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Angaben zur Quelle [Bearbeiten]

Autor     H. Iwasaki, K. Akashi
Titel    Hematopoietic developmental pathways: on cellular basis
Zeitschrift    Oncogene
Verlag    Nature Publishing Group
Ausgabe    26
Jahr    2007
Seiten    6687-6696
URL    http://www.nature.com/onc/journal/v26/n47/pdf/1210754a.pdf

Literaturverz.   

no
Fußnoten    no
Fragmente    4


Fragmente der Quelle:
[1.] Pak/Fragment 013 17 - Diskussion
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The long-term reconstitution potential of human HSCs has been described in SCID mouse repopulating assays. In the most advanced xenotransplant models by utilizing the Rag2 and IL-2Rγ double-deficient mouse40 or the NOD/SCID IL2Rγ deficient mouse.41 The CD34+CD38- or the CD34+CD90+ fractions of human bone marrow and cord blood have been shown to reconstitute all human hematolymphoid lineage cells for a long term, indicating that these CD34+ fractions contains normal human HSCs. An injection of at least 1000 cells of the human CD34+CD38- bone marrow cells is required to obtain multi-lineage, longterm reconstitution in xenotransplant models. The percent of hCD34+CD38- or hCD34+CD90+ cells that are multipotent, long-term HSCs is still difficult to determine in a engraft model.

40. Traggiai E, Chicha L, Mazzucchelli L, et al. Development of a human adaptive immune system in cord blood cell-transplanted mice. Science. 2004;304:104-107.

41. Ishikawa F, Yasukawa M, Lyons B, et al. Development of functional human blood and immune systems in NOD/SCID/IL2 receptor {gamma} chain(null) mice. Blood. 2005;106:1565-1573.

The long-term reconstitution potential of human HSCs has been directly shown in SCID mouse repopulating assays. In the most advanced xenotransplant models by utilizing the Rag2 and IL-2Rγ double-deficient mouse (Traggiai et al., 2004) or the NOD–SCID IL2Rγ deficient mouse (Ishikawa et al., 2005), hCD34+hCD38- or the hCD34+hCD90+ fractions of human bone marrow and cord blood can reconstitute all human hematolymphoid lineage cells for a long term, indicating that these hCD34+ fractions contains normal human HSCs. [...] injection of at least 1000 cells of the human hCD34+hCD38- bone marrow cells is required to obtain multi-lineage, long-term reconstitution in xenotransplant models. Thus, it is unknown whether the HSC that is capable of reconstitution of all lineages at the single cell level exists in human hematopoiesis, and if so, what percent of hCD34+hCD38- or hCD34+hCD90+ cells are multipotent, longterm HSCs.

Traggiai E, Chicha L, Mazzucchelli L, Bronz L, Piffaretti JC, Lanzavecchia A et al. (2004). Development of a human adaptive immune system in cord blood cell-transplanted mice. Science 304: 104–107.

Ishikawa F, Yasukawa M, Lyons B, Yoshida S, Miyamoto T, Yoshimoto G et al. (2005). Development of functional human blood and immune systems in NOD/SCID/IL2 receptor {gamma} chain(null) mice. Blood 106: 1565–1573.

Anmerkungen

The source is not given.

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(Hindemith) Schumann

[2.] Pak/Fragment 014 01 - Diskussion
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1.2.2. The subsets of human lymphoid and myeloid progenitor.

The existence of lymphoid-committed progenitors in the human bone marrow with the hCD34+CD38+CD45RA+CD10+ phenotype has been reported.42 In human cord blood, common lymphoid progenitors (CLP) activity is found in the CD7+ fraction of CD34+CD38-CD45RA+ population. The hCD34+CD38- CD45RA+CD7+ population do not exist in the adult bone marrow.43 IL-7Rα, a critical marker for the murine CLP, is expressed in human hCD10+ CLPs in the bone marrow, but not in hCD7+ CLPs in the cord blood. These data suggest that the CLP phenotype and the requirement of IL-7 signaling might have changed during the human ontogeny. In the myelo-erythroid pathway, CMP, GMP and MEP subsets can be isolated from the hCD34+CD38+ fraction in both the bone marrow and cord blood (Manz et al., 2002). All these fractions of cells are negative for the early lymphoid markers hCD10, hCD7 or hIL-7Rα. These myelo-erythroid progenitors can be prospectively isolated according to the expression of hCD45RA and hIL-3Rα. CD45RA-hIL-3Rαlo (CMPs), hCD45RA+hIL-3Rαlo (GMPs) and hCD45RA-hIL-3Rα(MEPs) efficiently form distinct myelo-erythroid colony types according to their definitions (Fig.1.1.2). CMPs give rise to MEPs and GMPs in vitro, and a significant proportion of CMPs possess clonal GM and MegE potentials.44 Thus, the hierarchical myeloid progenitor relationships demonstrated in mice is well preserved in human haematopoiesis.

Phenotypic comparisons between mouse and human subsets show that CD34, a marker positive only for murine CMPs and GMPs, is uniformly expressed on all three human subsets, and that the FcγRII/III (CD16/CD32), marking murine CMPs and GMPs, was not detectable in any of the human myeloid progenitors44 All haemato/lymphoid progenitors develop from CD34+CD38- HSC population 41but themselves have no self-renewal activity in xenogenic transplantation models 45, indicating that they are downstream of human LTHSCs in both the bone marrow and the cord blood.

Flt3 shows a significant difference in its distribution in human and mouse hematopoiesis. This suggests a critical role of Flt3 signaling in hematopoietic [development in humans.]


41. Ishikawa F, Yasukawa M, Lyons B, et al. Development of functional human blood and immune systems in NOD/SCID/IL2 receptor {gamma} chain(null) mice. Blood. 2005;106:1565-1573.

42. Galy AH, Cen D, Travis M, Chen S, Chen BP. Delineation of T-progenitor cell activity within the CD34+ compartment of adult bone marrow. Blood. 1995;85:2770-2778.

43. Hao Z, Rajewsky K. Homeostasis of peripheral B cells in the absence of B cell influx from the bone marrow. J Exp Med. 2001;194:1151-1164.

44. Manz MG, Miyamoto T, Akashi K, Weissman IL. Prospective isolation of human clonogenic common myeloid progenitors. Proc Natl Acad Sci U S A. 2002;99:11872-11877.

45. Ishikawa F, Niiro H, Iino T, et al. The developmental program of human dendritic cells is operated independently of conventional myeloid and lymphoid pathways. Blood. 2007;110:3591-3660.

Human lymphoid and myeloid progenitor subsets within the hCD34+hCD38+ MPP fraction

Galy et al. (1995) first reported the existence of lymphoid-committed progenitors in the human bone marrow with the hCD34+hCD38+hCD45RA+hCD10+ phenotype. [...] In human cord blood, CLP activity is found in the hCD7+ fraction of hCD34+hCD38-hCD45RA+ population (Hao et al., 2001). Interestingly, the hCD7+ hCD34+hCD38-hCD45RA+ population does not exist in the adult bone marrow (Hao et al., 2001). IL-7Rα, a critical marker for the murine CLP, is expressed in human hCD10+ CLPs in the bone marrow, but not in hCD7+ CLPs in the cord blood. These data suggest that the CLP phenotype and the requirement of IL-7 signaling may change during human ontogeny.

In the myelo-erythroid pathway, CMP, GMP and MEP subsets are isolatable within the hCD34+hCD38+ fraction in both the bone marrow and cord blood (Manz et al., 2002). All are negative for the early lymphoid markers hCD10, hCD7 or hIL-7Rα. These myeloerythroid progenitors are prospectively isolatable according to the expression of hCD45RA and hIL-3Rα. hCD45RA-hIL-3Rαlo (CMPs), hCD45RA+hIL-3Rαlo (GMPs) and hCD45RA-hIL-3Rα- (MEPs) efficiently formed distinct myelo-erythroid colony types according to their definitions. CMPs give rise to MEPs and GMPs in vitro, and a significant proportion of CMPs possess clonal GM and MegE potentials (Manz et al., 2002). Thus, the hierarchical myeloid progenitor relationships demonstrated in mice is well preserved in human hematopoiesis. Phenotypic comparisons between mouse and human subsets show that CD34, a marker positive for only murine CMPs and GMPs, is uniformly expressed on all three human subsets, and that the FcγRII/III (CD16/CD32), marking murine CMPs and GMPs, was not detectable in none of human myeloid progenitors (Manz et al., 2002).

All of these hematolymphoid progenitors develop from hCD34+hCD38- HSC population (Ishikawa et al., 2005), but themselves have no self-renewal activity in xenogeneic transplantation models (Ishikawa et al., 2007), indicating that they are downstream of human LT-HSCs in both the bone marrow and the cord blood.

[page 6693]

The significant difference of Flt3 distribution in human and mouse hematopoiesis suggests that the critical role of Flt3 signaling in hematopoietic development could also be different.


Galy A, Travis M, Cen D, Chen B. (1995). Human T, B, natural killer, and dendritic cells arise from a common bone marrow progenitor cell subset. Immunity 3: 459–473.

Hao QL, Zhu J, Price MA, Payne KJ, Barsky LW, Crooks GM. (2001). Identification of a novel, human multilymphoid progenitor in cord blood. Blood 97: 3683–3690.

Ishikawa F, Niiro H, Iino T, Yoshida S, Saito N, Onohara S et al. (2007). The developmental program of human dendritic cells is operated independently of conventional myeloid and lymphoid pathways. Blood (in press).

Ishikawa F, Yasukawa M, Lyons B, Yoshida S, Miyamoto T, Yoshimoto G et al. (2005). Development of functional human blood and immune systems in NOD/SCID/IL2 receptor {gamma} chain(null) mice. Blood 106: 1565–1573.

Manz MG, Miyamoto T, Akashi K, Weissman IL. (2002). Prospective isolation of human clonogenic common myeloid progenitors. Proc Natl Acad Sci USA 99: 11872–11877.

Anmerkungen

The source is not mentioned at all.

Note that the reference "(Manz et al., 2002)" is atypical here as typically a reference would refer by a number to the bibliography, without giving the author's name in the main body of text.

Sichter
(Hindemith) Schumann

[3.] Pak/Fragment 015 01 - Diskussion
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hFlt3 is expressed in leukemic blasts in most cases with acute myelogenous leukemia (AML)46,47 (Carow et al., 1996; Rosnet et al., 1996), and FLT3 is one of the most frequently mutated genes in AML.48,49 The signal from FLT3 mutations should be controlled under the regulation of normal Flt3

[FIGURE 1.2.2, see: Pak/Fragment 015 05]

expression machinery, signaling from FLT3 mutations should involve HSCs and GMPs, both of which are critical targets for leukemic transformation in mouse AML models.51-54 Thus, special considerations are required in utilizing mouse models to understand the role of FLT3 mutations in human leukemogenesis.


46.Carow CE, Levenstein M, Kaufmann SH, et al. Expression of the hematopoietic growth factor receptor FLT3 (STK-1/Flk2) in human leukemias. Blood. 1996;87:1089-1096.

47.Rosnet O, Buhring HJ, Marchetto S, et al. Human FLT3/FLK2 receptor tyrosine kinase is expressed at the surface of normal and malignant hematopoietic cells. Leukemia. 1996;10:238-248.

48.Gilliland DG, Griffin JD. The roles of FLT3 in hematopoiesis and leukemia. Blood. 2002;100:1532- 1542.

49.Stirewalt DL, Meshinchi S, Kussick SJ, et al. Novel FLT3 point mutations within exon 14 found in patients with acute myeloid leukaemia. Br J Haematol. 2004;124:481-484.

51.Cozzio A, Passegue E, Ayton PM, Karsunky H, Cleary ML, Weissman IL. Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors. Genes Dev. 2003;17:3029-3035.

52.So CW, Karsunky H, Passegue E, Cozzio A, Weissman IL, Cleary ML. MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice. Cancer Cell. 2003;3:161-171.

53.Huntly BJ, Shigematsu H, Deguchi K, et al. MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors. Cancer Cell. 2004;6:587-596.

54.Wang GG, Pasillas MP, Kamps MP. Meis1 programs transcription of FLT3 and cancer stem cell character, using a mechanism that requires interaction with Pbx and a novel function of the Meis1 Cterminus. Blood. 2005;106:254-264.

hFlt3 is expressed in leukemic blasts in most cases with acute myelogenous leukemia (AML) (Carow et al., 1996; Rosnet et al., 1996), and FLT3 is one of the most frequently mutated genes in AML (Gilliland, 2002; Stirewalt and Radich, 2003). [...] Because the signal from FLT3 mutations should be controlled under the regulation of normal Flt3 expression machinery, signaling from FLT3 mutations should involve HSCs and GMPs, both of which are critical targets for leukemic transformation in mouse AML models (see the next section) (Cozzio et al., 2003; So et al., 2003; Huntly et al., 2004; Wang et al., 2005). Thus, special considerations are required in utilizing mouse models to understand the role of FLT3 mutations in human leukemogenesis.

Carow CE, Levenstein M, Kaufmann SH, Chen J, Amin S, Rockwell P et al. (1996). Expression of the hematopoietic growth factor receptor FLT3 (STK-1/Flk2) in human leukemias. Blood 87: 1089–1096.

Cozzio A, Passegue E, Ayton PM, Karsunky H, Cleary ML, Weissman IL. (2003). Similar MLL-associated leukemias arising from self-renewing stem cells and short-lived myeloid progenitors. Genes Dev 17: 3029–3035.

Gilliland DG. (2002). Molecular genetics of human leukemias: new insights into therapy. Semin Hematol 39: 6–11.

Huntly BJ, Shigematsu H, Deguchi K, Lee BH, Mizuno S, Duclos N et al. (2004). MOZ-TIF2, but not BCR-ABL, confers properties of leukemic stem cells to committed murine hematopoietic progenitors. Cancer Cell 6: 587–596.

Rosnet O, Buhring HJ, Marchetto S, Rappold I, Lavagna C, Sainty D et al. (1996). Human FLT3/FLK2 receptor tyrosine kinase is expressed at the surface of normal and malignant hematopoietic cells. Leukemia 10: 238–248.

So CW, Karsunky H, Passegue E, Cozzio A, Weissman IL, Cleary ML. (2003). MLL-GAS7 transforms multipotent hematopoietic progenitors and induces mixed lineage leukemias in mice. Cancer Cell 3: 161–171.

Stirewalt DL, Radich JP. (2003). The role of FLT3 in haematopoietic malignancies. Nat Rev Cancer 3: 650–665.

Wang J, Iwasaki H, Krivtsov A, Febbo PG, Thorner AR, Ernst P et al. (2005). Conditional MLL-CBP targets GMP and models therapyrelated myeloproliferative disease. EMBO J 24: 368–381.

Anmerkungen

The source is not given.

Note that against the usual convention in the thesis the references "(Carow et al., 1996; Rosnet et al., 1996)" are given in the main body of text.

Sichter
(Hindemith) Schumann

[4.] Pak/Fragment 016 01 - Diskussion
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Further phenotypic and functional characterization of human hematopoietic cells should be performed by utilizing improved efficient xenotransplant models. These approaches will eventually help to identify LSCs that should be a critical cellular target in leukemia treatment.55

55.Iwasaki H, Mizuno S, Mayfield R, et al. Identification of eosinophil lineage-committed progenitors in the murine bone marrow. J Exp Med. 2005;201:1891-1897.

Further phenotypic and functional characterization of human hematopoietic cells should be performed by utilizing improved efficient xenotransplant models. These approaches will eventually help to identify LSCs that should be a critical cellular target in leukemia treatment.
Anmerkungen

The source is not given.

The text cannot be found in the referenced publication.

Sichter
(Hindemith) Schumann

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