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Ectopic expression of the homeobox gene Cdx2 is the key transforming event in a mouse model of t(12;13)(p13;q12) acute myeloid leukemia; a novel mechanism in AML

von Dr. Vpr

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[1.] Vpr/Fragment 004 10 - Diskussion
Zuletzt bearbeitet: 2014-04-04 23:00:39 Hindemith
BauernOpfer, Fragment, Gesichtet, Jamieson et al 2004, SMWFragment, Schutzlevel sysop, Vpr

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BauernOpfer
Bearbeiter
Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 4, Zeilen: 10-17
Quelle: Jamieson et al 2004
Seite(n): 531, Zeilen: col 1: 1-11
Human cancer stem cells, identified in acute myelogenous leukemia (AML) (Bonnet and Dick, 1997), myeloid blast crisis of chronic myelogenous leukemia (Jamieson et. al., 2004), breast cancer and brain tumors (Al-Hajj et. al., 2003; Singh et. al., 2003) share functional properties with normal stem cells such as self-renewal, high proliferative potential, some differentiation capacity and ability to be serially transplanted (Jamieson et. al., 2004b; Passegue et. al., 2003).

Al-Hajj, M., Wicha, M. S., Benito-Hernandez, A., Morrison, S. J., and Clarke, M. F. (2003). Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci U S A 100, 3983-3988.

Bonnet, D., and Dick, J. E. (1997). Human acute myeloid leukemia is organized as a hierarchy that originates from a primitive hematopoietic cell. Nat Med 3, 730-737.

Jamieson, C. H., Ailles, L. E., Dylla, S. J., Muijtjens, M., Jones, C., Zehnder, J. L., Gotlib, J., Li, K., Manz, M. G., Keating, A., et al. (2004a). Granulocyte-macrophage progenitors as candidate leukemic stem cells in blast-crisis CML. N Engl J Med 351, 657- 667.

Jamieson, C. H., Weissman, I. L., and Passegue, E. (2004b). Chronic versus acute myelogenous leukemia; A question of self-renewal. Cancer Cell 6, 531-533.

Passegue, E., Jamieson, C. H., Ailles, L. E., and Weissman, I. L. (2003). Normal and leukemic hematopoiesis: are leukemias a stem cell disorder or a reacquisition of stem cell characteristics? Proc Natl Acad Sci U S A 100 Suppl 1, 11842-11849.

Singh, S. K., Clarke, I. D., Terasaki, M., Bonn, V. E., Hawkins, C., Squire, J., and Dirks, P. B. (2003) Identification of a cancer stem cell in human brain tumors. Cancer Res 63, 5821-5828.

Human cancer stem cells, identified in acute myelogenous leukemia (Bonnet and Dick, 1997), myeloid blast crisis of chronic myelogenous leukemia (Jamieson et al, 2004), breast cancer (Al-Hajj et al., 2003), and brain tumors (Singh et al., 2003), share functional properties with normal stem cells, such as high proliferative potential, some differentiation capacity, and the ability to be serially transplanted (reviewed in Passegué et al., 2003).

Al-Hajj, M., Wicha, M., Benito-Hernandez, A., Morrison, S., and Clarke, M. (2003). Proc. Natl. Acad. Sci. USA 100, 3983–3988.

Bonnet, D., and Dick, J.E. (1997). Nat. Med. 3, 730–737.

Jamieson, C.H., Ailles, L.E., Dylla, S.J., Muijtjens, M., Jones, C., Zehnder, J.L., Gotlib, J., Li, K., Manz, M.G., Keating, A., et al. (2004). N. Engl. J. Med. 351, 657–667.

Passegué, E., Jamieson, C.H.M., Ailles, L.E., and Weissman, I.L. (2003). Proc. Natl. Acad. Sci. USA 100, 11842–11849.

Singh, S.K., Clarke, I.D., Terasaki, M., Bonn, V.E., Hawkins, C., Squire, J., and Dirks, P.B. (2003). Cancer Res. 63, 5821–5828.

Anmerkungen

The source is mentioned, but it is not clear that the overview of the literature is taken from it. The reader rather assumes that the given source is just one more reference.

Sichter
(Hindemith) Schumann

[2.] 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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SleepyHollow02
Gesichtet
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Untersuchte Arbeit:
Seite: 4, Zeilen: 23-31
Quelle: Reya et al 2001
Seite(n): 107, Zeilen: left col., 23-28 - right col. 1-7
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.

Sichter
(SleepyHollow02) Schumann


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