ArticleExperimental & molecular medicine2017
High prevalence of TP53 mutations is associated with poor survival and an EMT signature in gliosarcoma patients.
Article in Experimental & molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.
- Depression and glioblastoma, complicated concomitant diseases: a systemic review of published literature.Neurosurgical review · 2020Pooled it
- Advances in Brain Tumor Biomarkers: From Molecular Profiling to Liquid Biopsy and AI-Driven Detection.Cancers · 2026Review
- Distal noncontiguous recurrence and sarcomatous transformation of glioblastoma with stable molecular profile: illustrative case.Journal of neurosurgery. Case lessons · 2026Article
- Rare osseous mastoid invasion of secondary gliosarcoma: illustrative case.Journal of neurosurgery. Case lessons · 2025Article
- Gliosarcoma: A Multi-Institutional Analysis on Clinical Outcomes and Prognostic Factors.Cancer medicine · 2024Article
- Unveiling divergent treatment prognoses in IDHwt-GBM subtypes through multiomics clustering: a swift dual MRI-mRNA model for precise subtype prediction.Journal of translational medicine · 2024Article
- TGIF2 is a potential biomarker for diagnosis and prognosis of glioma.Frontiers in immunology · 2024Article
- Primary Intracranial Gliosarcoma: Is It Really a Variant of Glioblastoma? An Update of the Clinical, Radiological, and Biomolecular Characteristics.Journal of clinical medicine · 2023Review
- Pediatric gliosarcoma, a rare central nervous system tumor in children: Case report and literature review.Heliyon · 2023Article
- Article
- An overview of glioblastoma multiforme and temozolomide resistance: can LC-MS-based proteomics reveal the fundamental mechanism of temozolomide resistance?Frontiers in oncology · 2023Review
- Primary gliosarcoma with widespread extracranial metastases-spatiotemporal morphological variation.Chinese neurosurgical journal · 2022Article
- Identification of hub genes and biological pathways in glioma via integrated bioinformatics analysis.The Journal of international medical research · 2022Article
- Tumor Suppressor Role of Wild-Type P53-Dependent Secretome and Its Proteomic Identification in PDAC.Biomolecules · 2022Article
- Review
- Mutated RAS-associating proteins and ERK activation in relapse/refractory diffuse large B cell lymphoma.Scientific reports · 2022Article
- Gliosarcoma: The Distinct Genomic Alterations Identified by Comprehensive Analysis of Copy Number Variations.Analytical cellular pathology (Amsterdam) · 2022Article
- Article
- eTumorMetastasis: A Network-based Algorithm Predicts Clinical Outcomes Using Whole-exome Sequencing Data of Cancer Patients.Genomics, proteomics & bioinformatics · 2021Article
- Gliosarcoma vs. glioblastoma: a retrospective case series using molecular profiling.BMC neurology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 7 institutions in 2 countries.
Funding
Abstract
Gliosarcoma (GS) is a rare variant (2%) of glioblastoma (GBM) that poses clinical genomic challenges because of its poor prognosis and limited genomic information. To gain a comprehensive view of the genomic alterations in GS and to understand the molecular etiology of GS, we applied whole-exome sequencing analyses for 28 GS cases (6 blood-matched fresh-frozen tissues for the discovery set, 22 formalin-fixed paraffin-embedded tissues for the validation set) and copy-number variation microarrays for 5 blood-matched fresh-frozen tissues. TP53 mutations were more prevalent in the GS cases (20/28, 70%) compared to the GBM cases (29/90, 32%), and the GS patients with TP53 mutations showed a significantly shorter survival (multivariate Cox analysis, hazard ratio=23.9, 95% confidence interval, 2.87-199.63, P=0.003). A pathway analysis showed recurrent alterations in MAPK signaling (EGFR, RASGRF2 and TP53), phosphatidylinositol/calcium signaling (CACNA1s, PLCs and ITPRs) and focal adhesion/tight junction (PTEN and PAK3) pathways. Genomic profiling of the matched recurrent GS cases detected the occurrence of TP53 mutations in two recurrent GS cases, which suggests that TP53 mutations play a role in treatment resistance. Functionally, we found that TP53 mutations are associated with the epithelial-mesenchymal transition (EMT) process of sarcomatous components of GS. We provide the first comprehensive genome-wide genetic alternation profiling of GS, which suggests novel prognostic subgroups in GS patients based on their TP53 mutation status and provides new insight in the pathogenesis and targeted treatment of GS.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.