ArticleNature communications2019
Lsd1 as a therapeutic target in Gfi1-activated medulloblastoma.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 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
60 citing papers in PubMed, 84 citations in OpenAlex.
- Cancer-associated KBTBD4 mutations induce differentiation defects and confer a unique therapeutic vulnerability.Cancer gene therapy · 2026Article
- A tumor-associated photoreceptor signature unifies distinct central nervous system malignancies.Cancer cell · 2026Article
- Mechanisms of HIV Latency in Hematopoietic Progenitors: GFI1 as a Key Regulator.bioRxiv : the preprint server for biology · 2026Article
- Therapeutic targeting of chromatin alterations in leukemia and solid tumors.International journal of cancer · 2026Review
- The role of DNA methylation in directing treatment in medulloblastoma.Epigenomics · 2025Review
- Chromatin Regulatory Targets for Anticancer Therapeutics.Chemical reviews · 2025Review
- Reinforced plant-derived lipid nanoparticles for oral precise epigenome editing in colonic diseases.Science advances · 2025Article
- Maternal high fat and high sugar diet impacts on key DNA methylation enzymes in offspring brain in a sex-specific manner.Journal of neuroendocrinology · 2025Article
- Small-Molecule Drugs in Pediatric Neuro-Oncology.Current oncology (Toronto, Ont.) · 2025Review
- CoREST in pieces: Dismantling the CoREST complex for cancer therapy and beyond.Science advances · 2025Review
- In Silico Identification of LSD1 Inhibition-Responsive Targets in Small Cell Lung Cancer.Bioengineering (Basel, Switzerland) · 2025Article
- Lysine-specific demethylase 1 deletion reshapes tumour microenvironment to overcome acquired resistance to anti-programmed death 1 therapy in liver cancer.Clinical and translational medicine · 2025Article
- The dual HDAC/PI3K inhibitor CUDC-907 inhibits the growth and proliferation of MYC-driven Group 3 medulloblastoma.Cell death discovery · 2025Article
- Discovery of novel dual-target inhibitors of LSD1/EGFR for non-small cell lung cancer therapy.Acta pharmacologica Sinica · 2025Article
- Bone marrow mesenchymal stem cells-derived exosomes deliver microRNA-142-3p to disturb glioma progression by down-regulating GFI1.Discover oncology · 2025Article
- Arrested development: the dysfunctional life history of medulloblastoma.Genes & development · 2025Review
- Epigenetic modifications and their roles in pediatric brain tumor formation: emerging insights from chromatin dysregulation.Frontiers in oncology · 2025Review
- Aberrant histone modifications in pediatric brain tumors.Frontiers in oncology · 2025Review
- Single-cell multi-omics sequencing uncovers region-specific plasticity of glioblastoma for complementary therapeutic targeting.Science advances · 2024Article
- Prediction of the 3D cancer genome from whole-genome sequencing using InfoHiC.Molecular systems biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
17 authors at 9 institutions in 3 countries.
Funding
Abstract
Drugs that modify the epigenome are powerful tools for treating cancer, but these drugs often have pleiotropic effects, and identifying patients who will benefit from them remains a major clinical challenge. Here we show that medulloblastomas driven by the transcription factor Gfi1 are exquisitely dependent on the enzyme lysine demethylase 1 (Kdm1a/Lsd1). We demonstrate that Lsd1 physically associates with Gfi1, and that these proteins cooperate to inhibit genes involved in neuronal commitment and differentiation. We also show that Lsd1 is essential for Gfi1-mediated transformation: Gfi1 proteins that cannot recruit Lsd1 are unable to drive tumorigenesis, and genetic ablation of Lsd1 markedly impairs tumor growth in vivo. Finally, pharmacological inhibitors of Lsd1 potently inhibit growth of Gfi1-driven tumors. These studies provide important insight into the mechanisms by which Gfi1 contributes to tumorigenesis, and identify Lsd1 inhibitors as promising therapeutic agents for Gfi1-driven medulloblastoma.
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.