Abstract
Chronic myeloid leukemia (CML) is a clonal malignancy initiated by the occurrence of a t (9;22) translocation, generating Ph1 chromosome and BCR-ABL oncogene in a primitive hematopoietic stem cell (HSC). The resistance of HSC to targeted therapies using tyrosine kinase inhibitors remains a major obstacle towards the cure. We have generated an iPSC line from a patient with CML using leukemic CD34+ cells cryopreserved at diagnosis. Ph1+ CML cells were reprogrammed by non-integrative viral transduction. These iPSCs harboured Ph1 chromosome and expressed pluripotency hallmarks as well as BCR-ABL. Teratoma assays revealed normal differentiation after injection in immunodeficient mice.
Copyright © 2016 Helmholtz Zentrum München. Published by Elsevier B.V. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Animals
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Antigens, CD34 / metabolism
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Cell Differentiation
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Cellular Reprogramming*
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Fusion Proteins, bcr-abl / genetics
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Fusion Proteins, bcr-abl / metabolism
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Humans
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Induced Pluripotent Stem Cells / cytology
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Induced Pluripotent Stem Cells / metabolism*
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Induced Pluripotent Stem Cells / transplantation
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Karyotype
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / genetics
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / metabolism
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Leukemia, Myelogenous, Chronic, BCR-ABL Positive / pathology*
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Leukocytes, Mononuclear / cytology*
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Leukocytes, Mononuclear / metabolism
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Male
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Mice
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Mice, Inbred NOD
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Teratoma / metabolism
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Teratoma / pathology
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Transcription Factors / genetics
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Transcription Factors / metabolism
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Transplantation, Heterologous
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Tumor Cells, Cultured
Substances
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Antigens, CD34
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Transcription Factors
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Fusion Proteins, bcr-abl