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Expression von SDF-1/CXCL12 und CXCR4 in der sequenziellen DMBA-induzierten Karzinogenese des Hamsters / Expression of SDF-1/CXCL12 and CXCR4 in the sequentially DMBA induced carcinogenesis in a hamster modelNadenau, Eva 16 March 2015 (has links)
No description available.
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Molecular Mechanisms Associated with Chromosomal and Microsatellite Instability in Sporadic Glioblastoma multiformeMartinez, Ramon, Schackert, Hans-K., Plaschke, Jens, Baretton, Gustavo, Appelt, Hella, Schackert, Gabriele 12 February 2014 (has links) (PDF)
Objective: Two chromosomal instability (CIN) pathways are described in glioblastoma multiforme (GBM), type 1 and type 2, which can be observed in up to 70% of the cases. Microsatellite instability (MSI) plays a pathogenic role in sporadic cancers such as colon, gastric and endometrial carcinomas with deficient mismatch repair (MMR). We aimed to perform a comprehensive analysis of the relationship between CIN and MSI mechanisms in sporadic glioblastomas.
Methods: 129 GBMs were examined (109 newly diagnosed and 20 relapses) investigating MSI, immunohistochemical expression of MMR proteins as well as sequencing and promoter methylation of hMLH1. We characterized the molecular changes frequently correlated with CIN in MSI+ GBMs and compared them with 26 microsatellite-stable tumors.
Results: Low-level MSI was observed in 11 of 129 (8.5%) cases and was higher in relapses than in primary GBMs (25 vs. 5.5%, p = 0.027). High-level MSI was not found in any case. A deficient expression of MLH1 and PMS2 without hMLH1 inactivation was observed only in one giant cell GBM. 55% of the MSI+ GBMs showed a profile which did not correspond to one of the known CIN pathways. An inverse association was observed between MSI and mutations of both p53 and PTEN.
Conclusions: Our data suggest that CIN and MSI contribute to the genomic instability in GBMs via independent pathways. Since MSI was significantly more frequent in relapses, it might play a role in the malignant progression of GBM. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Molecular Mechanisms Associated with Chromosomal and Microsatellite Instability in Sporadic Glioblastoma multiformeMartinez, Ramon, Schackert, Hans-K., Plaschke, Jens, Baretton, Gustavo, Appelt, Hella, Schackert, Gabriele January 2004 (has links)
Objective: Two chromosomal instability (CIN) pathways are described in glioblastoma multiforme (GBM), type 1 and type 2, which can be observed in up to 70% of the cases. Microsatellite instability (MSI) plays a pathogenic role in sporadic cancers such as colon, gastric and endometrial carcinomas with deficient mismatch repair (MMR). We aimed to perform a comprehensive analysis of the relationship between CIN and MSI mechanisms in sporadic glioblastomas.
Methods: 129 GBMs were examined (109 newly diagnosed and 20 relapses) investigating MSI, immunohistochemical expression of MMR proteins as well as sequencing and promoter methylation of hMLH1. We characterized the molecular changes frequently correlated with CIN in MSI+ GBMs and compared them with 26 microsatellite-stable tumors.
Results: Low-level MSI was observed in 11 of 129 (8.5%) cases and was higher in relapses than in primary GBMs (25 vs. 5.5%, p = 0.027). High-level MSI was not found in any case. A deficient expression of MLH1 and PMS2 without hMLH1 inactivation was observed only in one giant cell GBM. 55% of the MSI+ GBMs showed a profile which did not correspond to one of the known CIN pathways. An inverse association was observed between MSI and mutations of both p53 and PTEN.
Conclusions: Our data suggest that CIN and MSI contribute to the genomic instability in GBMs via independent pathways. Since MSI was significantly more frequent in relapses, it might play a role in the malignant progression of GBM. / Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Regulation von Connexinen als Gap-Junction-Strukturprotein in der sequenziellen Karzinogenese des DMBA-induzierten Wangentaschenkarzinoms des Hamsters / Regulation of connexins as structure proteins of gap junctions in the sequential carcinogenesis of the DMBA-induced cheek pouch carcinoma of hamstersHillebrand, Rebekka Simone 07 August 2013 (has links)
Da vorliegende Studien unserer Arbeitsgruppe auf eine Beteiligung von Connexinen an der oralen Plattenepithelkarzinogenese hindeuten, war es Ziel dieser Arbeit in-vivo am Hamstermodell die Expression der Connexine 26, 43 und 45 im Verlauf der Karzinogenese zu untersuchen.
Die durch 9,10-Dimethyl-1,2-Benzanthrazen (DMBA) induzierten Karzinome wurden makroskopisch, histologisch, sowie auf ihren Inflammationsgrad hin untersucht, um die Effektivität des Tiermodells zu prüfen. Weiterhin erfolgte sie Genexpressionsanalyse mittels RNA-Isolation, PCR-Analyse und statistischer Auswertung.
Es konnte insgesamt gezeigt werden, dass die Applikation von DMBA in Abhängigkeit von Behandlungsdauer makroskopisch, histologisch und inflammatorisch einen deutlichen karzinogenen Effekt hatte und, dass das histopathologische Grading signifikant mit der Länge der Behandlungsdauer korrelierte. Im Rahmen der Genexpressionsanalyse konnte im Verlauf der DMBA-Behandlung für Connexin 26 und 45 eine signifikante Überexpression beschrieben werden. Connexin 43 zeigte sich als nicht differentiell exprimiert. Ein Zusammenhang zwischen histologischem Grading und Genexpression war nicht nachvollziehbar.
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Mathematical modeling of oncogenesis control in mature T-cell populationsGerdes, Sebastian, Newrzela, Sebastian, Glauche, Ingmar, von Laer, Dorothee, Hansmann, Martin-Leo, Röder, Ingo 06 February 2014 (has links) (PDF)
T-cell receptor (TCR) polyclonal mature T cells are surprisingly resistant to oncogenic transformation after retroviral insertion of T-cell oncogenes. In a mouse model, it has been shown that mature T-cell lymphoma/leukemia (MTCLL) is not induced upon transplantation of mature, TCR polyclonal wild-type (WT) T cells, transduced with gammaretroviral vectors encoding potent T-cell oncogenes, into RAG1-deficient recipients. However, further studies demonstrated that quasi-monoclonal T cells treated with the same protocol readily induced MTCLL in the recipient mice. It has been hypothesized that in the TCR polyclonal situation, outgrowth of preleukemic cells and subsequent conversion to overt malignancy is suppressed through regulation of clonal abundances on a per-clone basis due to interactions between TCRs and self-peptide-MHC-complexes (spMHCs), while these mechanisms fail in the quasi-monoclonal situation. To quantitatively study this hypothesis, we applied a mathematical modeling approach. In particular, we developed a novel ordinary differential equation model of T-cell homeostasis, in which T-cell fate depends on spMHC-TCR-interaction-triggered stimulatory signals from antigen-presenting cells (APCs). Based on our mathematical modeling approach, we identified parameter configurations of our model, which consistently explain the observed phenomena. Our results suggest that the preleukemic cells are less competent than healthy competitor cells in acquiring survival stimuli from APCs, but that proliferation of these preleukemic cells is less dependent on survival stimuli from APCs. These predictions now call for experimental validation.
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"Eine vergleichende Genexpressionsanalyse von Gap- Junction- Strukturproteinen in oralen Plattenepithelkarzinomen und gesunder Schleimhaut" / A comparative gene expression study of gap-junction proteins in oral squamous cell carcinomas and normal mucosaBrodmann, Tobias 23 April 2012 (has links)
No description available.
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Mathematical modeling of oncogenesis control in mature T-cell populationsGerdes, Sebastian, Newrzela, Sebastian, Glauche, Ingmar, von Laer, Dorothee, Hansmann, Martin-Leo, Röder, Ingo 06 February 2014 (has links)
T-cell receptor (TCR) polyclonal mature T cells are surprisingly resistant to oncogenic transformation after retroviral insertion of T-cell oncogenes. In a mouse model, it has been shown that mature T-cell lymphoma/leukemia (MTCLL) is not induced upon transplantation of mature, TCR polyclonal wild-type (WT) T cells, transduced with gammaretroviral vectors encoding potent T-cell oncogenes, into RAG1-deficient recipients. However, further studies demonstrated that quasi-monoclonal T cells treated with the same protocol readily induced MTCLL in the recipient mice. It has been hypothesized that in the TCR polyclonal situation, outgrowth of preleukemic cells and subsequent conversion to overt malignancy is suppressed through regulation of clonal abundances on a per-clone basis due to interactions between TCRs and self-peptide-MHC-complexes (spMHCs), while these mechanisms fail in the quasi-monoclonal situation. To quantitatively study this hypothesis, we applied a mathematical modeling approach. In particular, we developed a novel ordinary differential equation model of T-cell homeostasis, in which T-cell fate depends on spMHC-TCR-interaction-triggered stimulatory signals from antigen-presenting cells (APCs). Based on our mathematical modeling approach, we identified parameter configurations of our model, which consistently explain the observed phenomena. Our results suggest that the preleukemic cells are less competent than healthy competitor cells in acquiring survival stimuli from APCs, but that proliferation of these preleukemic cells is less dependent on survival stimuli from APCs. These predictions now call for experimental validation.
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