Somatic RHOA mutation in angioimmunoblastic T cell lymphoma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-02

AUTHORS

Mamiko Sakata-Yanagimoto, Terukazu Enami, Kenichi Yoshida, Yuichi Shiraishi, Ryohei Ishii, Yasuyuki Miyake, Hideharu Muto, Naoko Tsuyama, Aiko Sato-Otsubo, Yusuke Okuno, Seiji Sakata, Yuhei Kamada, Rie Nakamoto-Matsubara, Nguyen Bich Tran, Koji Izutsu, Yusuke Sato, Yasunori Ohta, Junichi Furuta, Seiichi Shimizu, Takuya Komeno, Yuji Sato, Takayoshi Ito, Masayuki Noguchi, Emiko Noguchi, Masashi Sanada, Kenichi Chiba, Hiroko Tanaka, Kazumi Suzukawa, Toru Nanmoku, Yuichi Hasegawa, Osamu Nureki, Satoru Miyano, Naoya Nakamura, Kengo Takeuchi, Seishi Ogawa, Shigeru Chiba

ABSTRACT

Angioimmunoblastic T cell lymphoma (AITL) is a distinct subtype of peripheral T cell lymphoma characterized by generalized lymphadenopathy and frequent autoimmune-like manifestations. Although frequent mutations in TET2, IDH2 and DNMT3A, which are common to various hematologic malignancies, have been identified in AITL, the molecular pathogenesis specific to this lymphoma subtype is unknown. Here we report somatic RHOA mutations encoding a p.Gly17Val alteration in 68% of AITL samples. Remarkably, all cases with the mutation encoding p.Gly17Val also had TET2 mutations. The RHOA mutation encoding p.Gly17Val was specifically identified in tumor cells, whereas TET2 mutations were found in both tumor cells and non-tumor hematopoietic cells. RHOA encodes a small GTPase that regulates diverse biological processes. We demonstrated that the Gly17Val RHOA mutant did not bind GTP and also inhibited wild-type RHOA function. Our findings suggest that impaired RHOA function in cooperation with preceding loss of TET2 function contributes to AITL-specific pathogenesis. More... »

PAGES

171-175

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng.2872

DOI

http://dx.doi.org/10.1038/ng.2872

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1043585182

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/24413737


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