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ProteomicsATM Inhibition Exploits Checkpoint Defects and ATM-Dependent Double Strand Break Repair in TP53-Mutant Glioblastoma
Determining the balance between DNA double strand break repair (DSBR) pathways is essential for understanding treatment response in cancer. We report a novel method for simultaneously measuring non-homologous end joining (NHEJ), homologous recombination (HR), and microhomology-mediated end joining (...
ORGANISM(S): Homo sapiens (Human) 
2024-03-08 | PXD047837 | Pride
Dna double strand break repair Tp53-mutant glioblastoma Atm inhibition 
TranscriptomicsModulation of gene expression in U251 glioblastoma cells by binding of mutant p53 to intronic and intergenic sequences
Missense point mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines derived thereof. Mutant p53 (mutp53) proteins have lost sequence-specific DNA binding, but have retained the ability to interact in a structure-selective manner with non-B DNA and to act a...
ORGANISM(S): Homo sapiens 
2010-06-24 | E-GEOD-13991 | biostudies-arrayexpress
TranscriptomicsGene expression analysis of U251 human glioblastoma cell line
The human TP53 gene is frequently mutated in tumors and cell lines. Unlike other tumor suppressors that are commonly inactivated by deletions or nonsense mutations, the majority of p53-mutations are missense point mutations that result in the expression of a full-length protein with an altered amino...
ORGANISM(S): Homo sapiens 
2012-12-10 | E-GEOD-35454 | biostudies-arrayexpress
TranscriptomicsChIP analysis on a custom tiling array of U251 human glioblastoma cell line
Missense mutations in the TP53 gene are frequent genetic alterations in human tumor tissue and cell lines. In contrast to wild-type p53, the mutant p53 (mutp53) protein has lost the transcriptional activity towards pro-apoptotic and growth arrest genes, but retained the property to interact with DNA...
ORGANISM(S): Homo sapiens 
2012-12-10 | E-GEOD-35453 | biostudies-arrayexpress
UnknownATM inhibition exploits checkpoint defects and ATM-dependent double strand break repair in TP53-mutant glioblastoma.
Not available
S-EPMC11192742 | biostudies-literature
UnknownSingle-nucleus transcriptomics of IDH1- and TP53-mutant glioma stem cells displays diversified commitment on invasive cancer progenitors.
Not available
S-EPMC9643511 | biostudies-literature
TranscriptomicsCFIm25 links alternative polyadenylation to glioblastoma tumour suppression
Purpose: To identify all of the APA targets of CFIm25 on a global scale and develop an algorithm that can idenitify APA events from standard RNA-seq data Methods: RNA from HeLa cells treated with control siRNA and CFIm25 siRNA were subject to RNA-Seq. Using a custom-designed algorithm to mine RNA-s...
ORGANISM(S): Homo sapiens 
2014-05-15 | E-GEOD-42420 | biostudies-arrayexpress
TranscriptomicsGene expression and ChIP-chip analysis of U251 human glioblastoma cell line
Using human U251 glioblastoma cells with endogenous mutp53 expression as a model, we performed a ChIP-chip analysis of mutp53 binding sites on a custom tiling array, coupled with global expression profiling and an analysis of the epigenetic status of mutp53 regulated promoters. Mutp53 binds preferen...
ORGANISM(S): Homo sapiens 
2012-12-10 | E-GEOD-35500 | biostudies-arrayexpress
TranscriptomicsDistinct functions of wild-type and mutant Δ133p53α R273H differentially regulate glioblastoma aggressiveness and therapy-induced senescence
Mutations effects on p53 isoforms’ activities remain largely unknown, although they are mutated in 92% of TP53 mutant cancers. Therefore, exploring the effect of mutations on p53 isoforms activities is a critical, albeit unexplored area in the p53 field. Current glioblastoma treatments, including te...
ORGANISM(S): Homo sapiens 
2024-07-31 | GSE240377 | GEO
TranscriptomicsINSM1 governs a neuronal progenitor state that drives glioblastoma in a human stem cell model
Glioblastoma (GBM) is an aggressivea lethal brain tumorcancer marked by functional plasticity driven by the interplay between tumor cell-intrinsic mutations and -extrinsic heterogeneity, enabling rapid evolutiontheir interplay with developmental programs. To investigate how canonical GBM glioblastom...
ORGANISM(S): Homo sapiens 
2025-07-15 | GSE229901 | GEO
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