APC and [beta]-catenin degradation / Jennifer Kennell and Kenneth M. Cadigan -- Nuclear APC / Kristi L. Neufeld -- APC in cell migration / Sandrine Etienne-Manneville -- The APC-EB1 interaction / Ewan E. Morrison -- The role of APC in mitosis and in chromosome instability / Christine M. Caldwell and Kenneth B. Kaplan -- Role of APC and its binding partners in regulating microtubules in mitosis / Shirin Bahmanyar, W. James Nelson, and Angela I.M. Barth -- The adenomatous polyposis coli tumor suppressor and WNT signaling in the regulation of apoptosis / Hassina Benchabane and Yashi Ahmed -- APC and its modifiers in colon cancer / Lawrence N. Kwong and William F. Dove -- Tissue-specific tumour suppression by APC / Owen Sansom -- Extra-colonic manifestations of familial adenomatous polyposis coli / Alison H. Trainer
Summary
The initial identification of the Adenomatous polyposis coli (Apc) gene as the site of mutations in familial adenomatous polyposis (FA P) was described in 1992. A causal relationship between Apc mutations and intestinal tract tumours was confirmed three years later with the establishment of the Min mouse model. These mice are heterozygous for Apc and develop numerous intestinal tumours that mimic FA P. Subsequently, Apc has emerged as the most commonly mutated gene in colorectal cancer with reports varying between 50-80 per cent of sporadic tumours carrying such mutations. The search for how m
