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  • 1
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    A model of human acute lymphoblastic leukemia in immune-deficient SCID mice (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-12-22
    Description: A human acute lymphoblastic leukemia (ALL) cell line that was transplanted into immune-deficient SCID mice proliferated in the hematopoietic tissues, invaded various organs, and led to the death of the mice. The distribution of leukemic cells in SCID mice was similar to the course of the disease in children. A-1 cells marked with a retrovirus vector showed clonal evolution after the transplant. SCID mice that were injected with bone marrow from three patients with non-T ALL had leukemic cells in their bone marrow and spleen. This in vivo model of human leukemia is an approach to understanding leukemic growth and progression and is a novel system for testing new treatment strategies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamel-Reid, S -- Letarte, M -- Sirard, C -- Doedens, M -- Grunberger, T -- Fulop, G -- Freedman, M H -- Phillips, R A -- Dick, J E -- New York, N.Y. -- Science. 1989 Dec 22;246(4937):1597-600.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2595371" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/pathology ; Cell Line ; Clone Cells ; DNA, Neoplasm/isolation & purification ; Humans ; Immunologic Deficiency Syndromes/*pathology ; Kidney/pathology ; Liver/pathology ; Mice ; Mice, Mutant Strains ; Neoplasm Transplantation ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*pathology ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Isolation of single human hematopoietic stem cells capable of long-term multilineage engraftment (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-07-09
    Description: Lifelong blood cell production is dependent on rare hematopoietic stem cells (HSCs) to perpetually replenish mature cells via a series of lineage-restricted intermediates. Investigating the molecular state of HSCs is contingent on the ability to purify HSCs away from transiently engrafting cells. We demonstrated that human HSCs remain infrequent, using current purification strategies based on Thy1 (CD90) expression. By tracking the expression of several adhesion molecules in HSC-enriched subsets, we revealed CD49f as a specific HSC marker. Single CD49f(+) cells were highly efficient in generating long-term multilineage grafts, and the loss of CD49f expression identified transiently engrafting multipotent progenitors (MPPs). The demarcation of human HSCs and MPPs will enable the investigation of the molecular determinants of HSCs, with a goal of developing stem cell-based therapeutics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Doulatov, Sergei -- Laurenti, Elisa -- Poeppl, Armando -- Jurisica, Igor -- Dick, John E -- Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2011 Jul 8;333(6039):218-21. doi: 10.1126/science.1201219.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Stem Cell and Developmental Biology, Campbell Family Institute for Cancer Research/Ontario Cancer Institute, Toronto, Ontario, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21737740" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD34/analysis ; Antigens, Thy-1/analysis ; *Cell Lineage ; Cell Proliferation ; *Cell Separation ; Coculture Techniques ; Fetal Blood/cytology ; Flow Cytometry ; Gene Expression Profiling ; Hematopoiesis ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/cytology/immunology/*physiology ; Humans ; Integrin alpha6/analysis ; Mice ; Mice, Inbred NOD ; Multipotent Stem Cells/cytology/immunology/*physiology ; Stromal Cells/cytology/physiology ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Evolution of human BCR-ABL1 lymphoblastic leukaemia-initiating cells (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-01-21
    Description: Many tumours are composed of genetically diverse cells; however, little is known about how diversity evolves or the impact that diversity has on functional properties. Here, using xenografting and DNA copy number alteration (CNA) profiling of human BCR-ABL1 lymphoblastic leukaemia, we demonstrate that genetic diversity occurs in functionally defined leukaemia-initiating cells and that many diagnostic patient samples contain multiple genetically distinct leukaemia-initiating cell subclones. Reconstructing the subclonal genetic ancestry of several samples by CNA profiling demonstrated a branching multi-clonal evolution model of leukaemogenesis, rather than linear succession. For some patient samples, the predominant diagnostic clone repopulated xenografts, whereas in others it was outcompeted by minor subclones. Reconstitution with the predominant diagnosis clone was associated with more aggressive growth properties in xenografts, deletion of CDKN2A and CDKN2B, and a trend towards poorer patient outcome. Our findings link clonal diversity with leukaemia-initiating-cell function and underscore the importance of developing therapies that eradicate all intratumoral subclones.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Mullighan, Charles G -- Wang, Jean C Y -- Poeppl, Armando -- Doulatov, Sergei -- Phillips, Letha A -- Ma, Jing -- Minden, Mark D -- Downing, James R -- Dick, John E -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2011 Jan 20;469(7330):362-7. doi: 10.1038/nature09733.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Stem Cell and Developmental Biology, Campbell Family Institute for Cancer Research/Ontario Cancer Institute, Toronto, Ontario M5G 1L7, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21248843" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Clone Cells/*metabolism/*pathology ; Cyclin-Dependent Kinase Inhibitor p15/deficiency/genetics ; DNA Copy Number Variations/genetics ; Disease Progression ; *Evolution, Molecular ; Fusion Proteins, bcr-abl/*genetics ; Genes, p16 ; Humans ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Models, Biological ; Neoplasm Transplantation ; Oligonucleotide Array Sequence Analysis ; Philadelphia Chromosome ; Polymorphism, Single Nucleotide/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/*genetics/*pathology ; Survival Rate ; Transplantation, Heterologous
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 4
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    Comment on "Tumor growth need not be driven by rare cancer stem cells" (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-12-15
    Description: Kelly et al. (Brevia, 20 July 2007, p. 337) questioned xenotransplant experiments supporting the cancer stem cell (CSC) hypothesis because they found a high frequency of leukemia-initiating cells (L-IC) in some transgenic mouse models. However, the CSC hypothesis depends on prospective purification of cells with tumor-initiating capacity, irrespective of frequency. Moreover, we found similar L-IC frequencies in genetically comparable leukemias using syngeneic or xenogeneic models.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennedy, James A -- Barabe, Frederic -- Poeppl, Armando G -- Wang, Jean C Y -- Dick, John E -- New York, N.Y. -- Science. 2007 Dec 14;318(5857):1722; author reply 1722.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell and Molecular Biology, University Health Network, Toronto, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18079385" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/pathology ; Bone Marrow Transplantation ; Cell Separation ; Disease Models, Animal ; Humans ; Leukemia/*pathology/physiopathology ; Leukemia, Myeloid, Acute/pathology/physiopathology ; Mice ; Mice, Transgenic ; Neoplasm Transplantation ; Neoplastic Stem Cells/pathology/*physiology ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/pathology/physiopathology ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Engraftment of immune-deficient mice with human hematopoietic stem cells (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: A system in which immune-deficient mice are repopulated with cells from the human myeloid lineage, and that provides an in vivo stem cell assay for human hematopoietic cells is described. Generation of the chimeric human/immune-deficient (HID) mice was dependent on the use of immune-deficient bg/nu/xid mice. Infusion of these mice with human bone marrow gave rise to increases in human macrophage progenitors during more than 5 weeks of in vivo growth, indicating the seeding, proliferation, and differentiation of human stem cells. The human identity of the progenitors was confirmed by sequence analysis and their dependence on human growth factors. The creation of HID mice lays the foundation for establishing animal models for a wide variety of human hemopathies, from leukemia to infectious disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kamel-Reid, S -- Dick, J E -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1706-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Hospital for Sick Children, Toronto, Ontario.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2904703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Transplantation ; Cell Differentiation ; Cell Division ; Colony-Forming Units Assay ; Colony-Stimulating Factors/pharmacology ; Disease Models, Animal ; Granulocyte-Macrophage Colony-Stimulating Factor ; Growth Substances/pharmacology ; Hematologic Diseases ; *Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/pathology ; Humans ; *Immunologic Deficiency Syndromes/immunology/pathology ; Interleukin-3/pharmacology ; Killer Cells, Natural/immunology ; Macrophages/pathology ; Mice ; Mice, Inbred CBA ; Mice, Mutant Strains ; Mice, Nude ; Transplantation, Heterologous
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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