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Review
. 2004 Nov;53(11):1701-9.
doi: 10.1136/gut.2004.052704.

Apoptosis and colorectal cancer

A J M Watson  1
Affiliations
Review

Apoptosis and colorectal cancer

A J M Watson. Gut. 2004 Nov.
No abstract available

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Figures

Figure 1
Figure 1
A simplified diagram of the Wnt/APC pathway. DKK, dickkopf-1; DSH, dishevelled; APC, adenomatous polyposis coli; TCF, T cell factor; Eph, ephrin.
Figure 2
Figure 2
The intrinsic, or mitochondrial, pathway (after Danial and Korsmeyer29). See text for details.
Figure 3
Figure 3
The extrinsic, or death receptor, pathway (see text for details).
Figure 4
Figure 4
The chromosomal instability (CIN) pathway (see text for details).
Figure 5
Figure 5
Mitogenic signals are transduced by Ras which inhibits the retinoblastoma (Rb) protein allowing E2F and Myc to promote cell cycle progression. p16INK4a is a tumour suppressor whose mutation permits cyclin D dependent kinase (CDK) to inhibit Rb. High levels of E2F or Myc activates p14ARF and thereby p53 which has multiple outputs. A series of proapoptotic bcl-2 family members are stimulated and via PTEN the antiapoptotic actions of AKT are inhibited. Note that p53 can still respond to DNA damage, and therefore chemotherapy, if the Ras/Rb pathway is disabled.
Figure 6
Figure 6
The microsatellite instability (MSI) pathway (see text for details).
See this image and copyright information in PMC

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References

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