Coexistence of LMPP-like and GMP-like Leukemia Stem Cells in Acute Myeloid Leukemia
The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) act...
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| Published in | Cancer cell Vol. 19; no. 1; pp. 138 - 152 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Elsevier Inc
18.01.2011
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| Subjects | |
| Online Access | Get full text |
| ISSN | 1535-6108 1878-3686 1878-3686 |
| DOI | 10.1016/j.ccr.2010.12.012 |
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| Abstract | The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential.
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► Most human CD34+ AMLs have two molecularly distinct LSC populations ► They are hierarchically ordered in vivo and in vitro ► Molecularly, LSCs are most similar to normal progenitors rather than stem cells ► The more immature LSCs most closely mirror normal LMPPs |
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| AbstractList | The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential.
[Display omitted]
► Most human CD34+ AMLs have two molecularly distinct LSC populations ► They are hierarchically ordered in vivo and in vitro ► Molecularly, LSCs are most similar to normal progenitors rather than stem cells ► The more immature LSCs most closely mirror normal LMPPs The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in similar to 80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential. The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential. The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential.The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two expanded populations with hemopoietic progenitor immunophenotype coexist in most patients. Both populations have leukemic stem cell (LSC) activity and are hierarchically ordered; one LSC population gives rise to the other. Global gene expression profiling shows the LSC populations are molecularly distinct and resemble normal progenitors but not stem cells. The more mature LSC population most closely mirrors normal granulocyte-macrophage progenitors (GMP) and the immature LSC population a previously uncharacterized progenitor functionally similar to lymphoid-primed multipotential progenitors (LMPPs). This suggests that in most cases primary CD34+ AML is a progenitor disease where LSCs acquire abnormal self-renewal potential. |
| Author | Vyas, Paresh Marchi, Emanuele Jacobsen, Sten Eirik W. Cavenagh, Jamie Woll, Petter Gilkes, Amanda Price, Andrew Alford, Kate A. Virgo, Paul Bowen, David Quek, Lynn Standen, Graham Hunter, Hannah Craddock, Charles Goardon, Nicolas Macintyre, Elizabeth Killick, Sally Beldjord, Kheira Robinson, Lisa Atzberger, Ann Begum, Suriya Geddes, Nicola Mead, Adam Chaudhury, Salma Burnett, Alan Porcher, Catherine Soneji, Shamit Knapper, Steve Griffiths, Mike Rose, Susan Sternberg, Alexander Schuh, Anna Rout, Raj Enver, Tariq |
| Author_xml | – sequence: 1 givenname: Nicolas surname: Goardon fullname: Goardon, Nicolas organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 2 givenname: Emanuele surname: Marchi fullname: Marchi, Emanuele organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 3 givenname: Ann surname: Atzberger fullname: Atzberger, Ann organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 4 givenname: Lynn surname: Quek fullname: Quek, Lynn organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 5 givenname: Anna surname: Schuh fullname: Schuh, Anna organization: Department of Haematology, Oxford Radcliffe Hospitals NHS Trust, Oxford OX3 9DU, UK – sequence: 6 givenname: Shamit surname: Soneji fullname: Soneji, Shamit organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 7 givenname: Petter surname: Woll fullname: Woll, Petter organization: HSCB, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 8 givenname: Adam surname: Mead fullname: Mead, Adam organization: HSCB, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 9 givenname: Kate A. surname: Alford fullname: Alford, Kate A. organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 10 givenname: Raj surname: Rout fullname: Rout, Raj organization: Nuffield Department of Orthopedics Nuffield Orthopedic Hospital, Oxford, Oxford OX3 7LD, UK – sequence: 11 givenname: Salma surname: Chaudhury fullname: Chaudhury, Salma organization: Nuffield Department of Orthopedics Nuffield Orthopedic Hospital, Oxford, Oxford OX3 7LD, UK – sequence: 12 givenname: Amanda surname: Gilkes fullname: Gilkes, Amanda organization: Department of Haematology, College of Medicine, Cardiff University Heath Park Cardiff, Wales CF14 4XN, UK – sequence: 13 givenname: Steve surname: Knapper fullname: Knapper, Steve organization: Department of Haematology, College of Medicine, Cardiff University Heath Park Cardiff, Wales CF14 4XN, UK – sequence: 14 givenname: Kheira surname: Beldjord fullname: Beldjord, Kheira organization: CNRS UMR 8147 and Department of Haematology, Hôpital Necker-Enfants-Malades (AP-HP), Université Paris-5 75015, France – sequence: 15 givenname: Suriya surname: Begum fullname: Begum, Suriya organization: West Midlands Regional Cytogenetics Laboratory, Birmingham B15 2TG, UK – sequence: 16 givenname: Susan surname: Rose fullname: Rose, Susan organization: West Midlands Regional Cytogenetics Laboratory, Birmingham B15 2TG, UK – sequence: 17 givenname: Nicola surname: Geddes fullname: Geddes, Nicola organization: West Midlands Regional Cytogenetics Laboratory, Birmingham B15 2TG, UK – sequence: 18 givenname: Mike surname: Griffiths fullname: Griffiths, Mike organization: West Midlands Regional Cytogenetics Laboratory, Birmingham B15 2TG, UK – sequence: 19 givenname: Graham surname: Standen fullname: Standen, Graham organization: Bristol Royal Infirmary, Bristol BS2 8HW, UK – sequence: 20 givenname: Alexander surname: Sternberg fullname: Sternberg, Alexander organization: Department of Haematology, Great Western Hospital, Swindon SN3 6BB, UK – sequence: 21 givenname: Jamie surname: Cavenagh fullname: Cavenagh, Jamie organization: Department of Haematology, St Bartholomew's Hospital, London EC1A 7BE, UK – sequence: 22 givenname: Hannah surname: Hunter fullname: Hunter, Hannah organization: Department of Haematology, Plymouth Hospital, Plymouth PL6 8DH, UK – sequence: 23 givenname: David surname: Bowen fullname: Bowen, David organization: Department of Haematology, Leeds LS9 7TF, UK – sequence: 24 givenname: Sally surname: Killick fullname: Killick, Sally organization: Department of Haematology, Bournemouth Hospital, Bournemouth BH7 7DW, UK – sequence: 25 givenname: Lisa surname: Robinson fullname: Robinson, Lisa organization: Department of Haematology, Hereford Hospital, HR1 2BN, UK – sequence: 26 givenname: Andrew surname: Price fullname: Price, Andrew organization: Nuffield Department of Orthopedics Nuffield Orthopedic Hospital, Oxford, Oxford OX3 7LD, UK – sequence: 27 givenname: Elizabeth surname: Macintyre fullname: Macintyre, Elizabeth organization: CNRS UMR 8147 and Department of Haematology, Hôpital Necker-Enfants-Malades (AP-HP), Université Paris-5 75015, France – sequence: 28 givenname: Paul surname: Virgo fullname: Virgo, Paul organization: Department of Immunology, North Bristol NHS Trust, Bristol BS10 5NB, UK – sequence: 29 givenname: Alan surname: Burnett fullname: Burnett, Alan organization: Department of Haematology, College of Medicine, Cardiff University Heath Park Cardiff, Wales CF14 4XN, UK – sequence: 30 givenname: Charles surname: Craddock fullname: Craddock, Charles organization: Department of Haematology University of Birmingham and University Hospital of Birmingham, Birmingham B15 2TH, UK – sequence: 31 givenname: Tariq surname: Enver fullname: Enver, Tariq organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 32 givenname: Sten Eirik W. surname: Jacobsen fullname: Jacobsen, Sten Eirik W. organization: HSCB, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 33 givenname: Catherine surname: Porcher fullname: Porcher, Catherine organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK – sequence: 34 givenname: Paresh surname: Vyas fullname: Vyas, Paresh email: paresh.vyas@imm.ox.ac.uk organization: MRC MHU, WIMM, University of Oxford, Oxford OX3 9DS, UK |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/21251617$$D View this record in MEDLINE/PubMed |
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| Snippet | The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in ∼80% of primary human CD34+ acute myeloid leukemia (AML), two... The relationships between normal and leukemic stem/progenitor cells are unclear. We show that in similar to 80% of primary human CD34+ acute myeloid leukemia... |
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| SubjectTerms | Adult Aged Aged, 80 and over Animals Antigens, CD - metabolism Antigens, CD34 - metabolism Cell Differentiation - physiology Cell Lineage - physiology Gene Expression Profiling Graft Survival Granulocyte-Macrophage Progenitor Cells - cytology Granulocyte-Macrophage Progenitor Cells - metabolism Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - metabolism Humans Immunophenotyping Leukemia, Myeloid, Acute - metabolism Leukemia, Myeloid, Acute - pathology Leukocyte Common Antigens - metabolism Lymphoid Progenitor Cells - cytology Lymphoid Progenitor Cells - metabolism Mice Mice, Inbred NOD Mice, SCID Middle Aged Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology Neoplastic Stem Cells - transplantation Transplantation, Heterologous - pathology Young Adult |
| Title | Coexistence of LMPP-like and GMP-like Leukemia Stem Cells in Acute Myeloid Leukemia |
| URI | https://dx.doi.org/10.1016/j.ccr.2010.12.012 https://www.ncbi.nlm.nih.gov/pubmed/21251617 https://www.proquest.com/docview/846901065 https://www.proquest.com/docview/923193737 |
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