ArticleMolecular cancer2007
Nilotinib treatment in mouse models of P190 Bcr/Abl lymphoblastic leukemia.
Article in Molecular cancer, 2007. 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.
- O-acetylated N-acetylneuraminic acid as a novel target for therapy in human pre-B acute lymphoblastic leukemia.The Journal of experimental medicine · 2013Trial
- Targeting miR-126 in Ph+ acute lymphoblastic leukemia.Leukemia · 2023Article
- Cancer-Induced Muscle Wasting Requires p38β MAPK Activation of p300.Cancer research · 2021Article
- USP10 modulates the SKP2/Bcr-Abl axis via stabilizing SKP2 in chronic myeloid leukemia.Cell discovery · 2019Article
- Platinum pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via DUB inhibition-dependent caspase activation and Bcr-Abl downregulation.Cell death & disease · 2017Article
- Nickel pyrithione induces apoptosis in chronic myeloid leukemia cells resistant to imatinib via both Bcr/Abl-dependent and Bcr/Abl-independent mechanisms.Journal of hematology & oncology · 2016Article
- Aurora A Kinase Inhibitor AKI603 Induces Cellular Senescence in Chronic Myeloid Leukemia Cells Harboring T315I Mutation.Scientific reports · 2016Article
- HS-543 induces apoptosis of Imatinib-resistant chronic myelogenous leukemia with T315I mutation.Oncotarget · 2015Article
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- Gambogic acid induces apoptosis in imatinib-resistant chronic myeloid leukemia cells via inducing proteasome inhibition and caspase-dependent Bcr-Abl downregulation.Clinical cancer research : an official journal of the American Association for Cancer Research · 2014Article
- Animal models of leukemia: any closer to the real thing?Cancer metastasis reviews · 2013Review
- Nilotinib potentiates anticancer drug sensitivity in murine ABCB1-, ABCG2-, and ABCC10-multidrug resistance xenograft models.Cancer letters · 2013Article
- Expression of cassini, a murine gamma-satellite sequence conserved in evolution, is regulated in normal and malignant hematopoietic cells.BMC genomics · 2012Article
- Environment-mediated drug resistance in Bcr/Abl-positive acute lymphoblastic leukemia.Oncoimmunology · 2012Article
- Treatment of human pre-B acute lymphoblastic leukemia with the Aurora kinase inhibitor PHA-739358 (Danusertib).Molecular cancer · 2012Article
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- Article
- AMD3100 sensitizes acute lymphoblastic leukemia cells to chemotherapy in vivo.Blood cancer journal · 2011Article
- Tirosin kinase inhibitors in chronic graft versus host disease: from bench to bedside.TheScientificWorldJournal · 2011Review
- Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-kappaB signaling and depleting Bcr-Abl.Molecular cancer · 2010Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundPh-positive leukemias are caused by the aberrant fusion of the BCR and ABL genes. Nilotinib is a selective Bcr/Abl tyrosine kinase inhibitor related to imatinib, which is widely used to treat chronic myelogenous leukemia. Because Ph-positive acute lymphoblastic leukemia only responds transiently to imatinib therapy, we have used mouse models to test the efficacy of nilotinib against lymphoblastic leukemia caused by the P190 form of Bcr/Abl.
resultsAfter transplant of 10,000 highly malignant leukemic cells into compatible recipients, untreated mice succumbed to leukemia within 21 days, whereas mice treated with 75 mg/kg nilotinib survived significantly longer. We examined cells from mice that developed leukemia while under treatment for Bcr/Abl kinase domain point mutations but these were not detected. In addition, culture of such cells ex vivo showed that they were as sensitive as the parental cell line to nilotinib but that the presence of stromal support allowed resistant cells to grow out. Nilotinib also exhibited impressive anti-leukemia activity in P190 Bcr/Abl transgenic mice that had developed overt leukemia/lymphoma masses and that otherwise would have been expected to die within 7 days. Visible lymphoma masses disappeared within six days of treatment and leukemic cell numbers in peripheral blood were significantly reduced. Treated mice survived more than 30 days.
conclusionThese results show that nilotinib has very impressive anti-leukemia activity but that lymphoblastic leukemia cells can become unresponsive to it both in vitro and in vivo through mechanisms that appear to be Bcr/Abl independent.
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