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Total 151 results found since Jan 2013.
Abstract A84: Regulation of 6-phosphofructo-2-kinase (PFKFB3) by estradiol and implications for the treatment of ER+ metastatic breast cancer
Estradiol (E2) administered to estrogen receptor positive (ER+) breast cancer patients stimulates glucose uptake by tumors. This E2-induced metabolic flare is predictive of the clinical effectiveness of anti-estrogens and downstream metabolic regulators of E2 are expected to have utility as targets for the development of anti-breast cancer agents. While the stimulation of glucose metabolism by E2 has been demonstrated, relatively little is known about the precise downstream effectors required for E2 to stimulate glucose metabolism in breast cancer. The family of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases (PFKFB1...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Clem, B., Tapolsky, G., Chesney, J. Tags: Therapeutic Targets From Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract PR01: Role of mitochondrial folate transporter in metabolism of tumor cells
The objective of the present study is to identify modulators of cellular metabolism among transportome genes which could potentially be exploited as targets in pancreatic ductal adenocarcinoma (PDAC). Indeed cancer cells have the ability to adapt in order to survive stressful environment where oxygen and nutrients are limited due to the poor vasculature and outgrowth of stromal component. Thus, disrupting mechanisms of metabolic adaptation could inhibit tumor proliferation or sensitize tumor cells to treatment. Ion channels and transporters provide the link between cancer cells, stroma and matrix. Additionally these protei...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Kovalenko, I., Schockel, L., Glasauer, A., Haegebarth, A., Christian, S. Tags: Therapeutic Targets From Cancer: Oral Presentations - Proffered Abstracts Source Type: research
Abstract PR03: P53 inhibits the expression of the pyrimidine catabolic gene Dihydropyrimidine dehydrogenase (DPYD)
Fluorouracil (5-FU) a widely used chemotherapeutic drug whose unpredictable pharmacokinetics is controlled by the pyrimidine catabolic gene dihydropyrimidine dehydrogenase (DPYD), that has recently also been shown to be a gatekeeper of the epithelial-to-mesenchymal transition (EMT) in breast cancer. Relatively little is known about the transcriptional control of DPYD and here we show for the first time an interaction between p53 and DPYD (involved in catabolism of pyrimidines as well as 5-FU) where p53 represses both the base-line expression of DPYD and that following 5-FU administration in vitro and in vivo. This mechanis...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Gokare, P. R., Finnberg, N., Dai, J., El-Deiry, W. Tags: Cancer Metabolic Pathways: Oral Presentations - Proffered Abstracts Source Type: research
Abstract A12: Establishment of myeloid lineage cell line that resembles myeloid-derived suppressive cells
Myeloid-derived suppressive cells (MDSCs) are inflammatory cells that play critical roles in promoting cancer growth and metastasis. In order to facilitate characterization of biochemical and cellular mechanisms of MDSCs, it is urgent to establish an "MDSC-like" cell line for pharmacological and immunotherapeutic applications. Lysosomal acid lipase (LAL) is a critical lipid enzyme in the metabolic signaling pathway that hydrolyzes cholesteryl esters (CE) and triglycerides (TG) in lysosomes. In mice, lack of LAL in genetically ablated knockout mice (lal-/-) shows systemic expansion of MDSCs, which directly stimulate cancer ...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Yan, C., Ding, X., Wu, L., Du, H. Tags: Cancer Metabolic Pathways: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A21: ACC1 is required for prostate cancer initiation, but not progression?
The majority of cancers undergo metabolic alterations during initiation and progression of disease. Increased de novo lipogenesis is recognized as metabolic mark of cancer cells. The enzymes responsible for de novo fatty acid synthesis are often overexpressed in cancer, indicating that these enzymes are potential and promising targets for novel therapies. Acetyl CoA Carboxylase 1 (ACC1) is a cytosolic enzyme which catalyzes the rate limiting step of de novo fatty acid synthesis through the ATP and biotin-dependent carboxylation of acetyl-CoA to malonyl-CoA. In doing so, it regulates both fatty acid and acetate metabolism. ...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Davis, A. L., Scott, K., Jiansheng, W., Chen, Y. Q., Kridel, S. J. Tags: Cancer Metabolic Pathways: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B29: LRP16 is an essential mediator for DNA double-strand breaks induced NF-kappaB activation
In this study, we demonstrate that LRP16 constitutively interacts with PARP1 and IKKgamma. This interaction is essential for efficient interactions among PARP1, IKKgamma, and PIASy, the modifications of IKKgamma, and the activation of NF-kappaB following DSB induction. The regulation of LRP16 in NF-kappaB activation is dependent on its poly (ADP-ribose) binding capability through the unique macro domain. The depletion of the DSB-specific sensor Ku80 resulted in a significant reduction in the physical interactions among LRP16, PARP1 and IKKgamma. Additionally, the knockdown of either endogenous Ku80 or Ku70 by siRNA markedl...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Wu, Z., Wang, C., Bai, M., Li, X., Mei, Q., Li, X., Wang, Y., Fu, X., Luo, G., Han, W. Tags: Signaling Pathways and Cancer Metabolism: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B31: Disruption of Folliculin interacting protein-1 modulates Myc-driven metabolism, increasing cell death following metabolic stress
In this study, we examined the potential efficacy of Fnip1 disruption in cancer by disrupting Fnip1 in primary mouse and human B cell lines overexpressing the Myc oncogene. We show that constitutive depletion of Fnip1 in primary pre-B cells, conditional knockdown of Fnip1 in primary mouse mature B cells using the Cre-loxP system, or siRNA-mediated depletion of endogenous FNIP1 from a human B cell line expressing a conditional Myc allele, increase oxidative phosphorylation and Myc-induced glycolysis, which support cell division. Disruption of Fnip1 increases death of primary murine pre-B Eµ-Myc cells and human B cell ...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Ramirez, J. A., Tsang, M., Park, H., Margineantu, D., Gu, H., Raftery, D., Hockenbery, D. M., Iritani, B. M. Tags: Signaling Pathways and Cancer Metabolism: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B41: Post-transcriptional regulation of IDH1 by the RNA-binding protein HuR is important for pancreatic cancer cell survival under nutrient deprivation
Conclusions: HuR is important for pancreatic cancer cell survival under glutamine deprivation, as previously observed for glucose deprivation. Carbon flux from glutamine to fatty acid end products suggests a role for HuR in reductive carboxylation of glutamine-derived α-ketoglutarate by IDH1, as a way to maintain adequate lipid synthesis under glucose deprivation. Our Studies provide a rationale to pursue pharmacologic strategies that target HuR or its regulation of IDH1 as a novel treatment of PDA.Citation Format: Mahsa Zarei, Fernando F. Blanco, Laszlo G. Boros, Charles J. Yeo, Jonathan R. Brody, Jordan M. Winter. ...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Zarei, M., Blanco, F. F., Boros, L. G., Yeo, C. J., Brody, J. R., Winter, J. M. Tags: Alterations of Nutrient/Fuel Sensing in Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract B05: WHSC1L1 and estrogen-independent activation of estrogen receptor-alpha (ER{alpha}) in 8p11 amplicon-bearing cell lines
The 8p11-p12 genomic region is amplified in 15% of breast cancers and 21% of lung squamous cell carcinomas (LSCC) and is associated with poorer prognosis. This genomic region harbors several oncogenes, three of which are epigenetic modifiers of chromatin (WHSC1L1, KAT6A, ASH2L). WHSC1L1 is a histone methyltransferase (HMT) that is expressed in 2 isoforms. The long isoform (WH-long) encompasses the entire coding region and is associated with dimethylation of lysine 36 on histone 3 (H3K36me2) to facilitate transcriptional elongation. The short isoform (WH-short) is produced by alternative splicing at exon 10, resulting in a ...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Mills, J. N., Irish, J., Turner-Ivey, B., Ethier, S. P. Tags: Cancer Genomics and Epigenomics Source Type: research
Abstract PR06: Analysis of enhancer transcription reveals novel gene regulatory networks in breast cancer
Enhancer transcription is a defining feature of active enhancers. We and others have shown that enhancers that produce transcripts (so called “eRNAs”) are more likely to (1) be associated with active chromatin marks, such as H3K4me1 and K3K27ac, (2) loop to target gene promoters, and (3) be associated with target gene activation. Thus, enhancer transcription is a good predictor of active enhancers. In this regard, we have shown that enhancer transcription can be used in the absence of any other genomic information to predict enhancers. We have used Global Run-On coupled deep sequencing (GRO-seq) in 14 different breast ...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Franco, H. L., Nagari, A., Xi, Y., Li, W., Richardson, D., Tanaka, K., Li, J., The CPRIT LONESTAR Consortium, Barton, M. C., Shi, X., Keyomarsi, K., Bedford, M. T., , Dent, S. Y. R., Kraus, W. L. Tags: Enhancers Source Type: research
Abstract A16: Different epigenetic mechanisms involved in the regulation of SFRP1 gene in prostate cancer
Among men, prostate cancer (PCa)[1] is the second most common cancer and the fifth cause of death worldwide [2]. Androgens play an important role in the development of the disease. For advanced PCa the standard therapy is androgen depletion. However, after 2 or 3 years a high percentage of patients become resistant to this therapy and castration resistant prostate cancer (CRPC) is developed. There is no successful treatment for CRPC, leading into death [3, 4]. Wingless pathway (WNT) is aberrantly activated in several cancer types and in PCa it is involved in AR activity modulation, promoting cancer development [5]. Secrete...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Garcia–Tobilla, P., Uribe, O., Rodriguez–Dorantes, M. Tags: Epigenetic Control of Transcription/ Elongation Source Type: research
Abstract A24: PBRM1 alteration in clear cell renal cell carcinoma increases tumorigenicity through ALDH1A1 upregulation
In this study, we investigated the mechanisms by which PBRM1 functions as a tumor suppressor in clear cell renal cell carcinoma (ccRCC). PBRM1, also known as BAF180 or Polybromo, is a member of the PBAF SWI/SNF chromatin remodeling complex. Cancer sequencing studies have revealed that SWI/SNF components are widely mutated in cancer. PBRM1 mutations in particular are found in ~40% of ccRCC tumors, making it the second most highly mutated gene in ccRCC (behind VHL). Although many recent studies have looked at how other SWI/SNF components function in cancer control, relatively little is known about the tumor suppressive mecha...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Schoenfeld, D., Su, W., Zairis, S., Mathur, D., Rabadan, R., Parsons, R. Tags: Chromatin Organization Source Type: research
Abstract B37: The histone deacetylase inhibitor panobinostat sensitizes cyclin E-amplified ovarian cancer cells to poly ADP ribose polymerase inhibitors via E2F1 downregulation.
Conclusions: The development of a new PARPi combination therapy with panobinostat has immediate prospects for rapid translation to the clinic and great potential for improving clinical outcomes for non-BRCAness, chemoresistant ovarian cancer.Citation Format: Andrew J. Wilson, Jeanette Saskowski, Dineo Khabele. The histone deacetylase inhibitor panobinostat sensitizes cyclin E-amplified ovarian cancer cells to poly ADP ribose polymerase inhibitors via E2F1 downregulation.. [abstract]. In: Proceedings of the AACR Special Conference on Chromatin and Epigenetics in Cancer; Sep 24-27, 2015; Atlanta, GA. Philadelphia (PA): AACR;...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Wilson, A. J., Saskowski, J., Khabele, D. Tags: Epigenetic Cancer Therapies Source Type: research
Abstract B43: Dose and context-dependent roles for Arid1a in liver tumorigenesis
Frequent Arid1a loss-of-function mutations suggest tumor suppressive roles, but the functional impact of Arid1a and SWI/SNF chromatin-remodeling aberrations in human cancer are not clear. Liver-specific Arid1a knockout mice do not develop cancer after 15 months and surprisingly, homozygous mice are potently protected from diethylnitrosamine (DEN) + carbon tetrachloride induced hepatocellular carcinoma (HCC). This is likely due to the fact that Arid1a deficient livers are resistant to chemical damage in a Cytochrome P450 dependent fashion. To determine if genetic drivers of cancer might reveal additional roles for Arid1a, w...
Source: Cancer Research - January 14, 2016 Category: Cancer & Oncology Authors: Sun, X., Wang, S., Nguyen, L., Zhu, H. Tags: Epigenetic Cancer Therapies Source Type: research
Abstract C1: Harnessing the pro-inflammatory tumor microenvironment of castrate-resistant prostate cancer to promote apoptosis
ConclusionProstate cancer cell lines are inherently resistant to SMAC mimetic therapy even in the presence of TNFα or TRAIL. However, dual targeting of FLIP and IAPs sensitises CRPC cell lines to microenvironment-derived TNFα. Combined targeting of IAPs and FLIP, or single targeting of FLIP, may be an effective means of treating pro-inflammatory prostate cancer.Citation Format: Christopher McCann, Nyree Crawford, David Waugh, Daniel Longley. Harnessing the pro-inflammatory tumor microenvironment of castrate-resistant prostate cancer to promote apoptosis. [abstract]. In: Proceedings of the AACR-NCI-EORTC Interna...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: McCann, C., Crawford, N., Waugh, D., Longley, D. Tags: Apoptosis, Necrosis, and Autophagy: Poster Presentations - Proffered Abstracts Source Type: research
