ArticleFrontiers in immunology2024
Pan-cancer analysis of the transcriptional expression of histone acetylation enzymes in solid tumors defines a new classification scheme for gliomas.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- Histone deacetylase enzyme activity is not the universal anticancer target of HDAC inhibitors.Signal transduction and targeted therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: The altered expression of genes encoding histone acetyltransferases (HATs) and histone deacetylases (HDACs) has been implicated in the tumorigenesis and progression of various solid tumors. However, systematic characterization of the transcriptomic landscape and clinical relevance of HATs and HDACs in pan-cancer contexts remains lacking. Methods: Transcriptome and clinical data of 9,483 patients across 31 tumor types from The Cancer Genome Atlas were collected for systematic pan-cancer analysis. Additional glioma-specific datasets (Chinese Glioma Genome Atlas, GlioVis, GSE43378, and GSE182109) were also collected to validate the transcriptional characteristics of HATs and HDACs in gliomas. Consensus clustering analysis was applied to identify distinct expression patterns of HATs and HDACs. Results: Based on the transcriptomic data of 25 genes encoding 9 HATs and 16 HDACs, we identified five major subtypes across 31 cancer types (AC-I to AC-V). Notably, the AC-V subtype comprised over 95% of glioma patients, suggesting glioma patients exhibited distinct expression patterns of histone acetylation-modifying enzymes compared to patients with other solid tumors. Therefore, we re-conducted the consensus clustering analysis specifically within the context of gliomas and identified five subtypes, denoted "AC-GI" to "AC-GV", which were characterized by differences in HATs/HDACs expression patterns, biological and immune status, genetic alterations, and clinical outcomes. The AC-GII patients exhibited the best prognosis and were sensitive to temozolomide, while AC-GV patients had the poorest prognosis and the lowest sensitivity to temozolomide among all subtypes. Moreover, based on the Connectivity Map database analysis and experimental verification, we identified several pan-HDAC inhibitors that could serve as sensitizers for temozolomide therapy in AC-GV patients, such as panobinostat and scriptaid. Considering the distinctive clinical characteristics of patients with AC-GII and AC-GV, we constructed the "ACG score" model capable of effectively recognizing patients with these subtypes and predicting patient prognosis. Conclusion: Herein, we established novel biologically and clinically relevant molecular classifications for pan-solid tumors and gliomas based on transcriptional expression profiles of HATs and HDACs. Moreover, the ACG score model, calculated by the transcriptional expression of 29 genes, was not only an independent prognostic factor for glioma patients, but can also provide valuable references for promoting more effective therapeutic strategies.
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.