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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of human glioblastoma samples from a homogenous cohort of patients treated within clinical trial with eitehr radiotherapy or radiotherapy and temonzolomide

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Monika Hegi

PROVIDER: E-GEOD-7696 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Stem cell-related "self-renewal" signature and high epidermal growth factor receptor expression associated with resistance to concomitant chemoradiotherapy in glioblastoma.

Murat Anastasia A Migliavacca Eugenia E Gorlia Thierry T Lambiv Wanyu L WL Shay Tal T Hamou Marie-France MF de Tribolet Nicolas N Regli Luca L Wick Wolfgang W Kouwenhoven Mathilde C M MC Hainfellner Johannes A JA Heppner Frank L FL Dietrich Pierre-Yves PY Zimmer Yitzhak Y Cairncross J Gregory JG Janzer Robert-Charles RC Domany Eytan E Delorenzi Mauro M Stupp Roger R Hegi Monika E ME

Journal of clinical oncology : official journal of the American Society of Clinical Oncology 20080601 18

<h4>Purpose</h4>Glioblastomas are notorious for resistance to therapy, which has been attributed to DNA-repair proficiency, a multitude of deregulated molecular pathways, and, more recently, to the particular biologic behavior of tumor stem-like cells. Here, we aimed to identify molecular profiles specific for treatment resistance to the current standard of care of concomitant chemoradiotherapy with the alkylating agent temozolomide.<h4>Patients and methods</h4>Gene expression profiles of 80 gli ...[more]

PMID: 18565887

Publication: 1/2

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Glioblastoma from a homogenous cohort of patients treated within clinical trial

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

Human cerebrospinal fluid impacts chemo-radiotherapy sensitivities in tumour cells from glioblastoma patients

Project description:Cancers in the central nervous system resist therapies effective in other cancers, possibly due to the unique biochemistry of the human brain microenvironment comprised of cerebrospinal fluid (CSF). However, the impact of CSF on cancer cells and therapeutic efficacy is unknown. Here we examined the effect of human CSF on glioblastoma (GBM) tumours from 25 patients. We found that CSF induces tumour cell plasticity and resistance to standard GBM treatments (temozolomide and irradiation). We identified nuclear-protein-1 (NUPR1), a transcription factor hampering ferroptosis, as a mediator of therapeutic resistance in CSF. NUPR1 inhibition with a repurposed antipsychotic, trifluoperazine, enhanced the killing of GBM cells resistant to chemoradiation in CSF. The same chemo-effective doses of trifluoperazine were safe for human neurons and astrocytes derived from pluripotent stem cells. These findings reveal that chemoradiation efficacy decreases in human CSF and suggest that combining trifluoperazine with standard care may improve GBM patient survival.

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Rational targeting of dynamic tumor subclones in relapsing human glioblastoma

Project description:Glioblastoma therapy relies on the alkylating drug temozolomide (TMZ) administered to irradiated patients post-neurosurgery, which increases overall survival but cannot prevent fatal disease relapse. Using clinical samples and glioblastoma models, we here identify TMZ-driven enrichment of ALDH1A1+ tumor subclones acquiring AKT-dependent drug resistance en route to relapse. We demonstrate that this recurrent phenotype switch is predictable and can be countered by a sequential rather than simultaneous combinatorial treatment approach.

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Genomic Exploration of Distinct Molecular Phenotypes Steering Temozolomide Resistance Development in Patient-Derived Glioblastoma Cells

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2016-07-06 | E-GEOD-84010 | biostudies-arrayexpress

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2018-02-19 | PXD008984 | Pride

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2013-01-12 | E-GEOD-43452 | biostudies-arrayexpress

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