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Wnt signaling and gastrointestinal tumorigenesis in mouse models

Abstract

The canonical Wnt signaling plays important roles in embryonic development and tumorigenesis. For the latter, induced mutations in mice have greatly contributed to our understanding of the molecular mechanisms of cancer initiation and progression. Here, I will review recent reports on gastrointestinal cancer model mice, with an emphasis on the roles of the Wnt signal pathway. They include: mouse models for familial adenomatous polyposis; modifying factors that affect mouse intestinal polyposis, including the genes that help cancer progression; Wnt target genes that affect mouse intestinal polyposis; and a mouse model of gastric cancer that mimics Helicobacter pyroli infection.

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Abbreviations

AA:

arachidonic acid

ABI:

anaphase bridge index

ACF:

aberrant crypt foci

Chr:

(mouse) chromosome

CIN:

chromosomal instability

cM:

centimorgan(s)

COX:

cyclooxygenase

FAP:

familial adenomatous polyposis

GI:

gastrointestinal

HDAC:

histone deacetylase

HNPCC:

hereditary nonpolyposis colon cancer

IL:

interleukin

K19:

cytokeratin 19

LOH:

loss of heterozygosity

MSI:

microsatellite instability

NSAID:

non-steroidal anti-inflammatory drug

PG:

prostaglandin

mPGES:

microsomal prostaglandin E synthase

PI:

phosphoinositide

PLA2:

phospholipase A2

PPAR:

peroxysome proliferator activator receptor

SPEM:

spasmolytic polypeptide/trefoil factor 2-expressing metaplasia

TCF:

T-cell factor

TFF:

trefoil factor

Tg:

transgenic

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Acknowledgements

I thank M Bienz for comments on the manuscript. I also thank the members of my laboratory who have contributed to the papers I have cited here. The research programs in my laboratory have been supported by grants from MESSC, Japan; OPSR, Japan; University of Tokyo–Banyu Pharmaceutical Co. Joint Fund; Takeda Foundation, and Mitsubishi Foundation.

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Correspondence to M M Taketo.

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Taketo, M. Wnt signaling and gastrointestinal tumorigenesis in mouse models. Oncogene 25, 7522–7530 (2006). https://doi.org/10.1038/sj.onc.1210058

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