Evidence map›Paper›PMID 39256867›Full record

ArticleActa neuropathologica communications2024

A patient-derived cell model for malignant transformation in IDH-mutant glioma.

Olga Kim, Zach Sergi, Guangyang Yu, Kazutoshi Yamamoto, Martha Quezado, Zied Abdullaev, Danel R Crooks, Shun Kishimoto, Qi Li, Peng Lu and 12 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Biomolecules & biomedicine · 2025
    Article
  8. Article
  9. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

22 authors.

Olga KimNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Zach SergiNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Guangyang YuNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Kazutoshi YamamotoRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Martha QuezadoLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Zied AbdullaevLaboratory of Pathology, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Danel R CrooksUrologic Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Shun KishimotoRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Qi LiNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Peng LuNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Burchelle BlackmanChemistry and Synthesis Center, National Heart, Lung, and Blood Institute, Rockville, MD, 20850, USA.
Thorkell AndressonProtein Characterization Laboratory, Leidos Biomedical Inc / Frederick National Laboratory for Cancer Research, Frederick, MD, 21701, USA.
Xiaolin WuGenomics Technology Laboratory, Cancer Research Technology Program, Frederick National Laboratory for Cancer Research, Frederick, MD, 21701, USA.
Bao TranSequencing Facility, Leidos Biomedical Inc / Frederick National Laboratory for Cancer Research, Frederick, MD, 21701, USA.
Jun S WeiGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Wei ZhangNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Meili ZhangNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Hua SongNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA.
Javed KhanGenetics Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Murali C KrishnaRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Jeffrey R BrenderRadiation Biology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD, 20892, USA.
Jing WuNeuro-Oncology Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Building 37, Room 1142A, 37 Convent Drive, Bethesda, MD, 20892, USA. jing.wu3@nih.gov.ORCID 0000-0002-1686-9646

Funding

WORK ORDER 126643 B539 EXPAND IC SUITE75N91019D00024 · NIAID · LEIDOS BIOMEDICAL RESEARCH, INC. · PI BRISCOE, LYNN · 2019 to 2025
$3932.6M
NCI NIH HHS 75N91019D00024
6 · The paper itself

Abstract

Malignant transformation (MT) is commonly seen in IDH-mutant gliomas. There has been a growing research interest in revealing its underlying mechanisms and intervening prior to MT at the early stages of the transforming process. Here we established a unique pair of matched 3D cell models: 403L, derived from a low-grade glioma (LGG), and 403H, derived from a high-grade glioma (HGG), by utilizing IDH-mutant astrocytoma samples from the same patient when the tumor was diagnosed as WHO grade 2 (tumor mutational burden (TMB) of 3.96/Mb) and later as grade 4 (TMB of 70.07/Mb), respectively. Both cell models were authenticated to a patient's sample retaining endogenous expression of IDH1 R132H. DNA methylation profiles of the parental tumors referred to LGG and HGG IDH-mutant glioma clusters. The immunopositivity of SOX2, NESTIN, GFAP, OLIG2, and beta 3-Tubulin suggested the multilineage potential of both models. 403H was more prompt to cell invasion and developed infiltrative HGG in vivo. The differentially expressed genes (DEGs) from the RNA sequencing analysis revealed the tumor invasion and aggressiveness related genes exclusively upregulated in the 403H model. Pathway analysis showcased an enrichment of genes associated with epithelial-mesenchymal transition (EMT) and Notch signaling pathways in 403H and 403L, respectively. Mass spectrometry-based targeted metabolomics and hyperpolarized (HP) 1-

Indexed as

Brain NeoplasmsCell Transformation, NeoplasticGliomaIsocitrate DehydrogenaseMutationAnimalsHumansIDH1 protein, humanIsocitrate Dehydrogenase3D cell modelHigh-grade glioma (HGG)Hypermutator phenotype (HMP)IDH-mutant gliomaLow-grade glioma (LGG)Malignant transformation (MT)Matched patient-derived cellsTumor mutational burden (TMB)

Identifiers

PMID39256867
PMCPMC11385154

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Registered trials

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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.