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Find video protocols related to scientific articles indexed in Pubmed.
DCE-MRI biomarkers for monitoring an anti-angiogenic triple combination therapy in experimental hypopharynx carcinoma xenografts with immunohistochemical validation.
Acta Radiol
PUBLISHED: 03-11-2014
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Novel anti-angiogenic treatments are increasingly complementing established cancer therapy strategies in head and neck tumors. Contrast-enhanced magnetic resonance imaging (MRI) can be applied for early and non-invasive therapy monitoring by non-invasive quantitative assessment of tumor microcirculation as in vivo imaging biomarkers of therapy response.
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Monitoring early response to anti-angiogenic therapy: diffusion-weighted magnetic resonance imaging and volume measurements in colon carcinoma xenografts.
PLoS ONE
PUBLISHED: 01-01-2014
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To evaluate the use of diffusion-weighted MRI (DW-MRI) and volume measurements for early monitoring of antiangiogenic therapy in an experimental tumor model.
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Stem Cell-Like Side Populations in Esophageal Cancer: A Source of Chemotherapy Resistance and Metastases.
Stem Cells Dev.
PUBLISHED: 11-13-2013
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Dye-effluxing side population (SP) cells can be resistant to chemotherapy and are thought to resemble cancer stem cells. We characterized the relevance of the SP subpopulation in esophageal cancer cell lines and their relation to chemotherapy resistance and metastasis. The SP subpopulation was detected using Hoechst 33342 staining in five esophageal cancer cell lines OE19, OE21, OE33, PT1590, and LN1590. CTx-resistant cell lines were developed after long-term exposure to 5-fluorouracil (5-FU) and cisplatin and validated by analysis of resistance markers, thymidylate synthase and ERCC1. While neither LN1590 nor PT1590 had detectable SP cells, OE19, OE21, and OE33?cells were found to contain varying levels of SP cells. With increasing duration of 5-FU or cisplatin therapy, the SP subpopulation substantially emerged in PT1590 and LN1590. OE19-SP cells displayed significant higher tumorigenicity than OE19- non-SP (NSP) cells after subcutaneous tumor cell injection in vivo. SP cells isolated from OE19 and OE19/5-FUres were subsequently analyzed by an epithelial-to-mesenchymal transition (EMT) polymerase chain reaction array. Interestingly, the SP fraction of OE19/5-FUres showed a dramatic upregulation of EMT-related genes compared to the SP fraction of OE19. Our results provide evidence that (1) the proportion of SP cells is different in esophageal cancer, (2) SP cells exhibit stem cell properties and are associated to chemotherapy resistance, and (3) long-term CTx selects for SP cells with an upregulated EMT gene profile, which might be the source of systemic disease relapse. Further investigations are necessary to ideally target these EMT-associated SP cells in esophageal cancer.
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Regorafenib effects on human colon carcinoma xenografts monitored by dynamic contrast-enhanced computed tomography with immunohistochemical validation.
PLoS ONE
PUBLISHED: 01-01-2013
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To investigate dynamic contrast-enhanced computed tomography for monitoring the effects of regorafenib on experimental colon carcinomas in rats by quantitative assessments of tumor microcirculation parameters with immunohistochemical validation.
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Kinases as targets in the treatment of solid tumors.
Cell. Signal.
PUBLISHED: 01-13-2010
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The protein kinase family, one of the largest gene families in eukaryotes, plays an important role in regulating various cellular processes such as cell proliferation, cell death, cell cycle progression, differentiation and cell survival. Therefore, it is not surprising that the deregulation of many kinases is usually directly linked to cancer development. In all solid tumors, changes in protein kinase expression levels and activities, as well as alterations in the degree of posttranslational modifications can contribute to cancer development. Consequently, the identification of molecular targets and signaling pathways specific to cancer cells is becoming more and more important for cancer drug development and cancer therapies. Inhibition of various protein kinases has already been investigated in many pre-clinical and clinical trials targeting all stages of signal transduction, demonstrating promising results in cancer therapy. Conventional chemotherapeutics are often ineffective as well as harmful; hence a combination of both chemotherapeutics and protein kinase inhibitors may result in new and more successful therapeutic approaches. In this review we focus on protein kinases involved in different signaling pathways and their alterations in solid tumors.
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Analysis of cell type-specific expression of CK1 epsilon in various tissues of young adult BALB/c Mice and in mammary tumors of SV40 T-Ag-transgenic mice.
J. Histochem. Cytochem.
PUBLISHED: 09-15-2009
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Casein kinase 1 epsilon (CK1epsilon) is involved in various cellular processes, including cell growth, differentiation, and apoptosis, vesicle transport, and control of the circadian rhythm. Deregulation of CK1epsilon has been linked to neurodegenerative diseases and cancer. To better understand the cell type-specific functions of CK1epsilon, we determined its localization by immunhistochemistry in tissues of healthy, young adult BALB/c mice and in mammary tumors of SV40 T-antigen-transgenic mice. CK1epsilon expression was found to be highly regulated in normal tissues of endodermal, mesodermal, and ectodermal origin and in neoplastic tissue of mammary cancer. The data presented here give an overview of CK1epsilon reactivity in different organs under normal conditions and outline changes in its expression in mammary carcinomas. Our data suggest a cell/organ type-specific function of CK1epsilon and indicate that tumorigenic conversion of mammary glands in SV40 T-antigen-transgenic mice leads to downregulation of CK1epsilon. This manuscript contains online supplemental material at http://www.jhc.org. Please visit this article online to view these materials.
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3,4-Diaryl-isoxazoles and -imidazoles as potent dual inhibitors of p38alpha mitogen activated protein kinase and casein kinase 1delta.
J. Med. Chem.
PUBLISHED: 07-14-2009
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In this study, we report on the discovery of isoxazole 1 as a potent dual inhibitor of p38alpha (IC(50) = 0.45 microM) and CK1delta (IC(50) = 0.23 microM). Because only a few effective small molecule inhibitors of CK1 have been described so far, we aimed to develop this structural class toward specific agents. Molecular modeling studies comparing p38alpha/CK1delta suggested an optimization strategy leading to design, synthesis, biological characterization, and SAR of highly potent compounds including 9 (IC(50) p38alpha = 0.006 microM; IC(50) CK1delta = 1.6 microM), 13 (IC(50) p38alpha = 2.52 microM; IC(50) CK1delta = 0.033 microM), 17 (IC(50) p38alpha = 0.019 microM; IC(50) CK1delta = 0.004 microM; IC(50) CK1epsilon = 0.073 microM), and 18 (CKP138) (IC(50) p38alpha = 0.041 microM; IC(50) CK1delta = 0.005 microM; IC(50) CK1epsilon = 0.447 microM) possessing differentiated specificity. Selected compounds were profiled over 76 kinases and evaluation of their cellular efficacy showed 18 (CKP138) to be a highly potent and dual-specific inhibitor of CK1delta and p38alpha.
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Immunohistochemical characterisation of cell-type specific expression of CK1delta in various tissues of young adult BALB/c mice.
PLoS ONE
PUBLISHED: 01-12-2009
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Casein kinase 1 delta (CK1delta) phosphorylates many key proteins playing important roles in such biological processes as cell growth, differentiation, apoptosis, circadian rhythm and vesicle transport. Furthermore, deregulation of CK1delta has been linked to neurodegenerative diseases and cancer. In this study, the cell specific distribution of CK1delta in various tissues and organs of young adult BALB/c mice was analysed by immunohistochemistry.
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Impaired CK1 delta activity attenuates SV40-induced cellular transformation in vitro and mouse mammary carcinogenesis in vivo.
PLoS ONE
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Simian virus 40 (SV40) is a powerful tool to study cellular transformation in vitro, as well as tumor development and progression in vivo. Various cellular kinases, among them members of the CK1 family, play an important role in modulating the transforming activity of SV40, including the transforming activity of T-Ag, the major transforming protein of SV40, itself. Here we characterized the effects of mutant CK1? variants with impaired kinase activity on SV40-induced cell transformation in vitro, and on SV40-induced mammary carcinogenesis in vivo in a transgenic/bi-transgenic mouse model. CK1? mutants exhibited a reduced kinase activity compared to wtCK1? in in vitro kinase assays. Molecular modeling studies suggested that mutation N172D, located within the substrate binding region, is mainly responsible for impaired mutCK1? activity. When stably over-expressed in maximal transformed SV-52 cells, CK1? mutants induced reversion to a minimal transformed phenotype by dominant-negative interference with endogenous wtCK1?. To characterize the effects of CK1? on SV40-induced mammary carcinogenesis, we generated transgenic mice expressing mutant CK1? under the control of the whey acidic protein (WAP) gene promoter, and crossed them with SV40 transgenic WAP-T-antigen (WAP-T) mice. Both WAP-T mice as well as WAP-mutCK1?/WAP-T bi-transgenic mice developed breast cancer. However, tumor incidence was lower and life span was significantly longer in WAP-mutCK1?/WAP-T bi-transgenic animals. The reduced CK1? activity did not affect early lesion formation during tumorigenesis, suggesting that impaired CK1? activity reduces the probability for outgrowth of in situ carcinomas to invasive carcinomas. The different tumorigenic potential of SV40 in WAP-T and WAP-mutCK1?/WAP-T tumors was also reflected by a significantly different expression of various genes known to be involved in tumor progression, specifically of those involved in wnt-signaling and DNA repair. Our data show that inactivating mutations in CK1? impair SV40-induced cellular transformation in vitro and mouse mammary carcinogenesis in vivo.
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What is Visualize?

JoVE Visualize is a tool created to match the last 5 years of PubMed publications to methods in JoVE's video library.

How does it work?

We use abstracts found on PubMed and match them to JoVE videos to create a list of 10 to 30 related methods videos.

Video X seems to be unrelated to Abstract Y...

In developing our video relationships, we compare around 5 million PubMed articles to our library of over 4,500 methods videos. In some cases the language used in the PubMed abstracts makes matching that content to a JoVE video difficult. In other cases, there happens not to be any content in our video library that is relevant to the topic of a given abstract. In these cases, our algorithms are trying their best to display videos with relevant content, which can sometimes result in matched videos with only a slight relation.