ArticleBlood2016
Normal ABL1 is a tumor suppressor and therapeutic target in human and mouse leukemias expressing oncogenic ABL1 kinases.
Article in Blood, 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, 51 citations in OpenAlex.
- Identification of new dasatinib analogues targeting mutated BCR-ABL1: virtual screening, molecular docking, and dynamics simulations studies.Molecular diversity · 2026Article
- New Fusarochromanone Derivatives from the Marine FungusMarine drugs · 2024Article
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- MEK1/2 regulate normal BCR and ABL1 tumor-suppressor functions to dictate ATO response in TKI-resistant Ph+ leukemia.Leukemia · 2023Article
- ABL1 kinase as a tumor suppressor in AML1-ETO and NUP98-PMX1 leukemias.Blood cancer journal · 2023Article
- Molecular mechanism of Wilms' tumor (Wt1) (+/-KTS) variants promoting proliferation and migration of ovarian epithelial cells by bioinformatics analysis.Journal of ovarian research · 2023Article
- Abl kinases can function as suppressors of tumor progression and metastasis.Frontiers in oncology · 2023Article
- A Conformation Selective Mode of Inhibiting SRC Improves Drug Efficacy and Tolerability.Cancer research · 2021Article
- Molecular insights on ABL kinase activation using tree-based machine learning models and molecular docking.Molecular diversity · 2021Article
- Genome-wide DNA methylome analysis identifies methylation signatures associated with survival and drug resistance of ovarian cancers.Clinical epigenetics · 2021Article
- The mechanism of TiaoGanYiPi formula for treating chronic hepatitis B by network pharmacology and molecular docking verification.Scientific reports · 2021Article
- Review
- Philadelphia Chromosome-Positive Leukemia in the Lymphoid Lineage-Similarities and Differences with the Myeloid Lineage and Specific Vulnerabilities.International journal of molecular sciences · 2020Review
- In silico analysis of alternative splicing on drug-target gene interactions.Scientific reports · 2020Article
- Identifying functions and prognostic biomarkers of network motifs marked by diverse chromatin states in human cell lines.Oncogene · 2020Article
- Sphingosine-1-Phosphate Receptor 1 Activity Promotes Tumor Growth by Amplifying VEGF-VEGFR2 Angiogenic Signaling.Cell reports · 2019Article
- Autophagy and Apoptosis Specific Knowledgebases-guided Systems Pharmacology Drug Research.Current cancer drug targets · 2019Article
- Article
- Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
17 authors at 10 institutions in 5 countries.
Funding
Abstract
Leukemias expressing constitutively activated mutants of ABL1 tyrosine kinase (BCR-ABL1, TEL-ABL1, NUP214-ABL1) usually contain at least 1 normal ABL1 allele. Because oncogenic and normal ABL1 kinases may exert opposite effects on cell behavior, we examined the role of normal ABL1 in leukemias induced by oncogenic ABL1 kinases. BCR-ABL1-Abl1(-/-) cells generated highly aggressive chronic myeloid leukemia (CML)-blast phase-like disease in mice compared with less malignant CML-chronic phase-like disease from BCR-ABL1-Abl1(+/+) cells. Additionally, loss of ABL1 stimulated proliferation and expansion of BCR-ABL1 murine leukemia stem cells, arrested myeloid differentiation, inhibited genotoxic stress-induced apoptosis, and facilitated accumulation of chromosomal aberrations. Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1. Therefore, we postulate that normal ABL1 kinase behaves like a tumor suppressor and therapeutic target in leukemias expressing oncogenic forms of the kinase.
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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.