Contribution of ADAMs and ADAMTSs to Tumor Expansion and Metastasis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2009-08-28

AUTHORS

Antoni Xavier Torres-Collado , M. Luisa Iruela-Arispe

ABSTRACT

Inactivating mutations in extracellular protease-encoding genes are a recent and somewhat surprising finding, since these enzymes were long believed to be promoting tumor cell detachment and invasion. However, in recent years several inhibitory roles in cancer progression have been attributed to matrix metalloproteinases and also members of the adamalysin family. In a recent comprehensive genetic screen of breast and colorectal cancer mutations, loss-of-function mutations were found in ADAM12 (Dyczynska et al. 2008), ADAMTS15, and ADAMTS18 (Sjöblom et al. 2006). Additionally, local copy number alterations involving deletions of ADAMTS20 were detected in glioblastoma multiforme (Cancer Genome Atlas Research Network 2008), and ADAM23, a possible tumor suppressor gene, is frequently silenced in gastric cancers by homozygous deletion or aberrant promoter hypermethylation (Takada et al. 2005). The mechanisms underlying the involvement of ADAM and ADAMTS proteins in tumor progression are reviewed below. More... »

PAGES

293-314

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4419-0711-0_13

DOI

http://dx.doi.org/10.1007/978-1-4419-0711-0_13

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009488446


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