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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 014 01 - Diskussion
Zuletzt bearbeitet: 2014-04-05 19:44:18 Hindemith
BauernOpfer, Chawengsaksophak et al 2004, Fragment, Gesichtet, SMWFragment, Schutzlevel sysop, Vpr

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Untersuchte Arbeit:
Seite: 14, Zeilen: 1-20
Quelle: Chawengsaksophak et al 2004
Seite(n): 7641, Zeilen: left col., 17-34, 46-52
1.4.1 Role of Cdx2 in embryogenesis and intestine development

Cdx genes have developmental roles and overlap in their expression patterns. Cdx2 is expressed at 3.5 days postcoitum (dpc) in the trophectoderm but not in the inner cell mass (Beck et. al., 1995). At 7.5 dpc (Theiler stage 11), it is present in the chorion, ectoplacental cone, mesoderm of the developing allantoic bud, and posterior primitive streak. At 8.5 dpc (Theiler stage 13), expression is seen in all three germ layers at the posterior end of the embryo extending into the mesodermal root of the allantois, in the endodermal epithelium of the hindgut rudiment, and in the neural tube; the presegmented paraxial mesoderm expresses the gene, but the somites, lateral plate, and intermediate mesoderm do not. By 9.5 dpc (Theiler stage 15), the caudal pole of the embryo remains positive, as does the posterior neural tube and posterior gut endoderm. At 12.5 dpc (Theiler stage 20), expression is confined exclusively to the gut endoderm posterior to the foregut-midgut junction (Beck et. al., 1995; Chawengsaksophak et. al., 2004). Cdx1 expression extends most anteriorly, followed by Cdx2 and Cdx4, with all three genes expressed posteriorly.

Cdx2-null mutant embryos die between 3.5 and 5.5 dpc, and heterozygotes have tail abnormalities and exhibit anterior homeotic transformations involving the cervical and upper thoracic vertebrae, ribs, and midgut endoderm. [90% of Cdx2 heterozygote mutant mice develop multiple intestinal adenomatous polyps, particularly in the proximal colon, suggesting that Cdx2 mutations might be the primary event in the genesis of some intestinal tumours (Chawengsaksophak et. al., 2004; Chawengsaksophak et. al., 1997).]


Beck, F., Erler, T., Russell, A., and James, R. (1995). Expression of Cdx-2 in the mouse embryo and placenta: possible role in patterning of the extra-embryonic membranes. Dev Dyn 204, 219-227.

Chawengsaksophak, K., de Graaff, W., Rossant, J., Deschamps, J., and Beck, F. (2004). Cdx2 is essential for axial elongation in mouse development. Proc Natl Acad Sci U S A 101, 7641-7645.

Chawengsaksophak, K., James, R., Hammond, V. E., Kontgen, F., and Beck, F. (1997). Homeosis and intestinal tumours in Cdx2 mutant mice. Nature 386, 84-87.

The three mouse cad homologues, Cdx1, Cdx2 and Cdx4, (2–4) have developmental roles with overlap of expression patterns.

Cdx2 is expressed (5) at 3.5 days postcoitum (dpc) in the trophectoderm but not in the inner cell mass. At 7.5 dpc (Theiler stage 11), it is present in the chorion, ectoplacental cone, mesoderm of the developing allantoic bud, and posterior primitive streak. At 8.5 dpc (Theiler stage 13), expression is seen in all three germ layers at the posterior end of the embryo extending into the mesodermal root of the allantois, in the endodermal epithelium of the hindgut rudiment, and in the neural tube; the presegmented paraxial mesoderm expresses the gene, but the somites, lateral plate, and intermediate mesoderm do not. By 9.5 dpc (Theiler stage 15), the caudal pole of the embryo remains positive, as does the posterior neural tube and posterior gut endoderm. At 12.5 dpc (Theiler stage 20), expression is confined exclusively to the gut endoderm posterior to the foregut midgut junction (5). [...]

Cdx1 expression extends most anteriorly, followed by Cdx2 and Cdx4, respectively, with all three genes expressed posteriorly. Cdx2-null mutant embryos die between 3.5 and 5.5 dpc, and heterozygotes have tail abnormalities and exhibit anterior homeotic shifts involving the cervical and upper thoracic vertebrae, ribs, and midgut endoderm (7).


5. Beck, F., Erler, T., Russell, A. & James, R. (1995) Dev. Dyn. 204, 219–227.

7. Chawengsaksophak, K., James, R., Hammond, V. E., Kontgen, F. & Beck, F. (1997) Nature 386, 84–87.

Anmerkungen

The source is given two times, but it is not clear that Chawengsaksophak et al. are quoted literally here. Also the reader rather assumes that the given source is just one more reference.

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