Persistence of Leukemia-Initiating Cells in a Conditional Knockin Model of an Imatinib-Responsive Myeloproliferative Disorder
- 1 August 2009
- journal article
- research article
- Published by Elsevier BV in Cancer Cell
- Vol. 16 (2), 137-148
- https://doi.org/10.1016/j.ccr.2009.06.007
Abstract
No abstract availableFunding Information
- Burroughs Wellcome Fund
- Howard Hughes Medical Institute
- National Cancer Institute (CBTG CA009676, R01 CA098730-01, R01 CA82363-03)
This publication has 35 references indexed in Scilit:
- Malignant Transformation Initiated by Mll-AF9: Gene Dosage and Critical Target CellsCancer Cell, 2008
- Knock-in of an internal tandem duplication mutation into murine FLT3 confers myeloproliferative disease in a mouse modelBlood, 2008
- Leukaemia lineage specification caused by cell-specific Mll-Enl translocationsOncogene, 2007
- Leukemia stem cells in a genetically defined murine model of blast-crisis CMLBlood, 2007
- FLT3 Mutations Confer Enhanced Proliferation and Survival Properties to Multipotent Progenitors in a Murine Model of Chronic Myelomonocytic LeukemiaCancer Cell, 2007
- Five-Year Follow-up of Patients Receiving Imatinib for Chronic Myeloid LeukemiaNew England Journal of Medicine, 2006
- Huntingtin Interacting Protein 1 mutations lead to abnormal hematopoiesis, spinal defects and cataractsHuman Molecular Genetics, 2004
- Molecular genetics of human leukemias: New insights into therapySeminars in Hematology, 2002
- Transforming Properties of the Huntingtin Interacting Protein 1/ Platelet-derived Growth Factor β Receptor Fusion ProteinPublished by Elsevier BV ,1999
- Inducible Gene Targeting in MiceScience, 1995