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Article

Recurrent CDC25C mutations drive malignant transformation in FPD/AML.

Nature communications - 27 Aug 2014

Yoshimi Akihide, Toya Takashi, Kawazu Masahito, Ueno Toshihide, Tsukamoto Ayato, Iizuka Hiromitsu, Nakagawa Masahiro, Nannya Yasuhito, Arai Shunya, Harada Hironori, Usuki Kensuke, Hayashi Yasuhide, Ito Etsuro, Kirito Keita, Nakajima Hideaki, Ichikawa Motoshi, Mano Hiroyuki, Kurokawa Mineo

Abstract excerpt

Familial platelet disorder (FPD) with predisposition to acute myelogenous leukaemia (AML) is characterized by platelet defects with a propensity for the development of haematological malignancies. Its molecular pathogenesis is poorly understood, except for the role of germline RUNX1 mutations. Here we show that CDC25C mutations are frequently found in FPD/AML patients (53%). Mutated CDC25C disrupts the G2/M...

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Share to Blood Platelet Disorders
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Share to Core Binding Factor Alpha 2 Subunit

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Share to GATA2 Transcription Factor

Share to Leukemia, Myeloid, Acute

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Source

Identifiers

PMID: 25159113
DOI: 10.1038/ncomms5770

Genes

GATA2
RUNX1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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