ArticleBlood cancer discovery2022
ZNF384 Fusion Oncoproteins Drive Lineage Aberrancy in Acute Leukemia.
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 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 29 citations in OpenAlex.
- A genomic and epigenomic lens into the biology of acute lymphoblastic leukaemia.Nature reviews. Cancer · 2026Review
- Plasticity under pressure: biology and detection of lineage switch in acute leukemia.Leukemia · 2026Review
- Antigen Pressure, Clonal Evolution, and Lineage Plasticity in B-Cell Acute Lymphoblastic Leukemia: Resistance Biology in the Immunotherapy Era.Current hematologic malignancy reports · 2026Review
- Co-option of lineage plasticity as a hallmark of multipotent acute leukemias.Blood neoplasia · 2026Review
- Article
- Multiomic analysis of clonal development reveals new regulators of leukemic cell growth.Genes & development · 2026Article
- CD19-negative relapse after CAR-T cell therapy: mechanisms of antigen escape and lineage switch.Frontiers in immunology · 2026Review
- Case Report: Acute myeloid leukemia with mixed immunophenotypic features and TCF3::ZNF384 fusion in a pediatric patient with CNS involvement: a diagnostic and therapeutic challenge.Frontiers in pediatrics · 2026Article
- KAT6A and KAT7 Histone Acetyltransferase Complexes Are Molecular Dependencies and Therapeutic Targets in NUP98-Rearranged Acute Myeloid Leukemia.Cancer discovery · 2025Article
- Identification of Molecular Subtypes of B-Cell Acute Lymphoblastic Leukemia in Mexican Children by Whole-Transcriptome Analysis.International journal of molecular sciences · 2025Article
- Multipotent lineage potential in B cell acute lymphoblastic leukemia is associated with distinct cellular origins and clinical features.Nature cancer · 2025Article
- Single-cell panleukemia signatures of HSPC-like blasts predict drug response and clinical outcome.Blood · 2025Article
- Integrated Network Analysis Decipher ZNF384-Related miR-20b-5p and miR-424-5p in Colon Adenocarcinoma.Cancer reports (Hoboken, N.J.) · 2025Article
- Biologic and Clinical Analysis of Childhood Gamma Delta T-ALL Identifies LMO2/STAG2 Rearrangements as Extremely High Risk.Cancer discovery · 2024Article
- Multiomic single cell sequencing identifies stemlike nature of mixed phenotype acute leukemia.Nature communications · 2024Article
- SJPedPanel: A Pan-Cancer Gene Panel for Childhood Malignancies to Enhance Cancer Monitoring and Early Detection.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- RGS1 and CREB5 are direct and common transcriptional targets of ZNF384-fusion proteins.Cancer medicine · 2024Article
- Acute lymphoblastic leukaemia.Nature reviews. Disease primers · 2024Review
- Advancing Diagnostics and Therapy to Reach Universal Cure in Childhood ALL.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2023Review
- Multimodal classification of molecular subtypes in pediatric acute lymphoblastic leukemia.NPJ precision oncology · 2023Article
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 3 countries.
Funding
Abstract
ZNF384-rearranged fusion oncoproteins (FO) define a subset of lineage ambiguous leukemias, but their mechanistic role in leukemogenesis and lineage ambiguity is poorly understood. Using viral expression in mouse and human hematopoietic stem and progenitor cells (HSPC) and a Ep300::Znf384 knockin mouse model, we show that ZNF384 FO promote hematopoietic expansion, myeloid lineage skewing, and self-renewal. In mouse HSPCs, concomitant lesions, such as NRASG12D, were required for fully penetrant leukemia, whereas in human HSPCs, expression of ZNF384 FO drove B/myeloid leukemia, with sensitivity of a ZNF384-rearranged xenograft to FLT3 inhibition in vivo. Mechanistically, ZNF384 FO occupy a subset of predominantly intragenic/enhancer regions with increased histone 3 lysine acetylation and deregulate expression of hematopoietic stem cell transcription factors. These data define a paradigm for FO-driven lineage ambiguous leukemia, in which expression in HSPCs results in deregulation of lineage-specific genes and hematopoietic skewing, progressing to full leukemia in the context of proliferative stress. SIGNIFICANCE: Expression of ZNF384 FO early in hematopoiesis results in binding and deregulation of key hematopoietic regulators, skewing of hematopoiesis, and priming for leukemic transformation. These results reveal the interplay between cell of origin and expression of ZNF384 FO to mediate lineage ambiguity and leukemia development. This article is highlighted in the In This Issue feature, p. 171.
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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.