ArticleOncogene2016
Sleeping Beauty transposon screen identifies signaling modules that cooperate with STAT5 activation to induce B-cell acute lymphoblastic leukemia.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Lipopolymer/siRNA Nanoparticles Targeting the Signal Transducer and Activator of Transcription 5A Disrupts Proliferation of Acute Lymphoblastic Leukemia.ACS pharmacology & translational science · 2024Article
- Loss of Nudt15 thiopurine detoxification increases direct DNA damage in hematopoietic stem cells.Scientific reports · 2023Article
- Biological Functions of the KDM2 Family of Histone Demethylases.Advances in experimental medicine and biology · 2023Article
- Targeting SOS1 overcomes imatinib resistance with BCR-ABL independence through uptake transporter SLC22A4 in CML.Molecular therapy oncolytics · 2021Article
- 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
- Regulation of Normal and Malignant Hematopoiesis by FBOX Ubiquitin E3 Ligases.Trends in immunology · 2020Review
- Genome Engineering of Primary Human B Cells Using CRISPR/Cas9.Journal of visualized experiments : JoVE · 2020Article
- In vivo functional screening for systems-level integrative cancer genomics.Nature reviews. Cancer · 2020Review
- Transposon Insertion Mutagenesis in Mice for Modeling Human Cancers: Critical Insights Gained and New Opportunities.International journal of molecular sciences · 2020Review
- Review
- A Cell Density-Dependent Reporter in the Drosophila S2 Cells.Scientific reports · 2019Article
- Sleeping Beauty Mouse Models of Cancer: Microenvironmental Influences on Cancer Genetics.Frontiers in oncology · 2019Review
- Advances in functional genetic screening with transposons and CRISPR/Cas9 to illuminate cancer biology.Current opinion in genetics & development · 2018Review
- Identifying transposon insertions and their effects from RNA-sequencing data.Nucleic acids research · 2017Article
- Transposon mutagenesis identifies chromatin modifiers cooperating withProceedings of the National Academy of Sciences of the United States of America · 2017Article
- It is a differentiation game: STAT5 in a new role.Cell death and differentiation · 2017Article
- Antagonism of B cell enhancer networks by STAT5 drives leukemia and poor patient survival.Nature immunology · 2017Article
- KDM2A integrates DNA and histone modification signals through a CXXC/PHD module and direct interaction with HP1.Nucleic acids research · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Signal transducer and activator of transcription 5 (STAT5) activation occurs frequently in human progenitor B-cell acute lymphoblastic leukemia (B-ALL). To identify gene alterations that cooperate with STAT5 activation to initiate leukemia, we crossed mice expressing a constitutively active form of STAT5 (Stat5b-CA) with mice in which a mutagenic Sleeping Beauty transposon (T2/Onc) was mobilized only in B cells. Stat5b-CA mice typically do not develop B-ALL (<2% penetrance); in contrast, 89% of Stat5b-CA mice in which the T2/Onc transposon had been mobilized died of B-ALL by 3 months of age. High-throughput sequencing approaches were used to identify genes frequently targeted by the T2/Onc transposon; these included Sos1 (74%), Kdm2a (35%), Jak1 (26%), Bmi1 (19%), Prdm14 or Ncoa2 (13%), Cdkn2a (10%), Ikzf1 (8%), Caap1 (6%) and Klf3 (6%). Collectively, these mutations target three major cellular processes: (i) the Janus kinase/STAT5 pathway (ii) progenitor B-cell differentiation and (iii) the CDKN2A tumor-suppressor pathway. Transposon insertions typically resulted in altered expression of these genes, as well as downstream pathways including STAT5, extracellular signal-regulated kinase (Erk) and p38. Importantly, expression of Sos1 and Kdm2a, and activation of p38, correlated with survival, further underscoring the role these genes and associated pathways have in B-ALL.
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Registered trials
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