Expression data from high grade astrocytoma surgical samples
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE33331 | GEO | 2011/10/31
SECONDARY ACCESSION(S): PRJNA148955
REPOSITORIES: GEO
Similar Datasets
Project description:Survival in the majority of high grade astrocytoma (HGA) patients is very poor, with only a rare population of long-term survivors. A better understanding of the biological factors associated with long-term survival in HGA would aid development of more effective therapy and prognostication. We used microarray gene expression profiling of 26 patient surgical samples with known clinical outcomes to discover novel prognostic markers. Gene expression profiles were generated from surgical tumor samples using Affymetrix HG-U133plus2 chips. All genes were correlated with survival as a continuous variable in order to identify ontologys associated with risk of recurrence.
2011-10-31 | E-GEOD-33331 | biostudies-arrayexpress
Project description:Background: Long noncoding RNAs (lncRNAs) are pervasively transcribed and play a key role in tumorigenesis. The aim of the present study was to determine the lncRNA expression profile in astrocytoma patients and to assess the potential clinical value of the findings. Methods: The global lncRNA expression profile in astrocytoma was measured by lncRNA microarray. Next, the differentially expressed lncRNAs were validated using a Taqman probe-based quantitative real time-PCR (qRT-PCR) assay in 130 astrocytoma and 60 normal adjacent tissue (NAT) samples, which were randomly divided into a training set and a validation set. Finally, the correlation of the lncRNA levels with survival of the astrocytoma patients was estimated by performing a Kaplan-Meier survival analysis and a univariate/multivariate Cox proportional hazard regression analysis. Results: After a two-phase selection and validation process, 7 lncRNAs were found to have a significantly different expression profile in astrocytoma samples compared to the NAT samples. Unsupervised clustering analysis further revealed the potential of the 7-lncRNA profile to differentiate between tumors and NAT samples. Using Kaplan-Meier survival analysis, we found that the low expression of XLOC_005285 and XLOC_010967 and the high expression of HIT000260843.11 were significantly associated with poor patient survival. Moreover, Cox proportional hazard regression analysis revealed that this prognostic impact was independent of other clinicopathological factors. The lncRNA expression profiles of 3 astrocytoma tissues and 3 normal adjacent tissues were studied by microarray.
2014-06-07 | E-GEOD-58276 | biostudies-arrayexpress
Project description:Less than half of all patients with advanced-stage high-grade serous ovarian cancers (HGSC) survive more than five years post-diagnosis but those who have an exceptionally long survival could provide new insights into tumor biology and therapeutic approaches. We analyzed 60 patients with advanced-stage, HGSC who survived more than 10 years after diagnosis using whole-genome sequencing, transcriptome, and methylome profiling of their primary tumor samples, comparing this data to 66 short- or moderate-term survivors. Tumors of long-term survivors were more likely to have multiple alterations in genes associated with DNA repair, and more frequent somatic variants resulting in an increased predicted neoantigen load. Patients clustered into survival groups based on genomic and immune cell signatures, including three subsets of patients with BRCA1 alterations with distinctly different outcomes. Specific combinations of germline and somatic gene alterations, tumor cell phenotypes, and differential immune responses appear to contribute to long-term survival in HGSC.
2022-08-26 | GSE211669 | GEO
Project description:We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. Progression to high-grade astrocytomas (HGA) occurred stochastically, in part through location-specific acquisition of CNA. HGA transcriptomes were heterogeneous and consisted of three subtypes that were also evident in GEM HGA with different oncogenic drivers and cellular origins. HGA subtypes expressing immune/invasion, proliferation, and neuronal genes mimicked human mesenchymal, proneural, and neural GBM, respectively. HGA subtypes also expressed distinct neural lineage signatures and were correlated with astrocyte location, but not oncogenic driver mutations. These results suggest that oncogenic drivers influence LGA subtype and that regional astrocyte identity and progression-acquired CNA contribute strongly to HGA transcriptomal heterogeneity. Defining tumor-initiating and progression-acquired mutations and the cells in which they occur would facilitate molecular classification and development of molecularly targeted strategies to manage GBM.
2016-02-01 | GSE49268 | GEO
Project description:We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. Progression to high-grade astrocytomas (HGA) occurred stochastically, in part through location-specific acquisition of CNA. HGA transcriptomes were heterogeneous and consisted of three subtypes that were also evident in GEM HGA with different oncogenic drivers and cellular origins. HGA subtypes expressing immune/invasion, proliferation, and neuronal genes mimicked human mesenchymal, proneural, and neural GBM, respectively. HGA subtypes also expressed distinct neural lineage signatures and were correlated with astrocyte location, but not oncogenic driver mutations. These results suggest that oncogenic drivers influence LGA subtype and that regional astrocyte identity and progression-acquired CNA contribute strongly to HGA transcriptomal heterogeneity. Defining tumor-initiating and progression-acquired mutations and the cells in which they occur would facilitate molecular classification and development of molecularly targeted strategies to manage GBM.
2016-02-01 | GSE49267 | GEO
Project description:We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. Progression to high-grade astrocytomas (HGA) occurred stochastically, in part through location-specific acquisition of CNA. HGA transcriptomes were heterogeneous and consisted of three subtypes that were also evident in GEM HGA with different oncogenic drivers and cellular origins. HGA subtypes expressing immune/invasion, proliferation, and neuronal genes mimicked human mesenchymal, proneural, and neural GBM, respectively. HGA subtypes also expressed distinct neural lineage signatures and were correlated with astrocyte location, but not oncogenic driver mutations. These results suggest that oncogenic drivers influence LGA subtype and that regional astrocyte identity and progression-acquired CNA contribute strongly to HGA transcriptomal heterogeneity. Defining tumor-initiating and progression-acquired mutations and the cells in which they occur would facilitate molecular classification and development of molecularly targeted strategies to manage GBM.
2016-02-01 | GSE49266 | GEO
Project description:We used genetically-engineered mice (GEM) to target constitutive RTK effector pathway (KrasG12D and/or Pten deletion) mutations in G1/S checkpoint-defective adult mouse astrocytes. Genetic lineage tracing showed that these mutations potentiated tumor initiation in cortical, diencephalic, brainstem, and olfactory bulb astrocytes, producing low-grade astrocytomas (LGA). LGA lacked copy number abnormalities (CNA), but showed oncogenic driver- and astrocyte location-specific transcriptome profiles, suggesting that both driver mutations and cellular origin contribute to LGA genomic heterogeneity. Progression to high-grade astrocytomas (HGA) occurred stochastically, in part through location-specific acquisition of CNA. HGA transcriptomes were heterogeneous and consisted of three subtypes that were also evident in GEM HGA with different oncogenic drivers and cellular origins. HGA subtypes expressing immune/invasion, proliferation, and neuronal genes mimicked human mesenchymal, proneural, and neural GBM, respectively. HGA subtypes also expressed distinct neural lineage signatures and were correlated with astrocyte location, but not oncogenic driver mutations. These results suggest that oncogenic drivers influence LGA subtype and that regional astrocyte identity and progression-acquired CNA contribute strongly to HGA transcriptomal heterogeneity. Defining tumor-initiating and progression-acquired mutations and the cells in which they occur would facilitate molecular classification and development of molecularly targeted strategies to manage GBM.
2016-02-01 | GSE49265 | GEO
Project description:Background: Long noncoding RNAs (lncRNAs) are pervasively transcribed and play a key role in tumorigenesis. The aim of the present study was to determine the lncRNA expression profile in astrocytoma patients and to assess the potential clinical value of the findings. Methods: The global lncRNA expression profile in astrocytoma was measured by lncRNA microarray. Next, the differentially expressed lncRNAs were validated using a Taqman probe-based quantitative real time-PCR (qRT-PCR) assay in 130 astrocytoma and 60 normal adjacent tissue (NAT) samples, which were randomly divided into a training set and a validation set. Finally, the correlation of the lncRNA levels with survival of the astrocytoma patients was estimated by performing a Kaplan-Meier survival analysis and a univariate/multivariate Cox proportional hazard regression analysis. Results: After a two-phase selection and validation process, 7 lncRNAs were found to have a significantly different expression profile in astrocytoma samples compared to the NAT samples. Unsupervised clustering analysis further revealed the potential of the 7-lncRNA profile to differentiate between tumors and NAT samples. Using Kaplan-Meier survival analysis, we found that the low expression of XLOC_005285 and XLOC_010967 and the high expression of HIT000260843.11 were significantly associated with poor patient survival. Moreover, Cox proportional hazard regression analysis revealed that this prognostic impact was independent of other clinicopathological factors.
2014-06-07 | GSE58276 | GEO
Project description:Less than half of all patients with advanced-stage high-grade serous ovarian cancers (HGSC) survive more than five years post-diagnosis but those who have an exceptionally long survival could provide new insights into tumor biology and therapeutic approaches. We analyzed 60 patients with advanced-stage, HGSC who survived more than 10 years after diagnosis using whole-genome sequencing, transcriptome, and methylome profiling of their primary tumor samples, comparing this data to 66 short- or moderate-term survivors. Tumors of long-term survivors were more likely to have multiple alterations in genes associated with DNA repair, and more frequent somatic variants resulting in an increased predicted neoantigen load. Patients clustered into survival groups based on genomic and immune cell signatures, including three subsets of patients with BRCA1 alterations with distinctly different outcomes. Specific combinations of germline and somatic gene alterations, tumor cell phenotypes, and differential immune responses appear to contribute to long-term survival in HGSC. Methylation profiling was done on 58 high grade serous ovarian cancer samples, 53 of which were primary tumors and and 5 were relapse tumors. 73 primary tumors from GSE65820 were also used as part of the cohort.
2022-08-26 | GSE211686 | GEO
Project description:High-grade serous ovarian carcinoma (HGSOC) is generally associated with a very dismal prognosis. Nevertheless, patients with similar clinicopathological characteristics can have markedly different clinical outcomes. Our aim was the identification of novel molecular determinants influencing survival. Gene expression profiles of 12 HGSOC long-term and 27 short-term survivors (training set) were generated by microarray, and a prognostic signature was identified and further evaluated on an independent extensive HGSOC dataset through a meta-analysis approach.
2019-11-14 | GSE131978 | GEO