ArticleJournal of cellular and molecular medicine2010
Inhibition of IGF-IR tyrosine kinase induces apoptosis and cell cycle arrest in imatinib-resistant chronic myeloid leukaemia cells.
Article in Journal of cellular and molecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Exploitation of the fibrinolytic system by B-cell acute lymphoblastic leukemia and its therapeutic targeting.Nature communications · 2024Article
- Integrated drug profiling and CRISPR screening identify BCR::ABL1-independent vulnerabilities in chronic myeloid leukemia.Cell reports. Medicine · 2024Article
- Impact of metformin on tyrosine kinase inhibitor response in chronic myeloid leukemia.Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners · 2022Observational
- IGF‑IR promotes clonal cell proliferation in myelodysplastic syndromes via inhibition of the MAPK pathway.Oncology reports · 2020Article
- Dual inhibition of IGF-IR and ALK as an effective strategy to eradicate NPM-ALKJournal of hematology & oncology · 2019Article
- Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells.Environmental science and pollution research international · 2017Article
- Type I insulin-like growth factor receptor signaling in hematological malignancies.Oncotarget · 2017Review
- Co-exposure to amorphous silica nanoparticles and benzo[a]pyrene at low level in human bronchial epithelial BEAS-2B cells.Environmental science and pollution research international · 2016Article
- Article
- The transcription factors Ik-1 and MZF1 downregulate IGF-IR expression in NPM-ALK⁺ T-cell lymphoma.Molecular cancer · 2015Article
- Article
- Inhibition of type I insulin-like growth factor receptor tyrosine kinase by picropodophyllin induces apoptosis and cell cycle arrest in T lymphoblastic leukemia/lymphoma.Leukemia & lymphoma · 2014Article
- Molecular and functional characterizations of the association and interactions between nucleophosmin-anaplastic lymphoma kinase and type I insulin-like growth factor receptor.Neoplasia (New York, N.Y.) · 2013Article
- Expression and effects of inhibition of type I insulin-like growth factor receptor tyrosine kinase in mantle cell lymphoma.Haematologica · 2011Article
- A computational approach to analyze the mechanism of action of the kinase inhibitor bafetinib.PLoS computational biology · 2010Article
- Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Although signalling through the type I insulin-like growth factor receptor (IGF-IR) maintains the survival of haematopoietic cells, a specific role of IGF-IR in haematological neoplasms remains largely unknown. Chronic myeloid leukaemia (CML) is the most common subtype of chronic myeloproliferative diseases. Typically, CML evolves as a chronic phase (CP) disease that progresses into accelerated (AP) and blast phase (BP) stages. In this study, we show that IGF-IR is universally expressed in four CML cell lines. IGF-IR was expressed in only 30% and 25% of CP and AP patients, respectively, but its frequency of expression increased to 73% of BP patients. Increased expression levels of IGF-IR with CML progression was supported by quantitative real-time PCR that demonstrated significantly higher levels of IGF-IR mRNA in BP patients. Inhibition of IGF-IR decreased the viability and proliferation of CML cell lines and abrogated their growth in soft agar. Importantly, inhibition of IGF-IR decreased the viability of cells resistant to imatinib mesylate including BaF3 cells transfected with p210 BCR-ABL mutants, CML cell lines and primary neoplastic cells from patients. The negative effects of inhibition of IGF-IR were attributable to apoptosis and cell cycle arrest due to alterations of downstream target proteins. Our findings suggest that IGF-IR could represent a potential molecular target particularly for advanced stage or imatinib-resistant cases.
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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.