MAX inactivation is an early event in GIST development that regulates p16 and cell proliferation View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-03-08

AUTHORS

Inga-Marie Schaefer, Yuexiang Wang, Cher-wei Liang, Nacef Bahri, Anna Quattrone, Leona Doyle, Adrian Mariño-Enríquez, Alexandra Lauria, Meijun Zhu, Maria Debiec-Rychter, Susanne Grunewald, Jaclyn F. Hechtman, Armelle Dufresne, Cristina R. Antonescu, Carol Beadling, Ewa T. Sicinska, Matt van de Rijn, George D. Demetri, Marc Ladanyi, Christopher L. Corless, Michael C. Heinrich, Chandrajit P. Raut, Sebastian Bauer, Jonathan A. Fletcher

ABSTRACT

KIT, PDGFRA, NF1 and SDH mutations are alternate initiating events, fostering hyperplasia in gastrointestinal stromal tumours (GISTs), and additional genetic alterations are required for progression to malignancy. The most frequent secondary alteration, demonstrated in ∼70% of GISTs, is chromosome 14q deletion. Here we report hemizygous or homozygous inactivating mutations of the chromosome 14q MAX gene in 16 of 76 GISTs (21%). We find MAX mutations in 17% and 50% of sporadic and NF1-syndromic GISTs, respectively, and we find loss of MAX protein expression in 48% and 90% of sporadic and NF1-syndromic GISTs, respectively, and in three of eight micro-GISTs, which are early GISTs. MAX genomic inactivation is associated with p16 silencing in the absence of p16 coding sequence deletion and MAX induction restores p16 expression and inhibits GIST proliferation. Hence, MAX inactivation is a common event in GIST progression, fostering cell cycle activity in early GISTs. More... »

PAGES

14674

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms14674

DOI

http://dx.doi.org/10.1038/ncomms14674

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1084128902

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28270683


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