Evidence map›Paper›PMID 42479134›Full record

ArticleNeuro-oncology2026

The CoREST complex inhibitor, corin, decreases tumor growth, increases cellular differentiation and extends lifespan in ATRT xenograft models.

Anupa Geethadevi, Nikhil Vaidya, Robert J Fisher, Tyler R Findlay, Yiming Deng, Khoa Pham, Vikas Kumar, Samuel Beck, Jun Choe, Shiyu Liu and 8 more

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Article in Neuro-oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Anupa GeethadeviDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Nikhil VaidyaDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.
Robert J FisherDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.
Tyler R FindlayDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Yiming DengDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Khoa PhamDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA 21205.
Vikas KumarDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.
Samuel BeckDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.
Jun ChoeDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Shiyu LiuDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Calixto-Hope G LucasDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA 21205.
Charles G EberhartDepartment of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA 21205.
Jinchong XuNeuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Philip A ColeDivision of Genetics, Departments of Medicine and Biological Chemistry and Molecular Pharmacology, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts, USA 02115.
Jeffrey RubensDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Marianne CollardDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.
Eric H RaabeDivision of Pediatric Oncology, Johns Hopkins University School of Medicine and Johns Hopkins Hospital, Bloomberg Children's Center, Baltimore, MD, USA 21205.
Rhoda M AlaniDepartment of Dermatology, Boston University Chobanian and Avedisian School of Medicine, Boston, Massachusetts, USA 02118.

Funding

Translational Research Central ServicesP30CA006973 · NCI · JOHNS HOPKINS UNIVERSITY · PI ALAN KEITH MEEKER · 1985 to 2026
$208.6M
Chemical Approaches to Understanding Reversible Lysine ModificationsR35GM149229 · NIGMS · BRIGHAM AND WOMEN'S HOSPITAL · PI PHILIP A COLE · 2023 to 2026
$1.9M
NCI NIH HHS P30 CA006973NIGMS NIH HHS R35 GM149229
6 · The paper itself

Abstract

backgroundAtypical teratoid rhabdoid tumor (ATRT) is the most common malignant brain tumor in infants. ATRT is associated with inactivation/deletion of SMARCB1, a member of the SWI/SNF chromatin remodeling complex. SMARCB1 loss contributes to tumorigenicity by compromising SWI/SNF activity at specific loci associated with the CoREST repressor complex, which regulates transcription at critical gene promoters and enhancers. We therefore explored the role of the CoREST repressor complex in ATRT.

methodsWe evaluated the effects of the bifunctional LSD1/HDAC1/2 small molecule CoREST inhibitor, corin, on ATRT tumor cell growth, apoptosis, differentiation, gene expression and chromatin accessibility.

resultsCorin inhibited the growth of ATRT cells regardless of their epigenetic subgroup. Corin caused increased tumor cell apoptosis and differentiation. ATAC-seq showed increased chromatin accessibility in corin-treated ATRT cells, with changes seen at genes associated with neuronal differentiation and synaptic function. RNA-seq confirmed increased expression of neuronal differentiation genes in ATRT cells treated with corin. Knockdown of RCOR2 phenocopied the effects of corin, and desensitized the cells to the drug, confirming corin specificity to the CoREST complex. Corin suppressed orthotopic ATRT tumor growth, leading to significant extension of lifespan in ATRT mouse models. Corin caused increased histone acetylation (H3K9ac) and methylation (H3K4Me1) in ATRT orthotopic xenografts, consistent with on-target pharmacodynamics.

conclusionsThe CoREST inhibitor, corin, suppressed tumor growth, induced differentiation, and promoted apoptosis in ATRT leading to significantly increased survival of mice bearing ATRT orthotopic xenografts. Our results suggest a potential application of CoREST complex inhibitors in patients with ATRT.

Indexed as

epigenetic reprogrammingLSD1neuronal differentiationrhabdoidSWI/SNF

Identifiers

PMID42479134
PMCPMC13615391

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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.