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Cell adhesion and signal transduction in cancer
Author(s) -
Birchmeier Walter
Publication year - 2005
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400408
Subject(s) - catenin , cadherin , cancer , signal transduction , biology , microbiology and biotechnology , cell , wnt signaling pathway , genetics
The Centro Nacional de Investigaciones Oncologicas (CNIO) Cancer Conference on ‘Cadherins, Catenins and Cancer’ was held in Madrid, Spain, between 29 November and 1 December 2004. The conference was organized by A. Cano, H. Clevers, J. Palacios and F. van Roy![][1] Cadherin cell‐adhesion molecules and their intracellular binding partners, catenins, were discovered in the 1980s (for a review, see Takeichi, 1995). Interest in these molecules was sparked by the discovery that cadherins and, subsequently, catenins are important in the formation and metastasis of carcinomas (Behrens et al , 1989; Berx et al , 1998; Perl et al , 1998; Polakis, 2000). Twenty years later, interest in cadherins and catenins remains high, as seen at the Centro Nacional de Investigaciones Oncologicas (CNIO) Cancer Conference on ‘Cadherins, Catenins and Cancer’ in Madrid. The meeting covered research on all fronts, from the molecular aspects of cadherin and catenin regulation and signalling, to their role in human carcinogenesis and subsequent clinical applications.### E‐cadherin in cancer progressionIn 1998, germline mutations in the E‐cadherin gene were identified in New Zealand Maori families with diffuse‐type gastric cancer, which firmly established the importance of E‐cadherin in the progression of carcinomas (Guilford et al , 1998). At the Madrid meeting, F. Carneiro (Porto, Portugal) presented new data, which showed that hereditary diffuse gastric cancer is a dominantly inherited familial cancer syndrome that contributes up to 3% of all gastric cancers. Furthermore, E‐cadherin mutations are the causal genetic defect for up to 40% of these cases. About 80% of the mutations that have been identified in the E‐cadherin gene result in a truncated protein, whereas the remaining 20% are missense mutations. Germline mutations of E‐cadherin are distributed throughout the whole gene, in contrast to somatic mutations in sporadic diffuse gastric cancer, which cluster in exons 7‐9 (Berx et al , 1998). Inactivation of the remaining … [1]: /embed/graphic-1.gif