Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells
Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treate...
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| Published in | Blood Vol. 121; no. 20; pp. 4175 - 4183 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
16.05.2013
American Society of Hematology |
| Subjects | |
| Online Access | Get full text |
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| Abstract | Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP–like mice, such as TKI-resistant BCR-ABL1 mutations (E255K, T315I, H396P), deletions in Ikzf1 and Trp53, and additions in Zfp423 and Idh1. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP–like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients.
•Imatinib does not prevent accumulation of genomic instability in CML-CP.•Imatinib-refractory leukemia stem cells may be a source of genomic instability in CML-CP. |
|---|---|
| AbstractList | Imatinib does not prevent accumulation of genomic instability in CML-CP.
Imatinib-refractory leukemia stem cells may be a source of genomic instability in CML-CP.
Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP–like mice, such as TKI-resistant
BCR-ABL1
mutations (E255K, T315I, H396P), deletions in
Ikzf1
and
Trp53
, and additions in
Zfp423
and
Idh1
. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP–like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients. Imatinib does not prevent accumulation of genomic instability in CML-CP. Imatinib-refractory leukemia stem cells may be a source of genomic instability in CML-CP. Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP-like mice, such as TKI-resistant BCR-ABL1 mutations (E255K, T315I, H396P), deletions in Ikzf1 and Trp53, and additions in Zfp423 and Idh1. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP-like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients. Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP-like mice, such as TKI-resistant BCR-ABL1 mutations (E255K, T315I, H396P), deletions in Ikzf1 and Trp53, and additions in Zfp423 and Idh1. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP-like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients.Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP-like mice, such as TKI-resistant BCR-ABL1 mutations (E255K, T315I, H396P), deletions in Ikzf1 and Trp53, and additions in Zfp423 and Idh1. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP-like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients. Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase inhibitors (TKIs) and/or additional chromosomal aberrations leading to disease relapse and/or malignant progression. TKI-naive and TKI-treated leukemia stem cells (LSCs) and leukemia progenitor cells (LPCs) accumulate high levels of reactive oxygen species (ROS) and oxidative DNA damage. To determine the role of TKI-refractory LSCs in genomic instability, we used a murine model of CML-CP where ROS-induced oxidative DNA damage was elevated in LSCs, including quiescent LSCs, but not in LPCs. ROS-induced oxidative DNA damage in LSCs caused clinically relevant genomic instability in CML-CP–like mice, such as TKI-resistant BCR-ABL1 mutations (E255K, T315I, H396P), deletions in Ikzf1 and Trp53, and additions in Zfp423 and Idh1. Despite inhibition of BCR-ABL1 kinase, imatinib did not downregulate ROS and oxidative DNA damage in TKI-refractory LSCs to the levels detected in normal cells, and CML-CP–like mice treated with imatinib continued to accumulate clinically relevant genetic aberrations. Inhibition of class I p21-activated protein kinases by IPA3 downregulated ROS in TKI-naive and TKI-treated LSCs. Altogether, we postulate that genomic instability may originate in the most primitive TKI-refractory LSCs in TKI-naive and TKI-treated patients. •Imatinib does not prevent accumulation of genomic instability in CML-CP.•Imatinib-refractory leukemia stem cells may be a source of genomic instability in CML-CP. |
| Author | Skorski, Tomasz Bhatia, Ravi Maier, Jacqueline Flis, Sylwia Seferynska, Ilona Koptyra, Mateusz Kerstiens, Linda Koschmieder, Steffen Bolton-Gillespie, Elisabeth Hoser, Grazyna Lange, Thoralf Müller, Martin C. Stoklosa, Tomasz Modi, Hardik Schemionek, Mirle Holyoake, Tessa L. Klein, Hans-Ulrich Nieborowska-Skorska, Margaret |
| Author_xml | – sequence: 1 givenname: Elisabeth surname: Bolton-Gillespie fullname: Bolton-Gillespie, Elisabeth organization: Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA – sequence: 2 givenname: Mirle surname: Schemionek fullname: Schemionek, Mirle organization: Department of Medicine (Oncology, Hematology, and Stem Cell Transplantation), University Medical Center of Aachen, Aachen, Germany – sequence: 3 givenname: Hans-Ulrich surname: Klein fullname: Klein, Hans-Ulrich organization: Institute of Medical Informatics, University of Münster, Münster, Germany – sequence: 4 givenname: Sylwia surname: Flis fullname: Flis, Sylwia organization: Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA – sequence: 5 givenname: Grazyna surname: Hoser fullname: Hoser, Grazyna organization: Department of Clinical Cytology, Medical Center for Postgraduate Education, Warsaw, Poland – sequence: 6 givenname: Thoralf surname: Lange fullname: Lange, Thoralf organization: Abteilung für Hämatologie, Onkologie, Hämostaseologie, Universitätsklinikum Leipzig, Leipzig, Germany – sequence: 7 givenname: Margaret surname: Nieborowska-Skorska fullname: Nieborowska-Skorska, Margaret organization: Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA – sequence: 8 givenname: Jacqueline surname: Maier fullname: Maier, Jacqueline organization: Abteilung für Hämatologie, Onkologie, Hämostaseologie, Universitätsklinikum Leipzig, Leipzig, Germany – sequence: 9 givenname: Linda surname: Kerstiens fullname: Kerstiens, Linda organization: Department of Hematology/Oncology, University of Münster, Münster, Germany – sequence: 10 givenname: Mateusz surname: Koptyra fullname: Koptyra, Mateusz organization: Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA – sequence: 11 givenname: Martin C. surname: Müller fullname: Müller, Martin C. organization: Medizinische Fakultät Mannheim der Universität Heidelberg, Mannheim, Germany – sequence: 12 givenname: Hardik surname: Modi fullname: Modi, Hardik organization: Division of Hematopoietic Stem Cell and Leukemia Research, Department of Hematology and Hematopoietic Cell Transplantation, City of Hope National Medical Center, Duarte, CA – sequence: 13 givenname: Tomasz surname: Stoklosa fullname: Stoklosa, Tomasz organization: Department of Immunology, Medical University of Warsaw, Warsaw, Poland – sequence: 14 givenname: Ilona surname: Seferynska fullname: Seferynska, Ilona organization: Department of Hematology, Institute of Hematology and Blood Transfusion, Warsaw, Poland – sequence: 15 givenname: Ravi surname: Bhatia fullname: Bhatia, Ravi organization: Division of Hematopoietic Stem Cell and Leukemia Research, Department of Hematology and Hematopoietic Cell Transplantation, City of Hope National Medical Center, Duarte, CA – sequence: 16 givenname: Tessa L. surname: Holyoake fullname: Holyoake, Tessa L. organization: Paul O'Gorman Leukemia Research Centre, University of Glasgow, Glasgow, United Kingdom – sequence: 17 givenname: Steffen surname: Koschmieder fullname: Koschmieder, Steffen organization: Department of Medicine (Oncology, Hematology, and Stem Cell Transplantation), University Medical Center of Aachen, Aachen, Germany – sequence: 18 givenname: Tomasz surname: Skorski fullname: Skorski, Tomasz email: tskorski@temple.edu organization: Department of Microbiology and Immunology, School of Medicine, Temple University, Philadelphia, PA |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23543457$$D View this record in MEDLINE/PubMed |
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| Snippet | Genomic instability is a hallmark of chronic myeloid leukemia in chronic phase (CML-CP) resulting in BCR-ABL1 mutations encoding resistance to tyrosine kinase... Imatinib does not prevent accumulation of genomic instability in CML-CP. Imatinib-refractory leukemia stem cells may be a source of genomic instability in... Imatinib does not prevent accumulation of genomic instability in CML-CP. Imatinib-refractory leukemia stem cells may be a source of genomic instability in... |
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| SubjectTerms | Animals Antineoplastic Agents - therapeutic use Benzamides - therapeutic use Cells, Cultured DNA Damage - drug effects Drug Resistance, Neoplasm - genetics Genomic Instability - drug effects Genomic Instability - physiology Humans Imatinib Mesylate Leukemia, Myelogenous, Chronic, BCR-ABL Positive - drug therapy Leukemia, Myelogenous, Chronic, BCR-ABL Positive - genetics Leukemia, Myelogenous, Chronic, BCR-ABL Positive - pathology Mice Mice, Transgenic Myeloid Neoplasia Neoplastic Stem Cells - drug effects Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Neoplastic Stem Cells - physiology Oxidative Stress - drug effects Oxidative Stress - genetics Piperazines - therapeutic use Protein Kinase Inhibitors - pharmacology Protein Kinase Inhibitors - therapeutic use Pyrimidines - therapeutic use Reactive Oxygen Species - metabolism |
| Title | Genomic instability may originate from imatinib-refractory chronic myeloid leukemia stem cells |
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