SynthesisMolecular oncology2024
IDH mutation, glioma immunogenicity, and therapeutic challenge of primary mismatch repair deficient IDH-mutant astrocytoma PMMRDIA: a systematic review.
Synthesis in Molecular oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Targeting the DNA Damage Response in Cancer.MedComm · 2026Review
- Gasdermin as a Molecular Signature and Predictor of Adult-Type Diffuse Glioma Severity and Grading.Journal of clinical medicine · 2026Article
- Construction and external validation of a prognostic model for high-grade glioma based on IDH1 mutation status: implications for concurrent chemoradiotherapy efficacy.American journal of cancer research · 2026Article
- Hepatocellular Carcinoma Precursor Lesions: From Pathological Basis to Risk Stratification and Precision Intervention.Journal of hepatocellular carcinoma · 2026Review
- Patterns of hypermutation shape tumorigenesis and immunotherapy response in mismatch-repair-deficient glioma.Nature genetics · 2026Article
- Natural killer cell dysfunction in glioma: from immune evasion to immunotherapy.Frontiers in immunology · 2026Review
- Integrating quantitative DCE-MRI parameters and radiomic features for improved IDH mutation prediction in gliomas.Frontiers in oncology · 2025Article
- Understanding brain cancer and exploiting its vulnerabilities.Molecular oncology · 2024Article
- IDH-mutant gliomas in children and adolescents - from biology to clinical trials.Frontiers in oncology · 2024Article
- Convolutional neural networks: applications, challenges and future prospects in brain tumor research.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In 2021, Suwala et al. described Primary Mismatch Repair Deficient IDH-mutant Astrocytoma (PMMRDIA) as a distinct group of gliomas. In unsupervised clustering, PMMRDIA forms distinct cluster, separate from other IDH-mutant gliomas, including IDH-mutant gliomas with secondary mismatch repair (MMR) deficiency. In the published cohort, three patients received treatment with an immune checkpoint blocker (ICB), yet none exhibited a response, which aligns with existing knowledge about the decreased immunogenicity of IDH-mutant gliomas in comparison to IDH-wildtype. In the case of PMMRDIA, the inherent resistance to the standard-of-care temozolomide caused by MMR deficiency is an additional challenge. It is known that a gain-of-function mutation of IDH1/2 genes produces the oncometabolite R-2-hydroxyglutarate (R-2-HG), which increases DNA and histone methylation contributing to the characteristic glioma-associated CpG island methylator phenotype (G-CIMP). While other factors could be involved in remodeling the tumor microenvironment (TME) of IDH-mutant gliomas, this systematic review emphasizes the role of R-2-HG and the subsequent G-CIMP in immune suppression. This highlights a potential actionable pathway to enhance the response of ICB, which might be relevant for addressing the unmet therapeutic challenge of PMMRDIA.
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