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Source: Cancer Research
Condition: Brain Tumor
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Total 43 results found since Jan 2013.
Abstract 4944: Identification of B-cell lymphoma 6 as a novel therapeutic target in glioblastoma
ConclusionOur data suggest that BCL6 is involved in glioma tumorigenesis through regulating both the TP53 and MEK-ERK pathways, and that BCL6 is a potential therapeutic target for glioma treatment.Citation Format: Ye Chen, Liang Xu, Masaharu Hazawa, Anand M. Thippeswamy, Henry Yang, Markus Müschen, De-Chen Lin, Phillip Koeffler. Identification of B-cell lymphoma 6 as a novel therapeutic target in glioblastoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 4944. doi:...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Chen, Y., Xu, L., Hazawa, M., Thippeswamy, A. M., Yang, H., Muschen, M., Lin, D.–C., Koeffler, P. Tags: Molecular and Cellular Biology Source Type: research
Abstract 5222: Endothelial plasticity generates aberrant angiogenesis and therapy resistance in glioblastoma
Overgrown, abnormal vasculature characterizes the microenvironment that fuels cancer progression and induces therapeutic resistance. Here we reveal that endothelial plasticity drives excessive and abnormal tumor angiogenesis. Glioblastoma multiforme (GBM) is among the most lethal of human malignancies, distinguished by prominent vascularity and extreme vascular abnormality. We identify endothelial fibro-transformation (Endo-FT) in GBM, contributing significantly to aberrant vascularization, tumor progression, and therapeutic resistance. Utilizing human GBM specimens and allograft and genetic murine GBM models driven by RCA...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Huang, M., Fan, Y. Tags: Tumor Biology Source Type: research
Abstract 5328: Protein phosphatase 2A activity is a major determinant of therapy response in cancer cells
Protein phosphatase 2A (PP2A) dephosphorylates majority of Ser/Thr phosphorylated proteins. Consequently, PP2A is an antagonist of multiple oncogenic pathways and PP2A reactivation may provide an alternative route to target these pathways. Importantly, because PP2A reactivation would result in simultaneous dephosphorylation of both collateral and downstream effectors of kinase pathways, it might circumvent commonly encountered kinase inhibitor resistance mechanisms.To systematically study the role of PP2A in cancer therapy response we used RNAi targeting against PP2A inhibitor proteins CIP2A, PME-1 and SET (PP2A reactivati...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Kauko, O., Imanishi, S., Kaur, A., Laajala, D., Kulesskiy, E., Jumppanen, M., Corthals, G., Aittokallio, T., Wennerberg, K., Westermarck, J. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 5093: Pre-clinical assessment of a novel anti-invasion nanoparticle therapeutic in combination with bevacizumab for the treatment of glioblastoma
We report a novel strategy by which GBM tumours invade and proliferate via overexpression of the GEF beta-PIX which was shown to be increased at the invasive edge in 74% of GBM tumours assessed (n = 19) compared with tumour core (5). We have further shown that siRNA-mediated knockdown of beta-PIX in GBM patient-derived xenograft cell cultures and cell lines resulted in decreased cell invasion in 3D, cell proliferation and survival assays in vitro. Furthermore, we have uncovered a role for beta-PIX expression in endothelial cell function, as knockdown of beta-PIX inhibits HUVEC cell migration in vitro. To interrogate in viv...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Murray, D. W., O'Halloran, P., Jarzabek, M., MacCarthy, B., Sarkaria, J. N., Schiffelers, R. M., Symons, M., Byrne, A. T. Tags: Tumor Biology Source Type: research
Abstract 4610: Functional characterization of a multicancer risk locus on chr5p15.33 reveals regulation of TERT by ZNF148
Genome wide association studies (GWAS) have mapped multiple independent cancer risk loci (n = 6) to a small region on chr5p15.33 for at least ten distinct cancers, including bladder, breast, glioma, lung, melanoma, non-melanoma skin, ovarian, pancreas, prostate, and testicular germ cell cancer. This region harbors two plausible target genes, TERT which encodes the catalytic subunit of telomerase reverse transcriptase which maintains chromosome ends by adding telomeres repeats, and CLPTM1L which encodes the cleft lip and palate transmembrane protein 1-like protein which promotes cancer cell growth, protect cells from apopto...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Brown, K. M., Fang, J., Jia, J., Wang, Z., Makowski, M., Zhang, T., Hoskins, J., Choi, J., Han, Y., Zhang, M., Xu, M., Kanetsky, P., Thorkell, A., Petersen, G. M., Nathanson, K. L., Amos, C. I., Landi, M. T., Chanock, S. J., Vermeulen, M., Amundadottir, L Tags: Epidemiology Source Type: research
Abstract 4170: The role of VEGF-C for cell viability, tumor growth and bevacizumab resistance in glioblastoma multiforme
In conclusion, our current results show that VEGF-C is of importance for GBM cell viability and tumor growth presumable due to its ability to stimulate autocrine activation of VEGFR2. VEGF-C expression therefore could respresent a possible mechanism behind Bevacizumab resistance. An update on this will be presented.Citation Format: Signe R. Michaelsen, Mette K. Nedergaard, Thomas Urup, Mette Villingshoej, Andreas Kjaer, Lara Perryman, Janine T. Erler, Ulrik Lassen, Hans S. Poulsen. The role of VEGF-C for cell viability, tumor growth and bevacizumab resistance in glioblastoma multiforme. [abstract]. In: Proceedings of the 1...
Source: Cancer Research - August 2, 2015 Category: Cancer & Oncology Authors: Michaelsen, S. R., Nedergaard, M. K., Urup, T., Villingshoej, M., Kjaer, A., Perryman, L., Erler, J. T., Lassen, U., Poulsen, H. S. Tags: Tumor Biology Source Type: research
SAT1 Regulates BRCA1 Expression and HR in GBM
Glioblastoma multiforme (GBM) is the most common and severe form of brain cancer. The median survival time of patients is approximately 12 months due to poor responses to surgery and chemoradiation. To understand the mechanisms involved in radioresistance, we conducted a genetic screen using an shRNA library to identify genes in which inhibition would sensitize cells to radiation. The results were cross-referenced with the Oncomine and Rembrandt databases to focus on genes that are highly expressed in GBM tumors and associated with poor patient outcomes. Spermidine/spermine-N1-acetyltransferase 1 (SAT1), an enzyme involved...
Source: Cancer Research - November 30, 2014 Category: Cancer & Oncology Authors: Brett-Morris, A., Wright, B. M., Seo, Y., Pasupuleti, V., Zhang, J., Lu, J., Spina, R., Bar, E. E., Gujrati, M., Schur, R., Lu, Z.-R., Welford, S. M. Tags: Molecular and Cellular Pathobiology Source Type: research
Involvement of Polymerase {eta} in Anticancer Drug Resistance
DNA repair processes are a key determinant of the sensitivity of cancer cells to DNA-damaging chemotherapeutics, which may induce certain repair genes as a mechanism to promote resistance. Here, we report the results of a screen for repair genes induced in cancer cells treated with DNA crosslinking agents, which identified the translesion polymerase η (PolH) as a p53-regulated target acting as one defense against interstrand crosslink (ICL)-inducing agents. PolH was induced by fotemustine, mafosfamide, and lomustine in breast cancer, glioma, and melanoma cells in vitro and in vivo, with similar inductions observed in norm...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Tomicic, M. T., Aasland, D., Naumann, S. C., Meise, R., Barckhausen, C., Kaina, B., Christmann, M. Tags: Therapeutics, Targets, and Chemical Biology Source Type: research
Abstract 1600: Keeping glioblastoma (GBM)in check by targeting the CHK1-STAT3-CIP2A axis
Checkpoint kinase1 (CHK1) is a DNA damage kinase, which has been observed to be constitutively active in human cancers. Unfortunately a number of new generation CHK1 inhibitors, currently in clinical trials, have shown deleterious effects on normal cells, thus limiting their clinical utility. Therefore, identification and targeting of cancer specific effectors of CHK1 signaling has emerged as an attractive therapeutic alternative.
Analysis of the REMBRANDT and TCGA datasets revealed a strong positive correlation for CHK1 and CIP2A expression in 422/522 and 356/454 glioma patients respectively. By contrast, there was neglig...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Khanna, A., Stringer, B., Day, B., Ensbey, K., Shen, H., Boyd, A., McDonald, K., Pimanda, J. E. Tags: Carcinogenesis Source Type: research
Abstract 428: HIC-1: A gene silenced in cancer stem cells of glioma
Conclusion: Down-regulation of HIC-1, by i) epigenetic changes or ii) knockdown by siRNA or iii) using mutant p53 cell line, may be responsible for contributing to stem cell-like properties to tumor cells. Since HIC-1 is a tumor suppressor gene silenced in many cancers as a result of promoter hypermethylation, it could by itself be a new target for epigenetic therapy. Moreover, increase in stemness on knockdown of HIC-1 could provide new insights into the behavior of cancer-initiating stem cells.
Citation Format: Mohita Bhagat, Subrata Sinha, Parthaprasad Chattopadhyay. HIC-1: A gene silenced in cancer stem cells of glioma...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Bhagat, M., Sinha, S., Chattopadhyay, P. Tags: Molecular and Cellular Biology Source Type: research
Abstract 1774: Polysialyltransferase ST8SiaII: a new target for the treatment of metastatic tumors
Polysialic acid (polySia) is a carbohydrate polymer expressed on the surface of NCAM (neuronal cell adhesion molecule) in many cancer cells where it modulates cell-cell and cell-matrix adhesion, migration, invasion and metastasis. PolySia-NCAM expression is strongly associated with poor clinical prognosis and correlates with aggressive/invasive disease in small cell lung cancer, pancreatic cancer, neuroblastoma and many other tumors principally of neuroendocrine origin [1]. SiRNA knockdown of polysialyltransferase ST8SiaII (STX), the enzyme primarily responsible for polySia synthesis in tumors, has been shown to abolish tu...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Viprey, V., Springett, B. R., Al-Saraireh, Y., Northrop, M., Sutherland, M., Saeed, R., Loadman, P. M., Patterson, L. H., Shnyder, S. D., Falconer, R. A. Tags: Experimental and Molecular Therapeutics Source Type: research
Abstract 511: EGFR-initated NADPH oxidase activity regulates Fyn expression in glioblastoma multiforme
Glioblastoma multiforme (GBM) constitute the most aggressive and common form of primary brain tumors, conferring the worst clinical prognosis. Epidermal growth factor receptor (EGFR) amplification, mutation and re-arrangement are commonly observed genetic lesions in GBM. The most frequently occurring EGFR variant in GBM, EGFRvIII, is characterized by a truncated extracellular domain, leading to a receptor which is unable to bind ligand yet rendered constitutively active. In addition to increasing proliferation and survival signaling, EGFRvIII increases the production of reactive oxygen species (ROS); redox signaling in GBM...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Johnson, B., Chandra, J. Tags: Molecular and Cellular Biology Source Type: research
Abstract LB-207: mTORC2/Akt signaling is modulated by noncanonical mitochondrial Notch1/PINK1 interaction in myc-amplified medulloblastoma tumorigenesis
Medulloblastoma is known to be the most malignant pediatric brain tumor. The armamentarium of targeted therapies to currently treat medulloblastoma and similar pediatric central nervous system malignancies is extremely limited, often necessitating the need to combat such tumors with modified regimens of therapeutic options designed originally to target adult neoplasms. Given such limited therapies, a budding focus on the role of mitochondrial dysregulation in the tumorigenesis of such pathologies merits consideration. Mitochondria are known to play fundamental roles in multiple processes conserved across eukaryotic species...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Feroze, A. H., Lee, K.-S., Gholamin, S., Wu, Z., Weissman, I., Lu, B., Mitra, S. S., Cheshier, S. Tags: Tumor Biology Source Type: research
Abstract 1031: Blockade of radiation-induced neuropilin-1 in glioblastoma cells impairs migration of endothelial cells
In this study, we show that the IR-induced NRP-1 role in the VEGFR-2 mediated signaling cascade promotes migration of endothelial cells. We observed that IR (8Gy) significantly elevated levels of VEGF and NRP-1 expression in 4910 and 5310 human GBM xenograft cells. Endothelial cells cultured on tumor- conditioned media from IR induced xenograft cells showed a significant increase in migration of endothelial cells; whereas, conditioned medium (CM) from NRP-1 knockdown xenograft cells inhibited IR-induced migration effects in endothelial cells. Further, CM from NRP-1 inhibited cells downregulated IR-induced expression of VEG...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Maddirela, D. R., Kesanakurti, D., Gogineni, V. R., Chetty, C. Tags: Tumor Biology Source Type: research
Aurora-A Inhibition Is Effective against GB in Mice
Glioblastoma remains a devastating disease for which novel therapies are urgently needed. Here, we report that the Aurora-A kinase inhibitor alisertib exhibits potent efficacy against glioblastoma neurosphere tumor stem–like cells in vitro and in vivo. Many glioblastoma neurosphere cells treated with alisertib for short periods undergo apoptosis, although some regain proliferative activity upon drug removal. Extended treatment, however, results in complete and irreversible loss of tumor cell proliferation. Moreover, alisertib caused glioblastoma neurosphere cells to partially differentiate and enter senescence. These eff...
Source: Cancer Research - September 30, 2014 Category: Cancer & Oncology Authors: Van Brocklyn, J. R., Wojton, J., Meisen, W. H., Kellough, D. A., Ecsedy, J. A., Kaur, B., Lehman, N. L. Tags: Priority Reports Source Type: research
