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Anat Erdreich-epstein - One of the best experts on this subject based on the ideXlab platform.
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Pediatric brain Tumor Cell lines
Journal of Cellular Biochemistry, 2015Co-Authors: Jingying Xu, Shahab Asgharzadeh, Ashley Margol, Anat Erdreich-epsteinAbstract:Pediatric brain Tumors as a group, including medulloblastomas, gliomas, and atypical teratoid rhabdoid Tumors (ATRT) are the most common solid Tumors in children and the leading cause of death from childhood cancer. Brain Tumor-derived Cell lines are critical for studying the biology of pediatric brain Tumors and can be useful for initial screening of new therapies. Use of appropriate brain Tumor Cell lines for experiments is important, as results may differ depending on Tumor properties, and can thus affect the conclusions and applicability of the model. Despite reports in the literature of over 60 pediatric brain Tumor Cell lines, the majority of published papers utilize only a small number of these Cell lines. Here we list the approximately 60 currently-published pediatric brain Tumor Cell lines and summarize some of their central features as a resource for scientists seeking pediatric brain Tumor Cell lines for their research.
Gary A Piazza - One of the best experts on this subject based on the ideXlab platform.
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sulindac inhibits Tumor Cell invasion by suppressing nf κb mediated transcription of micrornas
Oncogene, 2012Co-Authors: Lin Gao, Bernard D. Gary, Q Cui, Donna Lynn Dyess, William R Taylor, Lalita A Shevde, Rajeev S Samant, Windy Deancolomb, Gary A PiazzaAbstract:Non-steroidal anti-inflammatory drugs (NSAIDs) have been widely reported to display strong efficacy for cancer chemoprevention, although their mechanism of action is poorly understood. The most well-documented effects of NSAIDs include inhibition of Tumor Cell proliferation and induction of apoptosis, but their effect on Tumor Cell invasion has not been well studied. Here, we show that the NSAID, sulindac sulfide (SS) can potently inhibit the invasion of human MDA-MB-231 breast and HCT116 colon Tumor Cells in vitro at concentrations less than those required to inhibit Tumor Cell growth. To study the molecular basis for this activity, we investigated the involvement of microRNA (miRNA). A total of 132 miRNAs were found to be altered in response to SS treatment, including miR-10b, miR-17, miR-21 and miR-9, which have been previously implicated in Tumor invasion and metastasis. We confirmed that these miRNA can stimulate Tumor Cell invasion and show that SS can attenuate their invasive effects by downregulating their expression. Employing luciferase and chromatin immunoprecipitation assays, NF-κB was found to bind the promoters of all four miRNAs to suppress their expression at the transcriptional level. We show that SS can inhibit the translocation of NF-κB to the nucleus by decreasing the phosphorylation of IKKβ and IκB. Analysis of the promoter sequences of the miRNAs suppressed by SS revealed that 81 of 115 sequences contained NF-κB-binding sites. These results show that SS can inhibit Tumor Cell invasion by suppressing NF-κB-mediated transcription of miRNAs.
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discovery of colon Tumor Cell growth inhibitory agents through a combinatorial approach
European Journal of Medicinal Chemistry, 2010Co-Authors: Ashraf H Abadi, Gary A Piazza, Bernard D. Gary, Heather N. Tinsley, Dalal A Abouelella, Jochen Lehmann, Mohammed A O AbdelfattahAbstract:Two series with the general formula of 4,6-diaryl-2-oxo-1,2 dihydropyridine-3-carbonitriles and their isosteric 4,6-diaryl-2-imino-1,2-dihydropyridine-3-carbonitrile were synthesized through one pot reaction of the appropriate acetophenone, aldehyde, ammonium acetate with ethyl cyanoacetate or malononitrile, respectively. The synthesized compounds were evaluated for their Tumor Cell growth inhibitory activity against the human HT-29 colon Tumor Cell line, as well as their PDE3 inhibitory activity. Compound 4-(2-Ethoxyphenyl)-2-oxo-6-thiophen-3-yl-1,2-dihydropyridine-3 carbonitrile (21) showed Tumor Cell growth inhibitory activity with an IC50 value of 1.25 microM. Meanwhile, 4-(4-Ethoxyphenyl)-2-imino-6-(thiophen-3-yl)-1,2-dihydropyridine-3-carbonitrile (26) showed inhibitory effect upon PDE3 using cAMP or cGMP as substrate. No correlation exists between PDE3 inhibition and the Tumor Cell growth inhibitory activity. Docking compound 21 to other possible molecular targets showed the potential to bind PIM1 Kinase.
Marjolein Van Egmond - One of the best experts on this subject based on the ideXlab platform.
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targeting fcαri on polymorphonuclear Cells induces Tumor Cell killing through autophagy
Journal of Immunology, 2011Co-Authors: Jantine E Bakema, Robert H J Beelen, Sonja H Ganzevles, Donna Fluitsma, Marco W Schilham, Thomas Valerius, Stefan Lohse, Martin J Glennie, Jan Paul Medema, Marjolein Van EgmondAbstract:Neutrophils are the most abundant circulating FcR-expressing WBCs with potent cytotoxic ability. Currently, they are recognized as promising effector Cells for Ab-mediated immunotherapy of cancer, because their capacity to kill Tumor Cells is greatly enhanced by Tumor Ag-specific mAbs. The FcαRI represents the most potent FcR on neutrophils for induction of Ab-mediated Tumor Cell killing. However, the mechanisms of Cell death that are induced are poorly understood. Because these mechanisms can be used for modulation of anticancer treatment, we investigated the Tumor Cell death induced by neutrophil-mediated Ab-dependent killing via FcαRI. Human mammary carcinoma Cells were efficiently killed when incubated with human neutrophils and Tumor-specific FcαRI bispecific or IgA Abs. Interestingly, we observed characteristics of autophagy such as autophagic structures by electron microscopy and LC3B + autophagosomes in different human epithelial carcinoma Cells, which resulted in Tumor Cell death. To a lesser extent, necrotic features, such as Cellular membrane breakdown and spillage of intraCellular content, were found. By contrast, apoptotic features including fragmented nuclei, Annexin V-positivity, and presence of cleaved caspase-3 were not observed. These findings indicate that neutrophils mainly facilitate autophagy to induce Tumor Cell death rather than the more commonly recognized apoptotic Cell death mechanisms induced by NK Cells or cytotoxic T Cells. This knowledge not only reveals the type of Tumor Cell death induced in neutrophil-mediated, Ab-dependent Cellular cytotoxicity, but importantly opens up additional perspectives for modulation of anticancer therapy in, for example, apoptosis-resistant Tumor Cells.
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immature neutrophils mediate Tumor Cell killing via iga but not igg fc receptors
Journal of Immunology, 2005Co-Authors: Marielle A Otten, Esther Rudolph, Michael Dechant, Cornelis W Tuk, Rogier M Reijmers, Robert H J Beelen, Jan G J Van De Winkel, Marjolein Van EgmondAbstract:AntiTumor Abs are promising therapeutics for cancer. Currently, most Ab-based therapies focus on IgG Ab, which interact with IgG FcR (FcgammaR) on effector Cells. In this study, we examined human and mouse neutrophil-mediated Tumor Cell lysis via targeting the IgA FcR, FcalphaRI (CD89), in more detail. FcalphaRI was the most effective FcR in triggering Tumor Cell killing, and initiated enhanced migration of neutrophils into Tumor colonies. Importantly, immature neutrophils that are mobilized from the bone marrow upon G-CSF treatment efficiently triggered Tumor Cell lysis via FcalphaRI, but proved incapable of initiating Tumor Cell killing via FcgammaR. This may provide a rationale for the disappointing results observed in some earlier clinical trials in which patients were treated with G-CSF and antiTumor Ab-targeting FcgammaR.
John S Condeelis - One of the best experts on this subject based on the ideXlab platform.
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Tumor Cell invadopodia invasive protrusions that orchestrate metastasis
Trends in Cell Biology, 2017Co-Authors: Robert J Eddy, Maxwell D Weidmann, Ved P Sharma, John S CondeelisAbstract:Invadopodia are a subset of invadosomes that are implicated in the integration of signals from the Tumor microenvironment to support Tumor Cell invasion and dissemination. Recent progress has begun to define how Tumor Cells regulate the plasticity necessary for invadopodia to assemble and function efficiently in the different microenvironments encountered during dissemination in vivo . Exquisite mapping by many laboratories of the pathways involved in integrating diverse invadopodium initiation signals, from growth factors, to extraCellular matrix (ECM) and Cell–Cell contact in the Tumor microenvironment, has led to insight into the molecular basis of this plasticity. Here, we integrate this new information to discuss how the invadopodium is an important conductor that orchestrates Tumor Cell dissemination during metastasis.
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multiparametric classification links Tumor microenvironments with Tumor Cell phenotype
PLOS Biology, 2014Co-Authors: Bojana Gligorijevic, Aviv Bergman, John S CondeelisAbstract:While it has been established that a number of microenvironment components can affect the likelihood of metastasis, the link between microenvironment and Tumor Cell phenotypes is poorly understood. Here we have examined microenvironment control over two different Tumor Cell motility phenotypes required for metastasis. By high-resolution multiphoton microscopy of mammary carcinoma in mice, we detected two phenotypes of motile Tumor Cells, different in locomotion speed. Only slower Tumor Cells exhibited protrusions with molecular, morphological, and functional characteristics associated with invadopodia. Each region in the primary Tumor exhibited either fast- or slow-locomotion. To understand how the Tumor microenvironment controls invadopodium formation and Tumor Cell locomotion, we systematically analyzed components of the microenvironment previously associated with Cell invasion and migration. No single microenvironmental property was able to predict the locations of Tumor Cell phenotypes in the Tumor if used in isolation or combined linearly. To solve this, we utilized the support vector machine (SVM) algorithm to classify phenotypes in a nonlinear fashion. This approach identified conditions that promoted either motility phenotype. We then demonstrated that varying one of the conditions may change Tumor Cell behavior only in a context-dependent manner. In addition, to establish the link between phenotypes and Cell fates, we photoconverted and monitored the fate of Tumor Cells in different microenvironments, finding that only Tumor Cells in the invadopodium-rich microenvironments degraded extraCellular matrix (ECM) and disseminated. The number of invadopodia positively correlated with degradation, while the inhibiting metalloproteases eliminated degradation and lung metastasis, consistent with a direct link among invadopodia, ECM degradation, and metastasis. We have detected and characterized two phenotypes of motile Tumor Cells in vivo, which occurred in spatially distinct microenvironments of primary Tumors. We show how machine-learning analysis can classify heterogeneous microenvironments in vivo to enable prediction of motility phenotypes and Tumor Cell fate. The ability to predict the locations of Tumor Cell behavior leading to metastasis in breast cancer models may lead towards understanding the heterogeneity of response to treatment.
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direct visualization of macrophage assisted Tumor Cell intravasation in mammary Tumors
Cancer Research, 2007Co-Authors: Jeffrey B. Wyckoff, Jeffrey E. Segall, Yarong Wang, Jeffrey W Pollard, Sumanta Goswami, Jiu Feng Li, Richard E Stanley, John S CondeelisAbstract:Although the presence of macrophages in Tumors has been correlated with poor prognosis, until now there was no direct observation of how macrophages are involved in hematogenous metastasis. In this study, we use multiphoton microscopy to show, for the first time, that Tumor Cell intravasation occurs in association with perivascular macrophages in mammary Tumors. Furthermore, we show that perivascular macrophages of the mammary Tumor are associated with Tumor Cell intravasation in the absence of local angiogenesis. These results show that the interaction between macrophages and Tumor Cells lying in close proximity defines a microenvironment that is directly involved in the intravasation of cancer Cells in mammary Tumors. [Cancer Res 2007;67(6):2649–56]
Jingying Xu - One of the best experts on this subject based on the ideXlab platform.
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Pediatric brain Tumor Cell lines
Journal of Cellular Biochemistry, 2015Co-Authors: Jingying Xu, Shahab Asgharzadeh, Ashley Margol, Anat Erdreich-epsteinAbstract:Pediatric brain Tumors as a group, including medulloblastomas, gliomas, and atypical teratoid rhabdoid Tumors (ATRT) are the most common solid Tumors in children and the leading cause of death from childhood cancer. Brain Tumor-derived Cell lines are critical for studying the biology of pediatric brain Tumors and can be useful for initial screening of new therapies. Use of appropriate brain Tumor Cell lines for experiments is important, as results may differ depending on Tumor properties, and can thus affect the conclusions and applicability of the model. Despite reports in the literature of over 60 pediatric brain Tumor Cell lines, the majority of published papers utilize only a small number of these Cell lines. Here we list the approximately 60 currently-published pediatric brain Tumor Cell lines and summarize some of their central features as a resource for scientists seeking pediatric brain Tumor Cell lines for their research.
