Influence of growth environment on the ganglioside composition of an experimental mouse brain tumor

1994 ◽  
Vol 21 (2-3) ◽  
pp. 273-285 ◽  
Author(s):  
Mohga El-Abbadi ◽  
Thomas N. Seyfried
Keyword(s):  
Brain Tumor ◽  
Mouse Brain ◽  
Growth Environment ◽  
Experimental Mouse ◽  
Ganglioside Composition

Immune gene therapy of experimental mouse brain tumor with adenovirus-mediated gene transfer of murine interleukin-4

2000 ◽  
Vol 49 (1) ◽  
pp. 23-33 ◽  
Author(s):  
Koichi Yoshikawa ◽  
Koji Kajiwara ◽  
Makoto Ideguchi ◽  
Tetsuya Uchida ◽  
Haruhide Ito
Keyword(s):  
Gene Therapy ◽  
Brain Tumor ◽  
Gene Transfer ◽  
Mouse Brain ◽  
Interleukin 4 ◽  
Immune Gene ◽  
Experimental Mouse

Ganglioside composition of a mouse brain tumor grown in the severe combined immunodeficiency (SCID) mouse

1998 ◽  
Vol 33 (1) ◽  
pp. 27-37 ◽  
Author(s):  
Thomas N. Seyfried ◽  
Mohga El-Abbadi ◽  
Jeffrey A. Ecsedy ◽  
Mary E. Griffin ◽  
Herbert C. Yohe
Keyword(s):  
Brain Tumor ◽  
Mouse Brain ◽  
Scid Mouse ◽  
Severe Combined Immunodeficiency ◽  
Combined Immunodeficiency ◽  
Ganglioside Composition

scholarly journals Heme oxygenase-1 protects regulatory T cells from hypoxia-induced cellular stress in an experimental mouse brain tumor model

2014 ◽  
Vol 266 (1-2) ◽  
pp. 33-42 ◽  
Author(s):  
Mahua Dey ◽  
Alan L. Chang ◽  
Derek A. Wainwright ◽  
Atique U. Ahmed ◽  
Yu Han ◽  
...  
Keyword(s):  
T Cells ◽  
Brain Tumor ◽  
Regulatory T Cells ◽  
Mouse Brain ◽  
Heme Oxygenase ◽  
Cellular Stress ◽  
Tumor Model ◽  
Heme Oxygenase 1 ◽  
Brain Tumor Model ◽  
Experimental Mouse

scholarly journals Examination of blood–brain barrier (BBB) integrity in a mouse brain tumor model

2012 ◽  
Vol 111 (2) ◽  
pp. 133-143 ◽  
Author(s):  
Ngoc H. On ◽  
Ryan Mitchell ◽  
Sanjot D. Savant ◽  
Corbin. J. Bachmeier ◽  
Grant M. Hatch ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Blood Brain Barrier ◽  
Mouse Brain ◽  
Tumor Model ◽  
Brain Barrier ◽  
Blood Brain ◽  
Brain Tumor Model

scholarly journals Stemness of the CT-2A Immunocompetent Mouse Brain Tumor Model: Characterization In Vitro

2012 ◽  
Vol 3 ◽  
pp. 166-174 ◽  
Author(s):  
Emanuela Binello ◽  
Zulekha A. Qadeer ◽  
Harini P. Kothari ◽  
Luni Emdad ◽  
Isabelle M. Germano
Keyword(s):  
Brain Tumor ◽  
Mouse Brain ◽  
Tumor Model ◽  
Immunocompetent Mouse ◽  
Brain Tumor Model

scholarly journals Comprehensive genomic profiling of glioblastoma tumors, BTICs, and xenografts reveals stability and adaptation to growth environments

2019 ◽  
Vol 116 (38) ◽  
pp. 19098-19108 ◽  
Author(s):  
Yaoqing Shen ◽  
Cameron J. Grisdale ◽  
Sumaiya A. Islam ◽  
Pinaki Bose ◽  
Jake Lever ◽  
...  
Keyword(s):  
Brain Tumor ◽  
Massively Parallel Sequencing ◽  
Treatment Options ◽  
Culture Conditions ◽  
Model Systems ◽  
Sample Type ◽  
Tumor Initiating Cells ◽  
Growth Environment

Glioblastoma multiforme (GBM) is the most deadly brain tumor, and currently lacks effective treatment options. Brain tumor-initiating cells (BTICs) and orthotopic xenografts are widely used in investigating GBM biology and new therapies for this aggressive disease. However, the genomic characteristics and molecular resemblance of these models to GBM tumors remain undetermined. We used massively parallel sequencing technology to decode the genomes and transcriptomes of BTICs and xenografts and their matched tumors in order to delineate the potential impacts of the distinct growth environments. Using data generated from whole-genome sequencing of 201 samples and RNA sequencing of 118 samples, we show that BTICs and xenografts resemble their parental tumor at the genomic level but differ at the mRNA expression and epigenomic levels, likely due to the different growth environment for each sample type. These findings suggest that a comprehensive genomic understanding of in vitro and in vivo GBM model systems is crucial for interpreting data from drug screens, and can help control for biases introduced by cell-culture conditions and the microenvironment in mouse models. We also found that lack of MGMT expression in pretreated GBM is linked to hypermutation, which in turn contributes to increased genomic heterogeneity and requires new strategies for GBM treatment.

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