ArticleBlood cancer discovery2022
BCOR and BCORL1 Mutations Drive Epigenetic Reprogramming and Oncogenic Signaling by Unlinking PRC1.1 from Target Genes.
Article in Blood cancer discovery, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 40 citations in OpenAlex.
- Azacitidine-induced remission enables allogeneic transplantation inHaematologica · 2026Article
- Oncometabolites in Cancer Metabolism: Mechanistic Insights and Biomarker Potential- A Narrative Review.Health science reports · 2026Article
- Inhibition of USP7 Destabilizes the Noncanonical PRC1.1 Complex and Induces Neuroblastoma Differentiation.Molecular cancer research : MCR · 2026Article
- Sustained PRC1.1 activity preserves gene repression independently of PRC2.2 and restrains leukemic cell differentiation.Nucleic acids research · 2026Article
- Critical Role of Molecular-Based Stratification in Low-Risk Myelodysplastic Syndrome with Direct Progression to Acute Myeloid Leukemia: A Case Report.International journal of molecular sciences · 2026Article
- Multiomic analysis of clonal development reveals new regulators of leukemic cell growth.Genes & development · 2026Article
- BCOR Mutations Deregulate Cell Cycle and Hypoxic Adaptation Pathways in Retinoblastoma.Molecular cancer research : MCR · 2026Article
- Reduced PRC2 function causes asparaginase resistance in T-ALL by decreasing WNT pathway activity.Blood advances · 2026Article
- BCOR mutations define a therapeutic vulnerability to DHODH Inhibition in acute myeloid leukemia.Annals of hematology · 2026Article
- Clinical management and therapeutic development for the rare disease rhabdomyosarcoma.Journal of Cancer · 2026Review
- Analysis and Interpretation of Somatic NMD-Escaping Variants in Oncogenes and Dual-Function Genes across Adult and Pediatric Cancer Cohorts.medRxiv : the preprint server for health sciences · 2025Article
- Targeting developmental vulnerabilities in childhood sarcomas.Cancer metastasis reviews · 2025Review
- Analysis of a BCOR internal tandem duplication in mouse embryonic stem cell to neuronal precursor differentiation.Genetics · 2025Article
- Hereditary Hematopoietic Malignancies: Considerations for Optimizing Diagnosis and Management.Current oncology reports · 2025Review
- CNS Tumor with BCOR/BCORL1 Fusion: A Rare Tumor Entity.International journal of molecular sciences · 2025Article
- Somatic gene delivery faithfully recapitulates a molecular spectrum of high-risk sarcomas.Nature communications · 2025Article
- The dynamic evolution of lineage switch under CD19 CAR-T treatment in non-KMT2A rearranged B-ALL patients.Leukemia · 2025Article
- NUP98 fusion proteins and KMT2A-MENIN antagonize PRC1.1 to drive gene expression in AML.Cell reports · 2024Article
- Article
- Identification of genetic fingerprint of type I interferon therapy in visceral metastases of melanoma.Scientific reports · 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
27 authors at 8 institutions in 1 country.
Funding
Abstract
Polycomb repressive epigenetic complexes are recurrently dysregulated in cancer. Unlike polycomb repressive complex 2 (PRC2), the role of PRC1 in oncogenesis and therapy resistance is not well-defined. Here, we demonstrate that highly recurrent mutations of the PRC1 subunits BCOR and BCORL1 in leukemia disrupt assembly of a noncanonical PRC1.1 complex, thereby selectively unlinking the RING-PCGF enzymatic core from the chromatin-targeting auxiliary subcomplex. As a result, BCOR-mutated PRC1.1 is localized to chromatin but lacks repressive activity, leading to epigenetic reprogramming and transcriptional activation at target loci. We define a set of functional targets that drive aberrant oncogenic signaling programs in PRC1.1-mutated cells and primary patient samples. Activation of these PRC1.1 targets in BCOR-mutated cells confers acquired resistance to treatment while sensitizing to targeted kinase inhibition. Our study thus reveals a novel epigenetic mechanism that explains PRC1.1 tumor-suppressive activity and identifies a therapeutic strategy in PRC1.1-mutated cancer. SIGNIFICANCE: We demonstrate that BCOR and BCORL1 mutations in leukemia unlink PRC1.1 repressive function from target genes, resulting in epigenetic reprogramming and activation of aberrant cell signaling programs that mediate treatment resistance. Our study provides mechanistic insights into the pathogenesis of PRC1.1-mutated leukemia that inform novel therapeutic approaches. This article is highlighted in the In This Issue feature, p. 85.
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.