ser236P] and high content microscopy to quantify rpS6 phosphorylation in the pancreatic ductal adenocarcinoma cancer cell line (PDAC) MiaPaCa-2. Applying a stringent selection, we retrieved over 600 genes wherein at least two RNAi gave significant reduction in S6 phosphorylation. This cohort is significantly enriched in genes whose depletion affects th...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Papageorgiou, A., Tamayo, P., Mesirov, J., Avruch, J., Rapley, J. Tags: PI3K-mTOR Activation in Human Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A36: Combined inhibition of PI3K isoforms and mTOR kinase is critical for cancer stem cell inhibition by VS-5584
We report here that VS-5584 is up to 30-fold more potent at inhibiting the proliferation and survival of CSCs than non-CSCs in breast cancer cell lines using multiple orthogonal CSC assays. Moreover, VS-5584 preferentially induced apoptosis in Aldefluor-positive CSCs relative to Aldefluor-negative non-CSCs as measured by Annexin V and Caspase 3/7 assays. In contrast, paclitaxel induced more apoptosis in non-CSCs than CSCs cells. VS-5584 also preferentially diminished CSCs in human breast and small cell lung cancer xenograft models in vivo, as evidenced by marked reduction of tumor-initiating capacity in an in vivo limiting...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Kolev, V. N., Wright, Q. G., Weaver, D. T., Padval, M. V., Pachter, J. A., Xu, Q. Tags: Preclinical and Clinical Studies in Breast Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract PR01: Inhibitory role of phosphatidylinositol-3,4-bisphosphate in triple-negative breast cancers
Triple-negative breast cancer (lacking expression of estrogen receptor, progesterone receptor and amplification of HER2/Neu) remains one of the most aggressive subtypes, affects the youngest patients and yet still lacks an effective targeted therapy. Novel insights into the molecular mechanisms that drive these cancers are imperative to guide development and application of such targeted therapies. Data from The Cancer Genome Atlas and other sources have suggested that phospho-Akt (pAkt) levels are significantly higher in triple-negative tumors compared to either hormone receptor positive tumors (express estrogen and/or pro...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Reed, D. E., Shokat, K. M. Tags: Molecular Regulation of the PI3K-mTOR Network: Oral Presentations - Proffered Abstracts Source Type: research
Abstract B04: NPM1: A new downstream effector of PI3K-AKT-mTOR pathway in prostate cancer?
Nucleophosmin NPM1 is a molecular chaperone involved in many aspect of cellular physiology, eg. ribosomal biogenesis and cell cycle regulation. NPM1 is overexpressed in numerous types of solid tumors, including prostate cancer but the underlying molecular mechanisms are largely unknown. Using both cell lines and transgenic mouse models, we show that NPM1 expression is significantly increased in cells where the PI3K-AKT-mTOR pathway is activated through PTEN deletion. This overexpression is reversed when cells are treated with the pharmacological inhibitor of mTOR rapamycin. In accordance, transfection of small interfering ...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Boudra, R., Loubeau, G., Lours-Calet, C., Dejoussineau, C., Morel, L., Beaudoin, C. Tags: Downstream Effectors Underlying Cancer Progression: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B05: PI3K/mTOR pathway-dependent regulation of oxygen metabolism via pyruvate dehydrogenase (PDH)-E1alpha phosphorylation
The PI3K/mTOR pathway plays a central role in coupling metabolic processes to the cellular proliferative state. In the current study we show that pharmacological inhibition of this pathway leads to a decrease in hypoxia within SQ20B human head and neck cancer xenografts. The mechanism underlying the effect appears in part to be due to reduced tumor cell oxygen consumption induced by the drug. Pharmacologic inhibitors of the PI3K/mTOR pathway or genetic inhibition of Akt/PI3K decreased the oxygen consumption rate (OCR) in transformed cell lines in vitro by 30-40%. Pharmacologic inhibition of this pathway increased phosphory...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Cerniglia, G., Dey, S., Gallagher-Colombo, S. M., Daurio, N., Tuttle, S., Busch, T. M., Lin, A., Esipova, T. V., Vinogradov, S., Koumenis, C., Maity, A. Tags: Downstream Effectors Underlying Cancer Progression: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A11: Ets transcription factor Etv5 regulates ductal morphogenesis and differentiation in association with Sox9 in vitro and increases susceptibility and delays recovery from pancreatitis in vivo
Conclusion: Our data suggest a novel role for Etv5 in pancreatic ductal morphogenesis and lumen formation that is at least in part mediated by Sox9. In addition, our data suggests that the loss of Etv5 expression increases susceptibility to pancreatitis and results in persistent pancreatitis with delayed regeneration.Citation Format: Koushik K. Das, Steffen Heeg, Maximilian Reichert, Shigetsugu Takano, Basil S. Bakir, Gregory P. Botta, Christopher Hahn, Andrew D. Rhim, Anil K. Rustgi. Ets transcription factor Etv5 regulates ductal morphogenesis and differentiation in association with Sox9 in vitro and increases susceptibil...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Das, K. K., Heeg, S., Reichert, M., Takano, S., Bakir, B. S., Botta, G. P., Hahn, C., Rhim, A. D., Rustgi, A. K. Tags: Development Source Type: research
Abstract A13: Mechanisms of E47 induced quiescence and acinar cell differentiation in human pancreatic cancer cells
Pancreatic ductal adenocarcinoma (PDA) initiates from quiescent acinar cells that attain a Kras mutation, undergo acinar-ductal metaplasia and rapidly acquire increased growth potential. During this process several transcription factors from the basic helix-loop-helix (bHLH) family are downregulated while expression of their inhibitor Id3 is induced. Previously we showed that Id3 knockdown with siRNA resulted in growth arrest in PDA cells. Here we queried whether aggressive PDA cells can be reprogrammed to revert to their original quiescent acinar cell phenotype by shifting bHLH transcription programs. In order to mitigate...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Kim, S., Yang, C., Riha, C., Lamy, R., Jakubison, B. L., Konieczny, S. F., Itkin-Ansari, P. Tags: Development Source Type: research
Abstract B19: Redox factor 1 (Ref-1) signaling in the interaction between pancreatic tumor cells and cancer-associated fibroblasts
The objective of this work is to determine the outcome of inhibiting Ref-1 in CAFs and the effects of that inhibition on proliferation and migration in PDAC. The central hypothesis of the proposed work is that Ref-1 redox activity plays a critical role in the signaling within the TME between tumor and CAFs. We are using several innovative methods to probe the tumor-CAF interaction including: 1) co-culture 2D and 3D models; 2) genetic approach via redox inactive-Ref-1 constructs and siRNA to Ref-1; 3) pharmacologic approach via a well-established small molecule inhibitor of Ref-1 redox activity, E3330; 4) quantitation of Re...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Fishel, M. L., Cheng, H., Korc, M., Kelley, M. R. Tags: Inflammation/Stroma Source Type: research
Abstract A39: The activation of {beta}1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells
In this study, we demonstrated that pancreatic cancer cells exhibited increased proliferation and decreased apoptosis in response to type I collagen. In addition, exposed to type I collagen, PDAC cells lost the expression of E-cadherin and increased expression of mesenchymal markers, including N-cadherin and vimentin, which was correlated with enhanced cell migration and invasiveness. Conversely, the knockdown of β1-integrin abolished the effects induced by type I collagen. Further investigation revealed that type I collagen activates β1-integrin accompanied with significant up-regulation of Gli-1. siRNA specific to Gli-...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Duan, W., Ma, Q., Ma, J., Xu, Q., Lei, J., Wu, E. Tags: Development Source Type: research
