ArticleGenes & development2014
Pax5 loss imposes a reversible differentiation block in B-progenitor acute lymphoblastic leukemia.
Article in Genes & development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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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.
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.
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Who cites it
65 citing papers in PubMed, 100 citations in OpenAlex.
- PAX5 modulates vascularization and contributes to neuroendocrine lineage transition during carcinoma progression.The Journal of clinical investigation · 2026Article
- Dysregulated NF-κB dynamics impair proteostasis and drive premature differentiation in aging B cell development.Cell press blue · 2026Article
- B-Cell Differentiation of Human Hematopoietic Progenitors Is Efficiently Supported by Wharton Jelly-Derived Mesenchymal Stem Cells.European journal of immunology · 2026Article
- Cancer-associated adipocytes confer CDK4/6 inhibitor resistance in ER+ breast cancer through an IL-6/STAT3/SREBF2 axis coupled with cholesterol metabolism and cell cycle reprogramming.International journal of biological sciences · 2026Article
- Sequence Diversity and Expression Profiles of T Cell Receptor Beta Chain Constant Genes TRBC1 and TRBC2 in Canine Lymphoid Tumour Cell Lines and Normal Lymphocytes.Veterinary and comparative oncology · 2025Article
- PD-1 Expression Promotes Immune Evasion in B-ALL.Hematology reports · 2025Article
- [Research progress on copy number alterations in pediatric B-cell acute lymphoblastic leukemia].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2025Review
- A novel stroma-dependent leukemia cell line from a patient with mixed-phenotype acute leukemia with Ph chromosome and PAX5 mutation.International journal of hematology · 2025Article
- CRISPR screening reveals ZNF217 as a vulnerability in high-risk B-cell acute lymphoblastic leukemia.Theranostics · 2025Article
- A SIRT7-dependent acetylation switch regulates early B cell differentiation and lineage commitment through Pax5.Nature immunology · 2024Article
- PAX5 functions as a tumor suppressor by RB-E2F-mediated cell cycle arrest in Kaposi sarcoma-associated herpesvirus-infected primary effusion lymphoma.Neoplasia (New York, N.Y.) · 2024Article
- Mycovirus-ContainingInternational journal of molecular sciences · 2024Article
- Article
- Concepts in B cell acute lymphoblastic leukemia pathogenesis.Journal of leukocyte biology · 2024Review
- Early B-Cell Factor 1: An Archetype for a Lineage-Restricted Transcription Factor Linking Development to Disease.Advances in experimental medicine and biology · 2024Review
- Comprehensive genomic characterization of hematologic malignancies at a pediatric tertiary care center.Frontiers in oncology · 2024Article
- Comprehensive summary: the role of PBX1 in development and cancers.Frontiers in cell and developmental biology · 2024Review
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- Deletion of the transcriptional regulator TFAP4 accelerates c-MYC-driven lymphomagenesis.Cell death and differentiation · 2023Article
- Identification of Inflammatory Gene in the Congenital Heart Surgery Patients following Cardiopulmonary Bypass via the Way of WGCNA and Machine Learning Algorithms.Disease markers · 2023Article
5 more citing papers are in PubMed but not listed here.
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 6 institutions in 3 countries.
Funding
Abstract
Loss-of-function mutations in hematopoietic transcription factors including PAX5 occur in most cases of B-progenitor acute lymphoblastic leukemia (B-ALL), a disease characterized by the accumulation of undifferentiated lymphoblasts. Although PAX5 mutation is a critical driver of B-ALL development in mice and humans, it remains unclear how its loss contributes to leukemogenesis and whether ongoing PAX5 deficiency is required for B-ALL maintenance. Here we used transgenic RNAi to reversibly suppress endogenous Pax5 expression in the hematopoietic compartment of mice, which cooperates with activated signal transducer and activator of transcription 5 (STAT5) to induce B-ALL. In this model, restoring endogenous Pax5 expression in established B-ALL triggers immunophenotypic maturation and durable disease remission by engaging a transcriptional program reminiscent of normal B-cell differentiation. Notably, even brief Pax5 restoration in B-ALL cells causes rapid cell cycle exit and disables their leukemia-initiating capacity. These and similar findings in human B-ALL cell lines establish that Pax5 hypomorphism promotes B-ALL self-renewal by impairing a differentiation program that can be re-engaged despite the presence of additional oncogenic lesions. Our results establish a causal relationship between the hallmark genetic and phenotypic features of B-ALL and suggest that engaging the latent differentiation potential of B-ALL cells may provide new therapeutic entry points.
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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.