ArticleLeukemia2009
The stem cell factor-c-KIT pathway must be inhibited to enable apoptosis induced by BCR-ABL inhibitors in chronic myelogenous leukemia cells.
Article in Leukemia, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Patient-specific and gene-corrected induced pluripotent stem cell-derived endothelial cells elucidate single-cell phenotype of pulmonary veno-occlusive disease.Stem cell reports · 2022Article
- Stem cell factor is implicated in microenvironmental interactions and cellular dynamics of chronic lymphocytic leukemia.Haematologica · 2021Article
- Redistribution, homing and organ-invasion of neoplastic stem cells in myeloid neoplasms.Seminars in cancer biology · 2020Review
- Expression differences of miR-142-5p between treatment-naïve chronic myeloid leukemia patients responding and non-responding to imatinib therapy suggest a link to oncogenic ABL2, SRI, cKIT and MCL1 signaling pathways critical for development of therapy resistance.Experimental hematology & oncology · 2020Article
- Discovery of the Oncogenic Parp1, a Target of bcr-abl and a Potential Therapeutic, in mir-181a/PPFIA1 Signaling Pathway.Molecular therapy. Nucleic acids · 2019Article
- A kinase profile-adapted drug combination elicits synergistic cooperative effects on leukemic cells carrying BCR-ABL1Leukemia research · 2019Article
- Design, synthesis and broad-spectrum Bcr-Abl inhibitory activity of novel thiazolamide-benzamide derivatives.RSC advances · 2019Article
- Pharmacogenetics and Pharmacogenomics of Targeted Therapeutics in Chronic Myeloid Leukemia.Molecular diagnosis & therapy · 2017Review
- Expression of CD25 on leukemic stem cells in BCR-ABL1Experimental hematology · 2017Review
- Opposing roles of KIT and ABL1 in the therapeutic response of gastrointestinal stromal tumor (GIST) cells to imatinib mesylate.Oncotarget · 2017Article
- Effect of tyrosine kinase inhibitors on stemness in normal and chronic myeloid leukemia cells.Leukemia · 2017Article
- Silencing stem cell factor attenuates stemness and inhibits migration of cancer stem cells derived from Lewis lung carcinoma cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Long noncoding RNA, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression.Molecular cancer · 2015Article
- PI3K/mTOR pathway inhibitors sensitize chronic myeloid leukemia stem cells to nilotinib and restore the response of progenitors to nilotinib in the presence of stem cell factor.Cell death & disease · 2013Article
- KIT signaling governs differential sensitivity of mature and primitive CML progenitors to tyrosine kinase inhibitors.Cancer research · 2013Article
- Phosphorylation of serine palmitoyltransferase long chain-1 (SPTLC1) on tyrosine 164 inhibits its activity and promotes cell survival.The Journal of biological chemistry · 2013Article
- Synthesis and biological evaluation of analogues of the kinase inhibitor nilotinib as Abl and Kit inhibitors.Bioorganic & medicinal chemistry letters · 2013Article
- Variable behavior of iPSCs derived from CML patients for response to TKI and hematopoietic differentiation.PloS one · 2013Article
- Potentiation of Nilotinib-mediated cell death in the context of the bone marrow microenvironment requires a promiscuous JAK inhibitor in CML.Leukemia research · 2012Article
- Knockdown of SOD1 sensitizes the CD34+ CML cells to imatinib therapy.Medical oncology (Northwood, London, England) · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Imatinib is an effective first-line therapy for chronic myelogenous leukemia (CML) that acts by targeting the tyrosine kinase activity of BCR-ABL. To overcome resistance, second-generation inhibitors of BCR-ABL have been developed. Among these, nilotinib is more potent against BCR-ABL than imatinib, and is effective against many imatinib-resistant BCR-ABL mutants. In this study, an in vitro flow cytometry assay to analyze imatinib- and nilotinib-induced apoptosis in CML cells has been developed. Both the drugs induced significant apoptosis in CD34+ cells from 36 CML bone marrow samples (P<10(-4)), whereas CD34+ cells from BCR-ABL negative samples were unaffected. When the experiments were carried out in the presence of a cocktail of cytokines, nilotinib- but not imatinib-induced apoptosis was inhibited. This differential inhibition was confirmed on K562 cells. A blocking anti-CD117 antibody alleviated the antiapoptotic effect of cytokines against nilotinib. Moreover, using short hairpin RNA against BCR-ABL, we showed that K562 cells were not dependent on BCR-ABL signaling as long as the stem cell factor (SCF) receptor pathway was activated. We conclude that the c-KIT pathway may substitute for BCR-ABL tyrosine kinase to activate survival signals, and that c-KIT must be inhibited besides Bcr-Abl to allow apoptosis of CML cells.
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