ArticleBMC cancer2015
Somatic drivers of B-ALL in a model of ETV6-RUNX1; Pax5(+/-) leukemia.
Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Copy number alterations in pediatric B-cell precursor acute lymphoblastic leukemia patients and their association with patients' outcome.Annals of hematology · 2025Article
- Article
- RNA binding protein IGF2BP1 synergizes with ETV6-RUNX1 to drive oncogenic signaling in B-cell Acute Lymphoblastic Leukemia.Journal of experimental & clinical cancer research : CR · 2023Article
- Childhood B-Cell Preleukemia Mouse Modeling.International journal of molecular sciences · 2022Review
- Oncogene-Induced Reprogramming in Acute Lymphoblastic Leukemia: Towards Targeted Therapy of Leukemia-Initiating Cells.Cancers · 2021Review
- Identification of mutations that cooperate with defects in B cell transcription factors to initiate leukemia.Oncogene · 2021Article
- Forward and Reverse Genetics of B Cell Malignancies: From Insertional Mutagenesis to CRISPR-Cas.Frontiers in immunology · 2021Review
- In vivo functional screening for systems-level integrative cancer genomics.Nature reviews. Cancer · 2020Review
- The SWI/SNF complex in cancer - biology, biomarkers and therapy.Nature reviews. Clinical oncology · 2020Review
- Transposon Insertion Mutagenesis in Mice for Modeling Human Cancers: Critical Insights Gained and New Opportunities.International journal of molecular sciences · 2020Review
- Sleeping Beauty Mouse Models of Cancer: Microenvironmental Influences on Cancer Genetics.Frontiers in oncology · 2019Review
- Driver mutations in Janus kinases in a mouse model of B-cell leukemia induced by deletion of PU.1 and Spi-B.Blood advances · 2018Article
- PAX5-ELN oncoprotein promotes multistep B-cell acute lymphoblastic leukemia in mice.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- A causal mechanism for childhood acute lymphoblastic leukaemia.Nature reviews. Cancer · 2018Review
- Molecular processes involved in B cell acute lymphoblastic leukaemia.Cellular and molecular life sciences : CMLS · 2018Review
- Modeling the process of childhoodOncotarget · 2017Review
- B lymphoblastic leukemia/lymphoma: new insights into genetics, molecular aberrations, subclassification and targeted therapy.Oncotarget · 2017Review
- Identifying transposon insertions and their effects from RNA-sequencing data.Nucleic acids research · 2017Article
- Overview of the Use of Murine Models in Leukemia and Lymphoma Research.Frontiers in oncology · 2017Review
- ZNF423 and ZNF521: EBF1 Antagonists of Potential Relevance in B-Lymphoid Malignancies.BioMed research international · 2015Review
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundB-cell precursor acute lymphoblastic leukemia (B-ALL) is amongst the leading causes of childhood cancer-related mortality. Its most common chromosomal aberration is the ETV6-RUNX1 fusion gene, with ~25% of ETV6-RUNX1 patients also carrying PAX5 alterations.
methodsWe have recreated this mutation background by inter-crossing Etv6-RUNX1 (Etv6 (RUNX1-SB)) and Pax5(+/-) mice and performed an in vivo analysis to find driver genes using Sleeping Beauty transposon-mediated mutagenesis and also exome sequencing.
resultsCombination of Etv6-RUNX1 and Pax5(+/-) alleles generated a transplantable B220 + CD19+ B-ALL with a significant disease incidence. RNA-seq analysis showed a gene expression pattern consistent with arrest at the pre-B stage. Analysis of the transposon common insertion sites identified genes involved in B-cell development (Zfp423) and the JAK/STAT signaling pathway (Jak1, Stat5 and Il2rb), while exome sequencing revealed somatic hotspot mutations in Jak1 and Jak3 at residues analogous to those mutated in human leukemias, and also mutation of Trp53.
conclusionsPowerful synergies exists in our model suggesting STAT pathway activation and mutation of Trp53 are potent drivers of B-ALL in the context of Etv6-RUNX1;Pax5(+/-).
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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.