Global ETD Search

1	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 model Nadenau, Eva 16 March 2015 (has links) No description available. 610 Plattenepithelkarzinom CXCL12 CXCR4 DMBA induzierte Karzinogenese Expression CXCL12 CXCR4 CXCL12 CXCR4 CXCL12/ CXCR4 DMBA induced Carcinogenesis expression of CXCL12 CXCR4 oral cancer Kieferchirurgie (PPN619876387)
2	Molecular Mechanisms Associated with Chromosomal and Microsatellite Instability in Sporadic Glioblastoma multiforme Martinez, 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. Glioblastom Glioblastoma multiforme Tumor Karzinogenese Tumorentwicklung Mismatch-Reparatur chromosomale Instabilität Glioblastoma multiforme Tumorigenesis Mismatch repair Chromosomal instability ddc:610 rvk:XA 10000
3	Molecular Mechanisms Associated with Chromosomal and Microsatellite Instability in Sporadic Glioblastoma multiforme Martinez, 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. info:eu-repo/classification/ddc/610 ddc:610
4	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 hamsters Hillebrand, 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. 610 Karzinogenese Expression Connexin oral Plattenepithelkarzinom Hamster Gap Junction Dimethyl-1,2-Benzanthracen DMBA carcinogenesis expression connexin oral squamous cell carcinoma hamster gap junction dimethyl-1,2-benzanthracen DMBA Medizin (PPN619874732)
5	Mathematical modeling of oncogenesis control in mature T-cell populations Gerdes, 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. T-Zellen Karzinogenese Tumorentwicklung T-Zell-Leukämie TU Dresden Publikationsfonds T-cell homeostasis T-cell niche gene therapy MTCL oncogenesis control T-cell receptor mature T-cell lymphoma/leukemia Technical University Dresden Publication funds ddc:610 rvk:XA 10000
6	"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 mucosa Brodmann, Tobias 23 April 2012 (has links) No description available. 610 Medizin, Gesundheit Medicine Connexin Connexine Gap Junction oral;Plattenepithelkarzinom PEC Genexpression Expression Karzinogenese GJIC Cx 45 Cx 26 Connexin 45 Connexin 26 connexin connexins gap junction GJIC Cx 45 Cx 26 Cx-45 Cx-26 oral squamous cell carcinoma carcinogenesis OSCC gene expression comparative gene expression 44.81 MED 000: Medizin
7	Mathematical modeling of oncogenesis control in mature T-cell populations Gerdes, 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. info:eu-repo/classification/ddc/610 ddc:610

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