Ontology highlight
ABSTRACT:
PROVIDER: PRJNA135841 | ENA |
REPOSITORIES: ENA
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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:Global analysis of mRNA expression in prospectively purified human prostate orthotopic xenograft tumor cells with varying S/TFE
| PRJNA142451 | ENA
Project description:Global analysis of miRNA expression in prospectively purified human prostate orthotopic xenograft tumor cells with varying S/TFE
| PRJNA142453 | ENA
Project description:Human prostate CWR22 OT-tumor cells were prospectively purified for expression of various stem cell markers (TRA-1-60/CD151/CD166/EpCAM/CD44/α2-Integrin). Unsorted total tumor cells or the additional marker positive cells that do not manifest stem-like characteristics were used as control. All these cells were subjected to molecular profiling of total RNA expression and the fold change data are tabulated according to S/TFE of the purified cells in relation to their control. Notes: Low S/TFE = Low sphere and tumor forming efficiency; Moderate S/TFE = Moderate sphere and tumor forming efficiency; High S/TFE = High sphere and tumor forming efficiency; FDR* = False Discovery Rate; FC = Fold Change; Signal = Average Expression Signal Level. Low-S/TFE, Moderate S/TFE, High S/TFE data sets were compared to No S/TFE control sets
2010-12-06 | E-GEOD-25690 | biostudies-arrayexpress
Project description:Human prostate CWR22 OT-tumor cells were prospectively purified for expression of various stem cell markers (TRA-1-60/CD151/CD166/EpCAM/CD44/α2-Integrin). Unsorted total tumor cells or the additional marker positive cells that do not manifest stem-like characteristics were used as control. All these cells were subjected to molecular profiling of total RNA expression and the fold change data are tabulated according to S/TFE of the purified cells in relation to their control. Notes: Low S/TFE = Low sphere and tumor forming efficiency; Moderate S/TFE = Moderate sphere and tumor forming efficiency; High S/TFE = High sphere and tumor forming efficiency; FDR* = False Discovery Rate; FC = Fold Change; Signal = Average Expression Signal Level. Low-S/TFE, Moderate S/TFE, High S/TFE data sets were compared to No S/TFE control sets
2010-12-06 | E-GEOD-25691 | biostudies-arrayexpress
Project description:Human prostate CWR22 OT-tumor cells were prospectively purified for expression of various stem cell markers (TRA-1-60/CD151/CD166/EpCAM/CD44/α2-Integrin). Unsorted total tumor cells or the additional marker positive cells that do not manifest stem-like characteristics were used as control. All these cells were subjected to molecular profiling of total RNA expression and the fold change data are tabulated according to S/TFE of the purified cells in relation to their control. Notes: Low S/TFE = Low sphere and tumor forming efficiency; Moderate S/TFE = Moderate sphere and tumor forming efficiency; High S/TFE = High sphere and tumor forming efficiency; FDR* = False Discovery Rate; FC = Fold Change; Signal = Average Expression Signal Level.
2010-12-06 | GSE25691 | GEO
Project description:Human prostate CWR22 OT-tumor cells were prospectively purified for expression of various stem cell markers (TRA-1-60/CD151/CD166/EpCAM/CD44/α2-Integrin). Unsorted total tumor cells or the additional marker positive cells that do not manifest stem-like characteristics were used as control. All these cells were subjected to molecular profiling of total RNA expression and the fold change data are tabulated according to S/TFE of the purified cells in relation to their control. Notes: Low S/TFE = Low sphere and tumor forming efficiency; Moderate S/TFE = Moderate sphere and tumor forming efficiency; High S/TFE = High sphere and tumor forming efficiency; FDR* = False Discovery Rate; FC = Fold Change; Signal = Average Expression Signal Level.
2010-12-06 | GSE25690 | 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:To identify molecular singnal alterations between androgen dependent prostate cancer and castration resistant prostate cancer, we performed interspecies comparative microarray analyses using RNAs prepared from uncastrasion and castration tumor from LNCAP Orhotopic xenograft models of prostate cancer. microarray data from uncastrasion and castration tumor revealed that the gene expression profile is most significantly altered in between androgen dependent prostate cancer and castration resistant prostate cancer. Comparative analyses of LNCAP Orhotopic xenograft models of prostate cancer showed that genes involved in androgen dependent and androgen independent tumor were significantly altered. We prepared RNA samples from 4 samples uncastrasion and 4 samples castration tumors from LNCAP Orhotopic xenograft models of prostate cancer . High-quality RNA samples were subjected to microarray analysis using the Affymetrix Human Gene 2.0 ST platform, and only those results that passed examinations for quality assurance and quality control of the Human Gene 2.0 ST arrays were retrieved. In total, we obtained gene expression profiles from the following samples: 4 samples uncastrasion and 4 samples castration tumors
2013-04-20 | E-GEOD-46218 | biostudies-arrayexpress
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.
2013-10-01 | E-GEOD-46385 | biostudies-arrayexpress