Glioblastoma Xenograft Comparative Genomic Hybridization Arrays
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Brock Armstrong
PROVIDER: E-GEOD-38815 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE38814: Glioblastoma Orthotopic Xenograft Transcriptome GSE38815: Glioblastoma Xenograft Comparative Genomic Hybridization Arrays Refer to individual Series
2012-07-10 | E-GEOD-39242 | biostudies-arrayexpress
Project description:Transcriptional profiling of glioblastoma orthotopic xenografts Descriptive experiment, comparison of 39 glioblastoma tumors as orthotopic xenografts
2012-07-10 | E-GEOD-38814 | biostudies-arrayexpress
Project description:Transcriptional profiling of glioblastoma orthotopic xenografts
2012-07-11 | GSE38814 | GEO
Project description:Frequent discrepancies between preclinical and clinical results of anti-cancer agents demand a reliable translational platform that can precisely recapitulate the biology of human cancers. Another critical unmet need is the ability to predict therapeutic responses for individual patients. Toward this goal, we have established a library of orthotopic glioblastoma (GBM) xenograft models using surgical samples of GBM patients. These patient-specific GBM xenograft tumors recapitulate histopathological properties and maintain genomic characteristics of parental GBMs in situ. Furthermore, in vivo irradiation, chemotherapy, and targeted therapy of these xenograft tumors mimic the treatment response of parental GBMs. We also found that establishment of orthotopic xenograft models portends poor prognosis of GBM patients and identified the gene signatures and pathways signatures associated with the clinical aggressiveness of GBMs. Together, the patient-specific orthotopic GBM xenograft library represent the preclinically and clinically valuable “patient tumor’s phenocopy” that represents molecular and functional heterogeneity of GBMs. aCGH experiments were performed for a human glioblastoma tissue (sample ID: PC-NS08-559) and the matching xenograft tumor tissue using the Agilent Human Whole Genome CGH 244K microarray according to manufacturer's protocol (2-color).
2013-01-18 | E-GEOD-42577 | biostudies-arrayexpress
Project description:DNA copy number profiling of 32 glioblastoma orthotopic xenografts
2012-07-11 | GSE38815 | GEO
Project description:This project describes the establishment and validation of a murine orthotopic xenograft model using fresh human tumor samples that recapitulates the critical components of human pancreatic adenocarcinoma. The authors discuss the proven and theoretical advantages of the model as well as future translational implications. Background: Relevant preclinical models that recapitulate the key features of human pancreatic ductal adenocarcinoma (PDAC) are needed in order to provide biologically tractable models to probe disease progression and therapeutic responses and ultimately improve patient outcomes for this disease. Here, we describe the establishment and clinical, pathological, molecular and genetic validation of a murine, orthotopic xenograft model of PDAC. Methods: Human PDACs were resected and orthotopically implanted and propagated in immunocompromised mice. Patient survival was correlated with xenograft growth and metastatic rate in mice. Human and mouse tumor pathology were compared. Tumors were analyzed for genetic mutations, gene expression, receptor tyrosine kinase (RTK) activation, and cytokine expression. Results: Fifteen human PDACs were propagated orthotopically in mice. Xenografts developed peritoneal and liver metastases. Time to growth and metastatic efficiency in mice each correlated with patient survival. Tumor architecture, nuclear grade and stromal content were similar in patient and xenografted tumors. Propagated tumors closely exhibited the genetic and molecular features known to characterize pancreatic cancer (e.g. high rate of KRAS, p53, SMAD4 mutation and EGFR activation). The correlation coefficient of gene expression between patient tumors and xenografts propagated through multiple generations was 93 to 99%. Analysis of gene expression demonstrated distinct differences between xenografts from fresh patient tumors versus commercially available PDAC cell lines. Conclusions: Our orthotopic xenograft model derived from fresh human PDACs closely recapitulates the clinical, pathologic, genetic and molecular aspects of human disease. This model has resulted in the identification of rational therapeutic strategies to be tested in clinical trials and will permit additional therapeutic approaches and identification of biomarkers of response to therapy. 47 Samples in total were generated for normal pancreatic tissue in patients, pancreatic tumors in patients, pancreatic tumors propagated in a mouse xenograft model, and pancreatic cancer cell lines in vitro. Clustering analysis was performed to evaluate the differences between patient tumors, xenograft tumors, established cancer cell lines, and cell lines derived from xenografts.
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Project description:This SuperSeries is composed of the following subset Series: GSE25690: Global analysis of mRNA expression in prospectively purified human prostate orthotopic xenograft tumor cells with varying S/TFE. GSE25691: Global analysis of miRNA expression in prospectively purified human prostate orthotopic xenograft tumor cells with varying S/TFE. Refer to individual Series
2010-12-06 | E-GEOD-25692 | biostudies-arrayexpress
Project description:Characterization of gene expression for a panel of 50 in vitro and in vivo models of glioblastoma (GBM). Models include subcutaneously established xenograft lines, orthotopically grown subcutaneously established xenograft lines, serum derived cell lines and stem cell media derived cell lines. Multiple replicates of each line were run on different dates to determine the effect of batch and processing date on reproducibility of gene expression profiles 117 samples analyzed from 50 distinct GBM xenografts or cell lines. Biological replicates from the same passage number were included for many, but not all, of the lines.
2011-12-01 | E-GEOD-26344 | biostudies-arrayexpress
Project description:Treatment with ionizing irradiation (IR) may lead to accumulation of tumor-infiltrating T regulatory (Treg) cells and subsequent tumor resistance to radiotherapy. Here we focused on the contribution of Langerhans cells (LCs) to this phenomenon because of their unique ability to resist depletion by high-dose IR. We found that LCs resisted apoptosis and rapidly repaired DNA damage post-IR. Particularly, we found that p21 was overexpressed in LCs, and that p21-deficient LCs underwent apoptosis and accumulated DNA damage following IR treatment. Wild-type, but not p21-deficient, LCs upregulated major histocompatibility complex class II molecules, migrated to the draining lymph nodes and increased Treg cell numbers upon exposure to IR. These findings suggest a means for manipulating LC IR-resistance to increase cutaneous tumor response to radiotherapy. See above Cells were purified by flow cytometry and pooled until >10,000 cells/sample. At least 2 replicates of each sample were submitted.
2015-07-25 | E-GEOD-71330 | biostudies-arrayexpress
Project description:Here we present genome-wide copy number variation data on two vehicle treated and two CC214-2 (an mTOR kinase inhibitor) resistant GlioBlastoma Multiforme 39 (GBM39) xenografts, showing the absence of significant differences between the two groups, demonstrating that resistance to CC214-2 is due to adaptation rather than gene mutations. The genomic DNA extracted from the 4 xenografts samples was analysed with genome-wide Affymetrix SNP6.0 array
2013-12-06 | E-GEOD-53042 | biostudies-arrayexpress