CEBPA


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CEBPA

A gene on chromosome 19q13.1 that encodes a transcription factor which binds as a homodimer to various promoters and enhancers, and as a heterodimer to CEBP-beta and CEBP-gamma. CEBP-alpha also interacts with CDK2 and CDK4, inhibiting them and causing growth arrest.
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Mutations of FLT3, DNMT3A, and NPM1 are often present concurrently, while other mutations of NPM1, RUNX1, CEBPA, and TP53 are almost always mutually exclusive both at diagnosis and during disease transformation (11-19).
Reliable detection of a point mutation in a GC-rich region of the CEBPA gene.
TET2 mutation is a recent finding that should be added to ELN classification to improve risk stratification TET2 mutation is found as an adverse prognostic factor even if it coexists with favourable19 or intermediate-risk cytogenetics.15 Adversity of TET mutation become higher in the presence of FLT3-ITD, NPM1 negative, or poor prognostic genotypes but not in FLT3-ITD negative patients andNPM1 and or CEBPA positive AML.20 Overall survival is reduced with TET mutation.15 However, others have shown no correlation of TET2 with AML prognosis.21
Of note, CEBPA, an important transcription factor in adipogenesis was identified as an upstream regulator in TPP and troglitazone-treated cells (not in the top 10) but not in IPTP.
[10] Human genes: CD117, synonym for KIT (KIT proto-oncogene receptor tyrosine kinase); EGFR, epidermal growth factor receptor; ALK, anaplastic lymphoma receptor tyrosine kinase; HER2, synonym for EBBR2 (erb-b2 receptor tyrosine kinase 2); BRAF, B-Raf proto-oncogene, serine/threonine kinase; KRAS, KRAS proto-oncogene, GTPase; CEBPA, CCAAT/enhancer binding protein alpha; APC,APC, WNTsignaling pathway regulator; RB1, RB transcriptional corepressor 1; PIK3CA, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha.
Nucleophosmin (NPM1) mutated AML and CCAAT / enhancer binding protein alpha (CEBPA) mutated AML are categorized as two provisional entities to this category.
found that, unlike mutations considered to be "first hit" mutations, such as NPM1 and CEBPA, DNMT3A mutations were always still detectable at relapse [43].
DDIT3 is normally expressed late in adipocyte differentiation together with the related transcription factor CEBPA [14].
Citation: "Temporal mapping of CEBPA and CEBPB binding during liver regeneration reveals dynamic occupancy and specific regulatory codes for homeostatic and cell cycle gene batteries"; Janus Schou Jakobsen et al.; Genome Research, advance online publication, DOI: 10.1101/gr.146399.112