ArticleBlood2015
PAX5 is a tumor suppressor in mouse mutagenesis models of acute lymphoblastic leukemia.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 83 citations in OpenAlex.
- PD-1 Expression Promotes Immune Evasion in B-ALL.Hematology reports · 2025Article
- In vivo CRISPR screening reveals cooperation of KMT2D and TP53 deficiencies in B-cell lymphomagenesis.Blood advances · 2025Article
- A SIRT7-dependent acetylation switch regulates early B cell differentiation and lineage commitment through Pax5.Nature immunology · 2024Article
- Article
- Unraveling Copy Number Alterations in Pediatric B-Cell Acute Lymphoblastic Leukemia: Correlation with Induction Phase Remission Using MLPA.Asian Pacific journal of cancer prevention : APJCP · 2024Observational
- Article
- Transcription factor networks link B-lymphocyte development and malignant transformation in leukemia.Genes & development · 2023Review
- Lessons from mouse models in the impact of risk factors on the genesis of childhood B-cell leukemia.Frontiers in immunology · 2023Review
- International Consensus Classification of acute lymphoblastic leukemia/lymphoma.Virchows Archiv : an international journal of pathology · 2023Review
- The MBNL1/circNTRK2/PAX5 pathway regulates aerobic glycolysis in glioblastoma cells by encoding a novel protein NTRK2-243aa.Cell death & disease · 2022Article
- Childhood B-Cell Preleukemia Mouse Modeling.International journal of molecular sciences · 2022Review
- Genetic Biomarkers and Their Clinical Implications in B-Cell Acute Lymphoblastic Leukemia in Children.International journal of molecular sciences · 2022Review
- Review
- Analysis of lncRNA and mRNA Repertoires in Lung From BAFF-R-DeficientFrontiers in immunology · 2022Article
- Oncogene-Induced Reprogramming in Acute Lymphoblastic Leukemia: Towards Targeted Therapy of Leukemia-Initiating Cells.Cancers · 2021Review
- Emerging molecular subtypes and therapeutic targets in B-cell precursor acute lymphoblastic leukemia.Frontiers of medicine · 2021Review
- Preventive Healthcare and Management for Acute Lymphoblastic Leukaemia in Adults: Case Report and Literature Review.Healthcare (Basel, Switzerland) · 2021Article
- Identification of novel, clonally stable, somatic mutations targeting transcription factors PAX5 and NKX2-3, the epigenetic regulator LRIF1, and BRAF in a case of atypical B-cell chronic lymphocytic leukemia harboring a t(14;18)(q32;q21).Cold Spring Harbor molecular case studies · 2021Article
- Advances in germline predisposition to acute leukaemias and myeloid neoplasms.Nature reviews. Cancer · 2021Review
- Forward and Reverse Genetics of B Cell Malignancies: From Insertional Mutagenesis to CRISPR-Cas.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
20 authors at 3 institutions in 3 countries.
Funding
Abstract
Alterations of genes encoding transcriptional regulators of lymphoid development are a hallmark of B-progenitor acute lymphoblastic leukemia (B-ALL) and most commonly involve PAX5, encoding the DNA-binding transcription factor paired-box 5. The majority of PAX5 alterations in ALL are heterozygous, and key PAX5 target genes are expressed in leukemic cells, suggesting that PAX5 may be a haploinsufficient tumor suppressor. To examine the role of PAX5 alterations in leukemogenesis, we performed mutagenesis screens of mice heterozygous for a loss-of-function Pax5 allele. Both chemical and retroviral mutagenesis resulted in a significantly increased penetrance and reduced latency of leukemia, with a shift to B-lymphoid lineage. Genomic profiling identified a high frequency of secondary genomic mutations, deletions, and retroviral insertions targeting B-lymphoid development, including Pax5, and additional genes and pathways mutated in ALL, including tumor suppressors, Ras, and Janus kinase-signal transducer and activator of transcription signaling. These results show that in contrast to simple Pax5 haploinsufficiency, multiple sequential alterations targeting lymphoid development are central to leukemogenesis and contribute to the arrest in lymphoid maturation characteristic of ALL. This cross-species analysis also validates the importance of concomitant alterations of multiple cellular growth, signaling, and tumor suppression pathways in the pathogenesis of B-ALL.
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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.