Primary and Secondary Events in Oncogene-Driven Tumor Development: Lessons from Transgenic Model Systems

2003 ◽  
pp. 245-294
Author(s):  
Michaela Herzig ◽  
Gerhard Christofori
Keyword(s):  
Tumor Development ◽  
Model Systems ◽  
Transgenic Model

TMOD-02. GENERATION OF A NOVEL MOUSE MODEL FOR BRAIN TUMORS OF THE DNA METHYLATION CLASS “GBM MYCN”

2021 ◽  
Vol 23 (Supplement_6) ◽  
pp. vi215-vi216
Author(s):  
Melanie Schoof ◽  
Carolin Göbel ◽  
Dörthe Holdhof ◽  
Sina Al-Kershi ◽  
Ulrich Schüller
Keyword(s):  
Dna Methylation ◽  
Brain Tumors ◽  
Molecular Mechanisms ◽  
Treatment Options ◽  
Tumor Development ◽  
Model Systems ◽  
Preclinical Research ◽  
Human Gbm

Abstract DNA methylation based classification of brain tumors has revealed a high heterogeneity between tumors and led to the description of multiple distinct subclasses. The increasing subdivision of tumors can help to understand molecular mechanisms of tumor development and to improve therapy if appropriate model systems for preclinical research are available. Multiple recent publications have described a subgroup of pediatric glioblastoma which is clearly separable from other pediatric and adult glioblastoma in its DNA methylation profile (GBM MYCN). Many cases in this group are driven by MYCN amplifications and harbor TP53 mutations. These tumors almost exclusively occur in children and were further described as highly aggressive with a median overall survival of only 14 months. In order to further investigate the biology and treatment options of these tumors, we generated hGFAP-cre::TP53 Fl/Fl ::lsl-MYCN mice. These mice carry a loss of TP53 and show aberrant MYCN expression in neural precursors of the central nervous system. The animals develop large forebrain tumors within the first 80 days of life with 100 % penetrance. These tumors resemble human GBM MYCN tumors histologically and are sensitive to AURKA and ATR inhibitors in vitro. We believe that further characterization of the model and in vivo treatment studies will pave the way to improve treatment of patients with these highly aggressive tumors.

scholarly journals Study оf dCTCF insulator activity in Drosophila melanogaster model systems

2019 ◽  
Vol 486 (2) ◽  
pp. 262-266
Author(s):  
N. E. Postika ◽  
T. A. Ivlieva ◽  
P. G. Georgiev ◽  
O. V. Kyrchanova
Keyword(s):  
Drosophila Melanogaster ◽  
Binding Sites ◽  
Model Systems ◽  
Transgenic Model ◽  
Insulator Activity ◽  
Architectural Proteins ◽  
Protein Functions ◽  
Architectural Protein

Using Drosophila transgenic model systems, we have shown that the four binding sites for the architectural protein dCTCF themselves have no insulator activity. They cannot block enhancers and protect from Polycomb-dependent repression. The results suggest that in the known Drosophila insulators, the dCTCF protein functions in cooperation with other architectural proteins.

JP-8 jet fuel exposure potentiates tumor development in two experimental model systems

2007 ◽  
Vol 23 (10) ◽  
pp. 617-623 ◽  
Author(s):  
DT Harris ◽  
D Sakiestewa ◽  
D Titone ◽  
X He ◽  
J Hyde ◽  
...  
Keyword(s):  
Experimental Model ◽  
Tumor Development ◽  
Jet Fuel ◽  
Model Systems ◽  
Experimental Model Systems

Abstract B17: Genetic deletion of sphingosine kinase 1 suppresses mouse breast tumor development in MMTV-neu transgenic model

2016 ◽  
Author(s):  
Yoshiko Shimizu ◽  
Hideki Furuya ◽  
Paulette M. Tamashiro ◽  
Steve Goodison ◽  
Owen Chan ◽  
...  
Keyword(s):  
Breast Tumor ◽  
Tumor Development ◽  
Sphingosine Kinase ◽  
Sphingosine Kinase 1 ◽  
Transgenic Model ◽  
Genetic Deletion

scholarly journals Genetic deletion of sphingosine kinase 1 suppresses mouse breast tumor development in an HER2 transgenic model

2017 ◽  
Vol 39 (1) ◽  
pp. 47-55 ◽  
Author(s):  
Yoshiko Shimizu ◽  
Hideki Furuya ◽  
Paulette M Tamashiro ◽  
Kayoko Iino ◽  
Owen T M Chan ◽  
...  
Keyword(s):  
Breast Tumor ◽  
Tumor Development ◽  
Sphingosine Kinase ◽  
Sphingosine Kinase 1 ◽  
Transgenic Model ◽  
Genetic Deletion

Altered thymic epithelial cells may be decisive for Moloney virus-induced lymphoma development

1983 ◽  
Vol 41 ◽  
pp. 784-785
Author(s):  
U.I. Heine ◽  
G.R.F. Krueger ◽  
E. Munoz ◽  
A. Karpinski
Keyword(s):  
Epithelial Cells ◽  
Leukemia Virus ◽  
Light And Electron Microscopy ◽  
Tumor Development ◽  
Current Evidence ◽  
Thymic Epithelial Cells ◽  
Thymic Tissue ◽  
Newborn Mice ◽  
Moloney Leukemia Virus ◽  
Differentiation Block

Infection of newborn mice with Moloney leukemia virus (M-MuLV) causes a T-cell differentiation block in the thymic cortex accompanied by proliferation and accumulation of prethymic lymphoblasts in the thymus and subsequent spreading of these cells to generate systemic lymphoma. Current evidence shows that thymic reticular epithelial cells (REC) provide a microenvironment necessary for the maturation of prethymic lymphoblasts to mature T-lymphocytes by secretion of various thymic factors. A change in that environment due to infection of REC by virus could be decisive for the failure of lymphoblasts to mature and thus contribute to lymphoma development.We have studied the morphology and distribution of the major thymic cell populations at different stages of tumorigenesis in Balb/c mice infected when newborn with 0.2ml M-MuLV suspension, 6.8 log FFU/ml. Thymic tissue taken at 1-2 weekly intervals up to tumor development was processed for light and electron microscopy, using glutaraldehyde-OsO4fixation and Epon-Araldite embedding.

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