ArticleThe Journal of experimental medicine2007
Activation-induced cytidine deaminase acts as a mutator in BCR-ABL1-transformed acute lymphoblastic leukemia cells.
Article in The Journal of experimental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
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Who cites it
45 citing papers in PubMed, 88 citations in OpenAlex.
- Ibrutinib therapy downregulates AID enzyme and proliferative fractions in chronic lymphocytic leukemia.Blood · 2019Trial
- Common origins of autoimmune diseases and lymphoid malignancies.Trends in immunology · 2025Review
- Ultra-Deep Sequencing Reveals the Mutational Landscape of Classical Hodgkin Lymphoma.Cancer research communications · 2023Article
- Nonamer dependent RAG cleavage at CpGs can explain mechanism of chromosomal translocations associated to lymphoid cancers.PLoS genetics · 2022Article
- Review
- Support of BCP-ALL-cells by autologous bone marrow Th-cells involves induction of AID expression but not widespread AID off-target mutagenesis.Cancer immunology, immunotherapy : CII · 2021Article
- Small Molecule Inhibitors of Activation-Induced Deaminase Decrease Class Switch Recombination in B Cells.ACS pharmacology & translational science · 2021Article
- Alternative splicing of APOBEC3D generates functional diversity and its role as a DNA mutator.International journal of hematology · 2020Article
- Review
- Review
- Targeting CDK6 and BCL2 Exploits the "MYB Addiction" of PhCancer research · 2018Article
- Concomitant AID Expression and BCL7A Loss Associates With Accelerated Phase Progression and Imatinib Resistance in Chronic Myeloid Leukemia.Annals of laboratory medicine · 2017Article
- Article
- AID/APOBEC-network reconstruction identifies pathways associated with survival in ovarian cancer.BMC genomics · 2016Article
- CDKN2A-independent role of BMI1 in promoting growth and survival of Ph+ acute lymphoblastic leukemia.Leukemia · 2016Article
- HSP90 inhibitors decrease AID levels and activity in mice and in human cells.European journal of immunology · 2015Article
- Mechanisms of clonal evolution in childhood acute lymphoblastic leukemia.Nature immunology · 2015Article
- Deregulated expression of the HSP40 family members Auxilin-1 and -2 is indicative of proteostasis imbalance and predicts patient outcome in Ph(+) leukemia.Experimental hematology & oncology · 2015Article
- Generation and repair of AID-initiated DNA lesions in B lymphocytes.Frontiers of medicine · 2014Review
- Article
Corrections and comments
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Authors and funding
12 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Philadelphia chromosome (Ph) encoding the oncogenic BCR-ABL1 kinase defines a subset of acute lymphoblastic leukemia (ALL) with a particularly unfavorable prognosis. ALL cells are derived from B cell precursors in most cases and typically carry rearranged immunoglobulin heavy chain (IGH) variable (V) region genes devoid of somatic mutations. Somatic hypermutation is restricted to mature germinal center B cells and depends on activation-induced cytidine deaminase (AID). Studying AID expression in 108 cases of ALL, we detected AID mRNA in 24 of 28 Ph(+) ALLs as compared with 6 of 80 Ph(-) ALLs. Forced expression of BCR-ABL1 in Ph(-) ALL cells and inhibition of the BCR-ABL1 kinase showed that aberrant expression of AID depends on BCR-ABL1 kinase activity. Consistent with aberrant AID expression in Ph(+) ALL, IGH V region genes and BCL6 were mutated in many Ph(+) but unmutated in most Ph(-) cases. In addition, AID introduced DNA single-strand breaks within the tumor suppressor gene CDKN2B in Ph(+) ALL cells, which was sensitive to BCR-ABL1 kinase inhibition and silencing of AID expression by RNA interference. These findings identify AID as a BCR-ABL1-induced mutator in Ph(+) ALL cells, which may be relevant with respect to the particularly unfavorable prognosis of this leukemia subset.
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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.