Apc truncation mutations in intestinal tumors from MutL homolog deficient Apc1638N mice.

aCombined with previous data from Wong et al 2002 [36].bData from Kuraguchi et al 2000 [32] for comparison.

Figshare2015-12-02 更新00

Sequences of Apc mutations in MutL homolog deficient Apc1638N tumors.

aPrevious data from Wong et al 2002.

Figshare2015-12-02 更新00

Expression data from subpopulations of Apc1638N/+ intestinal adeno tumors versus Apc1638N/+ / KRAS v12G intestinal adenocarcinomas tumors

Constitutive activation of the Wnt pathway leads to adenoma formation, an obligatory step towards intestinal cancer. In view of the established role of Wnt in regulating stemness, we attempted the iso

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<i>Apc</i> truncation mutations in intestinal tumors from MutL homolog deficient Apc<sup>1638N</sup> mice.