F82b0dfa-5b5f-41fe-b2ba-d98108a045b9 - samples
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ABSTRACT:
PROVIDER: EGAD00001008568 | EGA |
REPOSITORIES: EGA
Similar Datasets
Project description:Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent). Experiment Overall Design: 80 glioblastoma specimen and 4 non-tumoral brain samples
2008-10-18 | E-GEOD-7696 | biostudies-arrayexpress
Project description:Analysis of 80 glioblastoma specimen of patients treated within clinical trials and 4 samples of "normal" brain tissue (non-tumoral). The data was used to identify factors of resistance to a chemoradiation therapy protocol of radiotherapy and concomitant and adjuvant temozolomide (alkylating agent). Keywords: Disease state comparison
2008-06-20 | GSE7696 | GEO
Project description:Combined model of in vitro and in vivo resistance to alkylating agents (BCNU and Temozolomide) in glioblastoma multiforme. Three matched pairs of surgical specimens from initial (DI, ME, LX) and repeat (DIR, MER, LXR) tumor resection were used to establish cell lines. Patients received BCNU chemotherapy between the two operations, which rendered the sublines from repeat surgery more resistant to BCNU than those from initial surgery. Each the pre-chemotherapeutic set and the post-chemotherapeutic set of cell lines was selected in vitro for resistance to either BCNU or Temozolomide. 9 in vitro selected sublines were established. Of those 4 (2 selected for BCNU [ME-BCNU, DI-BCNU] and 2 selected for Temozolomide [ME-TMZ, LX-TMZ) were generated from the parental/sensitive pre-chemotherapeutic set and 5 (2 selected for BCNU [DIR-BCNU, MER-BCNU] and 3 selected for Temozolomide [DIR-TMZ, MER-TMZ, LXR-TMZ) from the in vivo resistant post-chemotherapeutic set. The model included a total of 15 sublines. Genome-wide high-resolution gene copy number profiling was performed on each subline using 42,000-feature cDNA microarrays. Utilizing the same microarray platform genome-wide gene expression profiles were generated. Biostatistical tools were employed to identify signatures of resistance to alkylating agents both at the genetic as well as at the transcriptomic levels. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Series_type = Logical Set Keywords: other
2006-01-27 | GSE2221 | GEO
Project description:Glioblastoma is an aggressive incurable primary malignant brain tumor. Measles virus (MeV) therapy is a promising upcoming treatment strategy with proven preclinical efficacy and clinical safety. Using RNA Sequencing and immunopeptidome analyses, we aimed at identifying a synergistic combination regimen of MeV with conventional therapeutic strategies for glioblastoma patients, i.e. radiotherapy and temozolomide or lomustine, and to understand the underlying molecular mechanism.
2018-02-19 | PXD008984 | Pride
Project description:The androgen receptor splice variant 7 (AR-V7) lacks the ligand-binding domain; is detected with increased frequency in advanced prostate cancer and is postulated to be one crucial mechanism for disease progression and therapeutic resistance to androgen deprivation in castration–resistant prostate cancer (CRPC). Targeting AR-V7 or unique downstream targets could provide novel therapeutic approaches for CRPC. Here, we report that, independent of ligand, AR-V7 binds not only to the androgen-responsive element (ARE) sites inducing canonical AR signaling but also to non-canonical target sites where ligand-stimulated full-length AR (AR-FL) does not bind. These AR-V7 “solo” binding sites are mainly found at gene promoters and are co-occupied by a zinc-finger transcription factor ZFX and the co-activator BRD4, both of which physically interact with AR-V7. Consequently, AR-V7 not only recapitulates AR-FL action without androgen but uniquely regulates transcripts correlating with AR-V7 expression in the TCGA prostate cancer cohort. Mechanistically, ZFX appears to function as a pioneer factor for AR-V7 at solo-binding sites and BRD4 inhibitors but not anti-androgens suppress AR-V7 action at solo-binding sites as well as AR-V7-dependent growth. Additionally, knockdown of ZFX, or two downstream targets uniquely co-activated by AR-V7 (ZNF32 and FZD6), also suppressed growth of AR-V7-dependent CRPC cells. AR-V7 directly activated genes differentiate tumor from normal prostate tissues and predict poor prognosis in patients. Thus AR-V7 has both canonical and non-canonical regulatory functions in CRPC, which may provide new therapeutic avenues.
2018-10-02 | GSE94013 | GEO
Project description:The data contains Illumina 450k/EPIC array methylation files from 104 patients of the NOA-08 study comparing temozolomide alone vs. radiotherapy in elderly patients with glioblastoma
2019-10-31 | GSE122920 | GEO
Project description:Diffuse Intrinsic Pontine Glioma (DIPG) is an aggressive incurable pediatric brainstem cancer. Due to its inoperable tumor location and resistance to conventional chemotherapy agents such as temozolomide, radiotherapy is the current standard treatment. This study aimed to identify potential therapeutic agents for DIPG treatment using a computational drug screening pipeline. We hypothesized that drugs that can reverse a disease gene signature can be potential drug candidates for that disease. Because of lack of normal brain samples as control for creating disease signature, we implemented a deep learning autoencoder to select reference control samples. Using a systematic computational approach with publicly available gene expression databases for DIPG signature and gene expression data of pre and post drug treated cancer cell lines, we identified drug hits with potential to reverse a DIPG gene signature to one that matches normal tissue background. We then tested the identified drugs at their IC50 concentration for 24 hours on patient-derived DIPG4 cell lines. Overall Design: mRNA profiles of DIPG4 cell lines treated with Triptolide (TPL), Triamterene(TRIAM), Mycophenolate mofetil (MMF) and DMSO as control
2022-10-20 | GSE193855 | GEO
Project description:Glioblastoma (GBM) is the most common primary brain tumor in adults, characterized by an inherent aggressivity and resistance to treatment leading to poor prognoses. While some resistance mechanisms have been elucidated, a deeper understanding of these mechanisms is needed to increase therapeutic efficacy. In this study we first discovered glial-cell derived neurotrophic factor (GDNF) to be upregulated in patient-derived glioblastoma spheroid cultures after chemotherapeutic temozolomide (TMZ) treatment, through RNA-Seq experiments. Therefore, we investigated the role of the GDNF/GDNF receptor alpha 1 (GFRA1) signaling pathway as a resistance mechanism to chemotherapy with temozolomide and lomustine as well as irradiation using patient-derived glioblastoma spheroid cultures. With qPCR experiments we showed a consistent upregulation of GDNF and its primary receptor GFRA1 following all three lines of treatment. Moreover, CRISPR/Cas9 knock-outs of GDNF in two patient-derived models sensitized these cells to chemotherapy treatment, but not radiotherapy. The increased sensitivity was completely reversed by the addition of exogeneous GDNF, confirming the key role of this factor in chemoresistance. Finally, a CRISPR KO of GFRA1 demonstrated a similar increased sensitivity to temozolomide and lomustine treatment, as well as radiotherapy. Together, our findings support the role of the GDNF/GFRA1 signaling pathway in glioblastoma chemo and radioresistance.
2024-02-13 | GSE255581 | GEO
Project description:We performed a retrospective analysis of the SweBCG 91-RT trial, which randomized women with node-negative stage I-IIA breast cancer to whole breast radiotherapy or no radiotherapy following breast-conserving surgery with minimal use of adjuvant systemic treatment. Primary tumors were profiled with the GeneChip Human Exon 1.0 ST microarray.
2019-09-26 | GSE119295 | GEO
Project description:Glioblastoma multiforme (GBM) is the most common and aggressive primary human brain tumor. Although comprehensive therapies combining radiotherapy and chemotherapy after surgery can prolong survival, the prognosis is still poor with a median survival of only 14.6 months. Chemoresistance is one of the major causes of relapse as well as poor survival in glioma patients. Therefore, novel strategies to overcome chemoresistance are desperately needed for improved treatment of human GBM. Recent studies have demonstrated that long non‑coding RNAs are closely related to resistance to cancer chemotherapy. Here, we simultaneously detected, for the first time, the expression profiles of mRNAs, lncRNAs, and circRNAs in three pairs of secondary temozolomide-resistant glioblastoma (STRG) and matched primary glioblastoma tissues by microarrays. A total of 92 mRNA, 299lncRNAs, and 53 circRNAs were altered during the Chemoresistance. The functions of these differentially expressed RNAs were predicted by Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Co-expression networks of lncRNA-mRNA and circRNA-miRNA were conducted to uncovered the hidden ceRNA mechanisms. Our findings revealed the alteration of expression patterns of mRNAs, lncRNAs, and circRNAs in the secondary temozolomide-resistant glioblastoma. These mRNAs, lncRNAs, and circRNAs might be potential therapeutic targets for the treatment of glioblastoma.
2020-12-17 | GSE139826 | GEO