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Angaben zur Quelle [Bearbeiten]

Autor     Tannishtha Reya, Sean J. Morrison, Michael F. Clarke, Irving L. Weissman
Titel    Stem cells, cancer, and cancer stem cells
Zeitschrift    Nature
Ausgabe    414
Datum    November 2001
Seiten    105-111
URL    http://deepblue.lib.umich.edu/bitstream/handle/2027.42/62862/414105a0.pdf?sequence=1

Literaturverz.   

yes
Fußnoten    yes
Fragmente    3


Fragmente der Quelle:
[1.] Vpr/Fragment 002 26 - Diskussion
Zuletzt bearbeitet: 2014-03-17 12:28:44 Graf Isolan
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Quelle: Reya et al 2001
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In the hematopoietic system, stem cells are heterogeneous with respect to their ability to self-renew and can be divided into three different populations: long-term self-renewing HSCs, short-term self-renewing HSCs, and multipotent progenitors without detectable self-renewal potential (Morrison and Weissman, 1994; Morrison et. al., 1997). These populations form a lineage in which the long-term HSCs give rise to short-term HSCs, which in turn give rise to multi-[potent progenitors (Morrison et. al., 1997).]

Morrison, S. J., Wandycz, A. M., Hemmati, H. D., Wright, D. E., and Weissman, I. L. (1997). Identification of a lineage of multipotent hematopoietic progenitors. Development 124, 1929-1939.

Morrison, S. J., and Weissman, I. L. (1994). The long-term repopulating subset of hematopoietic stem cells is deterministic and isolatable by phenotype. Immunity 1, 661-673.

In the haematopoietic system, stem cells are heterogeneous with respect to their ability to self-renew. Multipotent progenitors constitute 0.05% of mouse bone-marrow cells, and can be divided into three different populations: long-term self-renewing HSCs, short-term self-renewing HSCs, and multipotent progenitors without detectable self-renewal potential2,11. These populations form a lineage in which the long-term HSCs give rise to short-term HSCs, which in turn give rise to multipotent progenitors11.

2. Morrison, S. J. & Weissman, I. L. The long-term repopulating subset of hematopoietic stem cells is deterministic and isolatable by phenotype. Immunity 1, 661–673 (1994).

11. Morrison, S. J., Wandycz, A. M., Hemmati, H. D., Wright, D. E. & Weissman, I. L. Identification of a lineage of multipotent hematopoietic progenitors. Development 124, 1929–1939 (1997).

Anmerkungen

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[2.] Vpr/Fragment 003 01 - Diskussion
Zuletzt bearbeitet: 2014-03-16 23:25:09 Hindemith
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As HSCs mature from the long-term self-renewing pool to multipotent progenitors, they progressively lose their potential to self-renew but become more mitotically active. Whereas long-term HSCs give rise to mature hematopoietic cells for the lifetime of the mouse, short-term HSCs and multipotent progenitors reconstitute lethally irradiated mice for less than eight weeks (Fig.2).

03a diss Vpr.png

Figure 2. Development of hematopoietic stem cells. HSCs can be subdivided into long-term self-renewing HSCs, short-term self-renewing HSCs and multipotent progenitors (red arrows indicate self-renewal). They give rise to common lymphoid progenitors (CLPs) and common myeloid progenitors (CMPs). Both CMPs/GMPs (granulocyte macrophage precursors) and CLPs can give rise to all known mouse hematopoietic cells (Figure adapted from Reya et. al., 2001)

[page 105]

As HSCs mature from the long-term self-renewing pool to multipotent progenitors, they progressively lose their potential to self-renew but become more mitotically active. Whereas long-term HSCs give rise to mature haematopoietic cells for the lifetime of the mouse, short-term HSCs and multipotent progenitors reconstitute lethally irradiated mice for less than eight weeks.

[page 106]

03a source Vpr.png

Development of haematopoietic stem cells. HSCs can be subdivided into long-term self-renewing HSCs, short-term self-renewing HSCs and multipotent progenitors (red arrows indicate self-renewal). They give rise to common lymphoid progenitors (CLPs; the precursors of all lymphoid cells) and common myeloid progenitors (CMPs; the precursors of all myeloid cells). Both CMPs/GMPs (granulocyte macrophage precursors) and CLPs can give rise to all known mouse dendritic cells.

Anmerkungen

The source is given, but only for the figure: "Figure adapted from Reya et. al., 2001" It is not clear to the reader that the text before the figure is also taken from this source, that the figure has not been "adapted" but copied and that also the figure caption is taken from the source.

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[3.] Vpr/Fragment 004 23 - Diskussion
Zuletzt bearbeitet: 2014-03-17 12:35:55 Graf Isolan
BauernOpfer, Fragment, Gesichtet, Reya et al 2001, SMWFragment, Schutzlevel sysop, Vpr

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If dysregulation of signaling pathways that normally regulate stem cell selfrenewal leads to tumorigenesis, then stem cells themselves might be the target of transformation in certain types of cancer. There are two reasons to think that this hypothesis may be correct: first, because stem cells have the machinery for self-renewal already activated, maintaining this activation may be simpler than turning it on de novo in a more differentiated cell; that is, fewer mutations may be required to maintain self-renewal than to activate it ectopically. Secondly, stem cells often persist for long periods of time, instead of dying like many mature cells in highly proliferative tissues. This means that there is a much greater [opportunity for mutations to accumulate in individual stem cells than in most mature cell types.] If the signalling pathways that normally regulate stem cell selfrenewal lead to tumorigenesis when dysregulated, then are stem cells themselves the target of transformation in certain types of cancer28,29? There are two reasons to think that this may be the case. First, because stem cells have the machinery for self-renewal already activated, maintaining this activation may be simpler than turning it on de novo in a more differentiated cell; that is, fewer mutations may be required to maintain self-renewal than to activate it ectopically. Second, by self-renewing, stem cells often persist for long periods of time, instead of dying after short periods of time like many mature cells in highly proliferative tissues. This means that there is a much greater opportunity for mutations to accumulate in individual stem cells than in most mature cell types (Fig. 3).
Anmerkungen

The source is mentioned two sentences further down, but it is not clear that Reya et al are quoted literally here.

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