Atlas of Genetics and Cytogenetics in Oncology and Haematology

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Taking over the Atlas
Dear Colleagues,
The Atlas, once more, is in great danger, and I will have to proceed to a collective economic lay-off of all the team involved in the Atlas before the begining of April 2015 (a foundation having suddenly withdrawn its commitment to support the Atlas). I ask you herein if any Scientific Society (a Society of Cytogenetics, of Clinical Genetics, of Hematology, or a Cancer Society, or any other...), any University and/or Hospital, any Charity, or any database would be interested in taking over the Atlas, in whole or in part. If taking charge of the whole lot is too big, a consortium of various actors could be the solution (I am myself trying to find partners). Could you please spread the information, contact the relevant authorities, and find partners.
Survival of the Atlas will be critically dependant upon your ability to find solutions (and urgently!).
Kind regards.
Jean-Loup Huret jlhuret@AtlasGeneticsOncology.org
Donations are also welcome
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Don't let the Atlas imminent demise
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CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha)

Identity

Other namesC/EBPa
CEBP
HGNC (Hugo) CEBPA
LocusID (NCBI) 1050
Location 19q13.1
Location_base_pair Starts at 33790840 and ends at 33793470 bp from pter ( according to hg19-Feb_2009)  [Mapping]

DNA/RNA

 
  Figure 1: Human C/EBPa mRNA.
Description Human C/EBPα is an intronless gene located on the minus strand of chromosome 19q.
Transcription The C/EBPa mRNA (RNA messenger) consists of a short 5' unstranslated region (5'-UTR), a unique protein coding sequence (CDS) and a long 3'-UTR (Hendricks-Taylor et al., 1992).

Protein

 
  Figure 2: C/EBPa protein domains and interactions.
Description Human C/EBPα mRNA gives rise to two protein products by using two different translation starting sites (Figure 1 and 2) (Calkhoven et al., 2000). Compared to full-length C/EBPA protein, P42, the shorter P30 isoform lacks N-terminal 117 amino acids (Lin et al., 1993).
As a transcription factor, C/EBPA protein consists of DNA-binding domain (DBD) in its carboxyl-terminal (C-terminal), which is conserved between C/ebp family members (Leutz et al., 2011). The highly conserved C-terminus includes the basic DNA binding leucine zipper domain (bZip). The bZip domain in turn consists of a basic region that represents the DNA binding domain (DBD), the fork domain and the leucine zipper domain (LZ). The bZip domain is indispensable for homodimerization and heterodimerization with other members of the C/EBP family. This region is also involved in the interaction with other transcription factors (e.g. E2F, PU.1, c-JUN, RUNX1 and ETS1) (McNagny et al., 1998; Yamaguchi et al., 1999; Ramji and Foka, 2002; Nerlov, 2004; Koschmieder et al., 2005; Leutz et al., 2011).
The N-terminus of C/EBPa consists of three transactivation domains (TA), which can interact with components of the transcriptional machinery (e.g. CBP/P300, TBP/TFIIB) (Nerlov and Ziff, 1995; Kovacs et al., 2003; Schwartz et al., 2003), cell cycle regulators (e.g. E2F, CDK2, CDK4) (Porse et al., 2001; Porse et al., 2006) and chromatin remodellers (e.g. SWI/SNF) (Pedersen et al., 2001).
Expression C/EBPa is mainly expressed in terminally differentiated cells, such as mature adipocytes and myelomonocytic cells. C/EBPa is also found expressed in skin, intestine, lung, adrenal gland, mammary gland, ovary, prostate, placenta (Oh and Smart, 1998; Birkenmeier et al., 1989).
Localisation C/EBPa protein is localized in nucleus.
Function C/EBPa homozygous null mice lack white adipose tissues (Wang et al., 1995), as well as mature granulocytes and granulocyte-macrophage precursors (Zhang et al., 1997; Heath et al., 2004). In addition, forced expression of C/EBPa can direct uncommitted progenitors to differentiate into adipocytes and granulocytes (Freytag et al., 1994; Radomska et al., 1998; Nerlov et al., 1998). Further studies suggest that C/EBPa plays important roles in lineage determination by activating lineage-specific genes (Nerlov, 2004; Graf and Enver, 2009).
In hematopoiesis, C/EBPa is one of the key factors driving myeloid cell differentiation from hematopoietic stem cells by interacting with other proteins, such as the ETS family transcription factor PU.1, the ATP dependent chromatin remodeling complex SWI/SNF, the DNA modifying enzyme TET2 (McNagny et al., 1998; Koschmieder et al., 2005; Leutz et al., 2011; Kallin et al., 2012). Ectopic expression of C/EBPa leads to cell cycle arrest via direct interaction with the key cell cycle regulators CDK2/4 and E2F (Porse et al., 2001; Porse et al., 2006). The N-terminal truncated form of C/EBPa, P30, has been shown to act as a dominant negative regulator of the full-length form, P42. Modulation of P30 expression level in mice can alter normal adipogenesis and granulopoiesis (Kirstetter et al., 2008).
Notably, ectopic expression of C/EBPa in B and T-lymphocyte precursors results in transdifferentiation into functional macrophages (Xie et al., 2004; Laiosa et al., 2006; Bussmann et al., 2009; Di Tullio et al., 2011; Kallin et al., 2012). Interestingly, C/EBPa mediated conversion of B lymphoma cells into macrophages impairs significantly its tumorigenicity, providing a novel strategy for lymphoma treatment (Rapino et al., 2013). Moreover, a recent study showed that transient C/EBPa expression is also capable of facilitating the conversion of B cells into induced pluripotent stem cells (iPS cells) (Di Stefano et al., 2014).
Moreover, C/EBPa has been shown involved in lung development and airway epithelial differentiation (Cassel et al., 2000a; Cassel et al., 2000b; Cassel et al., 2002). The conditional deletion of C/EBPa gene in respiratory epithelium results in respiratory arrest and death soon after birth. This phenotype is associated with proliferation of immature type II alveolar cells, which causes epithelial expansion and loss of air space (Martis et al., 2006; Basseres et al., 2006).
Homology C/EBPa belongs to the CCAAT/enhancer binging protein family and is highly conserved across vertebrate species. Sequence alignments show that C/EBP members share several conserved regions including the bZip and transactivation domains (Leutz et al., 2011).

Mutations

Note Mutations of the C/EBPα gene have been detected in 7%-15% of Acute Myeloid Leukemia (AML) (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005), around 4% of Myelodysplastic Syndrome (MDS) and Chronic Myeloid Leukemia (CML) (Shih et al., 2005). In addition, two familial cases of AML harboring C/EBPA mutations have been reported (Smith et al., 2004; Renneville et al., 2009).
Germinal Germ line mutations of C/EBPα have been described for two familial cases of AML. In one Inherited acute myeloid leukemia case, a heterozygous deletion of cytosine 212 has been reported (Smith et al., 2004). Recently, the second family contained a heterozygous insertion of cytosine at nucleotide 217 (Renneville et al., 2009). These mutations result in frameshifts, leading to a premature termination of full-length C/EBPa P42 isoform translation. Nonetheless, the alternative C/EBPa P30 isoform translation could be potentially privileged. P30 isoform has dominant-negative activity on the full-length P42 isoform.
Somatic It has been shown that 7%-15% of AML harbor somatic mutations of the C/EBPα gene (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005). In addition, C/EBPα mutations have been detected in MDS and CML patient samples. These mutations can be basically divided into two categories: C-terminal in-frame ins/del mutations altering C/EBPA DNA-binding activities, and N-terminal out-of-frame ins/del mutations impairing translation of full-length P42 isoform and leading aberrant expression of P30 isoform, which has dominant-negative activity on P42 isoform. The majority of leukemias with biallelic C/EBPA mutations harbor one allele with C-terminal mutations and the other one with N-terminal mutations. Tumors with homozygous N'-terminal or C'-terminal mutations are relatively rare.

Implicated in

Entity Acute myeloid leukemia (AML)
Disease Mutations in C/EBPα have been identified in 7-15% of AML cases (Pabst et al., 2001b; Preudhomme et al., 2002; Barjesteh van Waalwijk van Doorn-Khosrovani et al., 2003; Snaddon et al., 2003; Frohling et al., 2004; Lin et al., 2005). A meta-analysis of a cohort of 1175 patients reported that C/EBPα mutations are preferentially identified in M1, M2 and M4 FAB subtypes and associated with normal karyotype (Leroy et al., 2005).
Prognosis It has been shown that AML patients harboring C/EBPα mutations have favorable prognosis (Preudhomme et al., 2002).
Abnormal Protein C-terminal in-frame ins/del mutations can alter C/EBPa DNA-binding activities, and N-terminal out-of-frame ins/del mutations impairing translation of full-length P42 isoform and leading to aberrant expression of P30 isoform, which has dominant-negative activity on P42 isoform (Leroy et al., 2005).
Oncogenesis Mouse models harboring biallelic (C-terminal and N-terminal) C/EBPα mutations suggested that the co-existence of these mutations can increase the proliferation of long-term hematopoietic stem cells (LT-HSC) and override normal HSC homeostasis, leading to expansion of premalignant HSC (Kirstetter et al., 2008; Bereshchenko et al., 2009). Moreover, the fusion oncoproteins AML1-ETO (t(8;21)), CBFb-HYH11 (inv(16)) and PML-RARa (t(15;17)) suppress C/EBPA mRNA expression and/or protein activity in AML (Pabst et al., 2001a; Truong et al., 2003; Cilloni et al., 2003).
  
Entity B cell precursor acute lymphoblastic leukemia (BCP-ALL)
Note t(14;19)(q32;q13)
Disease It has been reported that C/EBPa is involved in several cases of BCP-ALL, although the prevalence of C/EBPa involved translocation need to be determined using larger cohorts (Chapiro et al., 2006; Akasaka et al., 2007; Jeffries et al., 2014). In these BCP-ALL cases, C/EBPa is aberrantly expressed by juxtaposition to the immunoglobulin gene enhancer upon its rearrangement with the immunoglobulin heavy-chain locus.
Oncogenesis Aberrant expression of C/EBPa in BCP-ALL samples harboring t(14;19)(q32;q13) suggests that C/EBPa may have oncogenic function in this disease, which is in contrast to its onco-suppressor role in AML (Chapiro et al., 2006). Further biological studies need to be performed to clarify this hypothesis.
  
Entity Non-small-cell lung cancer
Disease The chromosomal region including C/EBPa was reported deleted in 50% stage II and IIIA lung adenocarcinomas (Girard et al., 2000). However, mutations of C/EBPa in lung cancer are rare. It has been as well reported that an upstream promoter region of the C/EBPa gene is hypermethylated in approximately 65% of primary lung tumors (Tada et al., 2006). These evidences suggest that C/EBPa is a tumor suppressor in non-small-cell lung cancer.
Oncogenesis Ectopic expression of C/EBPa in lung cancer cell lines results in significant growth arrest (Halmos et al., 2002; Costa et al., 2007). A transcriptional analysis identified that differentiation associated gene FoxA2 is a direct target gene of C/EBPa in lung cancer cell line (Halmos et al., 2004). Recently, using urethane-induced lung cancer model, it has been shown that C/EBPa expression is extinguished through p38alpha MAP kinase inactivation, leading to tumor progression (Sato et al., 2013), confirming a tumor suppressor role of C/EBPa in lung cancer.
  
Entity Skin squamous cell carcinoma
Disease Although C/EBPa expression has been found in human precancerous skin lesions (Actinic Keratoses) and normal epidermis, its expression is undetectable in invasive squamous cell carcinoma samples (Thompson et al., 2011), suggesting a possible role as a tumor-suppressor in skin cancer.
Oncogenesis In normal epidermis, C/EBPa expression is located in basal and suprabasal keratinocytes (Maytin and Habener, 1998; Thompson et al., 2011). Forced C/EBPa expression in a skin cancer cell line inhibits cell proliferation (Shim et al., 2005). Moreover, C/EBPa-null mice are highly susceptible to 7,12-dimethylbenz[a]anthracene- and UVB-induced skin tumor development (Loomis et al., 2007; Thompson et al., 2011). Notably, It has been shown that down-regulation of C/EBPa in skin cancer cells is associated with oncogenic Ras activation (Shim et al., 2005; Loomis et al., 2007).
  
Entity Prostate cancer
Disease It has been shown that C/EBPa expression is down-regulated in prostate cancer sample comparing to normal prostate tissue (Yin et al., 2006). Interestingly, one study showed that C/EBPa expression is sequestered in cytosol, which could impair its transcription factor activity (Zhang et al., 2008). Although further studies need to be performed with larger prostate cancer cohorts for confirmation, these observations suggest an emerging tumor suppressor role of C/EBPa in prostate cancer.
Oncogenesis C/EBPa is mainly expressed in basal layer in normal prostate. In most prostate adenocarcinoma samples, its expression level is low (Yin et al., 2006; Zhang et al., 2008). Forced expression of C/EBPa in prostate cancer cell lines can inhibit PSA (Prostate Specific Antigen) expression and regulate negatively androgen receptor (AR) signaling (Chattopadhyay et al., 2006; Yin et al., 2006; Zhang et al., 2010). In addition, in AR-negative prostate cancer cell lines, ectopically expressed C/EBPA protein can physically interact with Ku proteins (Ku70, Ku80) and Poly [ADP-ribose] polymerase 1 (PARP-1), conferring prostate cancer cells an increased sensitivity to DNA-damaging agents (Yin and Glass, 2006).
  
Entity Hepatocellular carcinoma
Disease The expression of C/EBPa is reduced in hepatocellular carcinoma samples and higher expression of C/EBPa in hepatocellular carcinoma reversibly correlated with the tumor size and clinical stage (Tomizawa et al., 2003).
Oncogenesis Forced C/EBPa expression in hepatoma cell lines impairs proliferation and tumorigenicity (Watkins et al., 1996). Liver specific C/EBPa knock-in mice are resistant, at least partially, to diethylnitrosamine-induced hepatocellular carcinoma formation. These observations suggest a tumor suppressor role of C/EBPa in hepatocellular carcinoma (Tan et al., 2005).
  
Entity Head and neck squamous cell cancer
Disease It has been reported that C/EBPa expression is down-regulated in squamous cell cancers in head and neck region. This down-regulation correlates with the degree of C/EBPa promoter methylation (Bennett et al., 2007).
  

Other Leukemias implicated (Data extracted from papers in the Atlas)

Leukemias 11q23ChildAMLID1615 11q23ID1030 11q23secondLeukID1131 t1119ELLID1029 t0812q24q22ID2057
t0814ID1050

External links

Nomenclature
HGNC (Hugo)CEBPA   1833
Cards
AtlasCEBPAID40050ch19q13
Entrez_Gene (NCBI)CEBPA  1050  CCAAT/enhancer binding protein (C/EBP), alpha
GeneCards (Weizmann)CEBPA
Ensembl hg19 (Hinxton)ENSG00000245848 [Gene_View]  chr19:33790840-33793470 [Contig_View]  CEBPA [Vega]
Ensembl hg38 (Hinxton)ENSG00000245848 [Gene_View]  chr19:33790840-33793470 [Contig_View]  CEBPA [Vega]
ICGC DataPortalENSG00000245848
cBioPortalCEBPA
AceView (NCBI)CEBPA
Genatlas (Paris)CEBPA
WikiGenes1050
SOURCE (Princeton)CEBPA
Genomic and cartography
GoldenPath hg19 (UCSC)CEBPA  -     chr19:33790840-33793470 -  19q13.1   [Description]    (hg19-Feb_2009)
GoldenPath hg38 (UCSC)CEBPA  -     19q13.1   [Description]    (hg38-Dec_2013)
EnsemblCEBPA - 19q13.1 [CytoView hg19]  CEBPA - 19q13.1 [CytoView hg38]
Mapping of homologs : NCBICEBPA [Mapview hg19]  CEBPA [Mapview hg38]
OMIM116897   
Gene and transcription
Genbank (Entrez)BC027902 BC063874 BC160133 X87248 Y11525
RefSeq transcript (Entrez)NM_001285829 NM_001287424 NM_001287435 NM_004364
RefSeq genomic (Entrez)AC_000151 NC_000019 NC_018930 NG_012022 NT_011109 NW_001838492 NW_004929415
Consensus coding sequences : CCDS (NCBI)CEBPA
Cluster EST : UnigeneHs.76171 [ NCBI ]
CGAP (NCI)Hs.76171
Alternative Splicing GalleryENSG00000245848
Gene ExpressionCEBPA [ NCBI-GEO ]     CEBPA [ SEEK ]   CEBPA [ MEM ]
SOURCE (Princeton)Expression in : [Normal Tissue Atlas]  [carcinoma Classsification]  [NCI60]
Protein : pattern, domain, 3D structure
UniProt/SwissProtP49715 (Uniprot)
NextProtP49715  [Medical]
With graphics : InterProP49715
Splice isoforms : SwissVarP49715 (Swissvar)
Domaine pattern : Prosite (Expaxy)BZIP (PS50217)   
Domains : Interpro (EBI)bZIP    CCAAT/enhancer-binding   
Related proteins : CluSTrP49715
Domain families : Pfam (Sanger)bZIP_2 (PF07716)   
Domain families : Pfam (NCBI)pfam07716   
Domain families : Smart (EMBL)BRLZ (SM00338)  
DMDM Disease mutations1050
Blocks (Seattle)P49715
Human Protein AtlasENSG00000245848
Peptide AtlasP49715
HPRD00296
IPIIPI00292025   
Protein Interaction databases
DIP (DOE-UCLA)P49715
IntAct (EBI)P49715
FunCoupENSG00000245848
BioGRIDCEBPA
IntegromeDBCEBPA
STRING (EMBL)CEBPA
Ontologies - Pathways
QuickGOP49715
Ontology : AmiGOurea cycle  negative regulation of transcription from RNA polymerase II promoter  liver development  embryonic placenta development  DNA binding  sequence-specific DNA binding transcription factor activity  RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity  protein binding  nucleus  generation of precursor metabolites and energy  transcription, DNA-templated  transcription, DNA-templated  transcription from RNA polymerase II promoter  acute-phase response  mitochondrion organization  transcription factor binding  cholesterol metabolic process  negative regulation of cell proliferation  viral process  nuclear matrix  cytokine-mediated signaling pathway  myeloid cell differentiation  macrophage differentiation  lung development  organ regeneration  protein complex binding  response to vitamin B2  Rb-E2F complex  protein homodimerization activity  sequence-specific DNA binding  transcription regulatory region DNA binding  positive regulation of fat cell differentiation  positive regulation of osteoblast differentiation  positive regulation of transcription from RNA polymerase II promoter  positive regulation of transcription from RNA polymerase III promoter  protein heterodimerization activity  cell maturation  inner ear development  white fat cell differentiation  brown fat cell differentiation  response to glucocorticoid  cellular response to lithium ion  cellular response to organic cyclic compound  HMG box domain binding  
Ontology : EGO-EBIurea cycle  negative regulation of transcription from RNA polymerase II promoter  liver development  embryonic placenta development  DNA binding  sequence-specific DNA binding transcription factor activity  RNA polymerase II distal enhancer sequence-specific DNA binding transcription factor activity  protein binding  nucleus  generation of precursor metabolites and energy  transcription, DNA-templated  transcription, DNA-templated  transcription from RNA polymerase II promoter  acute-phase response  mitochondrion organization  transcription factor binding  cholesterol metabolic process  negative regulation of cell proliferation  viral process  nuclear matrix  cytokine-mediated signaling pathway  myeloid cell differentiation  macrophage differentiation  lung development  organ regeneration  protein complex binding  response to vitamin B2  Rb-E2F complex  protein homodimerization activity  sequence-specific DNA binding  transcription regulatory region DNA binding  positive regulation of fat cell differentiation  positive regulation of osteoblast differentiation  positive regulation of transcription from RNA polymerase II promoter  positive regulation of transcription from RNA polymerase III promoter  protein heterodimerization activity  cell maturation  inner ear development  white fat cell differentiation  brown fat cell differentiation  response to glucocorticoid  cellular response to lithium ion  cellular response to organic cyclic compound  HMG box domain binding  
Pathways : BIOCARTAMAPKinase Signaling Pathway [Genes]    Keratinocyte Differentiation [Genes]   
Pathways : KEGGNon-alcoholic fatty liver disease (NAFLD)    Pathways in cancer    Transcriptional misregulation in cancer    Acute myeloid leukemia   
REACTOMEP49715 [protein]
REACTOME PathwaysREACT_111045 Developmental Biology [pathway]
Protein Interaction DatabaseCEBPA
DoCM (Curated mutations)CEBPA
Wikipedia pathwaysCEBPA
Gene fusion - rearrangements
Polymorphisms : SNP, variants
NCBI Variation ViewerCEBPA [hg38]
dbSNP Single Nucleotide Polymorphism (NCBI)CEBPA
dbVarCEBPA
ClinVarCEBPA
1000_GenomesCEBPA 
Exome Variant ServerCEBPA
SNP (GeneSNP Utah)CEBPA
SNP : HGBaseCEBPA
Genetic variants : HAPMAPCEBPA
Genomic Variants (DGV)CEBPA [DGVbeta]
Mutations
ICGC Data PortalENSG00000245848 
Cancer Gene: CensusCEBPA 
Somatic Mutations in Cancer : COSMICCEBPA 
CONAN: Copy Number AnalysisCEBPA 
LOVD (Leiden Open Variation Database)Whole genome datasets
LOVD (Leiden Open Variation Database)LOVD 3.0 shared installation
Impact of mutations[PolyPhen2] [SIFT Human Coding SNP] [Buck Institute : MutDB] [Mutation Assessor] 
Diseases
DECIPHER (Syndromes)19:33790840-33793470
Mutations and Diseases : HGMDCEBPA
OMIM116897   
MedgenCEBPA
NextProtP49715 [Medical]
GENETestsCEBPA
Disease Genetic AssociationCEBPA
Huge Navigator CEBPA [HugePedia]  CEBPA [HugeCancerGEM]
snp3D : Map Gene to Disease1050
DGIdb (Drug Gene Interaction db)CEBPA
General knowledge
Homologs : HomoloGeneCEBPA
Homology/Alignments : Family Browser (UCSC)CEBPA
Phylogenetic Trees/Animal Genes : TreeFamCEBPA
Chemical/Protein Interactions : CTD1050
Chemical/Pharm GKB GenePA26376
Clinical trialCEBPA
Cancer Resource (Charite)ENSG00000245848
Other databases
Probes
Litterature
PubMed335 Pubmed reference(s) in Entrez
CoreMineCEBPA
GoPubMedCEBPA
iHOPCEBPA

Bibliography

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Impaired energy homeostasis in C/EBP alpha knockout mice.
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Absence of granulocyte colony-stimulating factor signaling and neutrophil development in CCAAT enhancer binding protein alpha-deficient mice.
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PMID 9012825
 
Transcription factors C/EBP alpha, C/EBP beta, and CHOP (Gadd153) expressed during the differentiation program of keratinocytes in vitro and in vivo.
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PMID 9506442
 
Regulation of eosinophil-specific gene expression by a C/EBP-Ets complex and GATA-1.
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Distinct C/EBP functions are required for eosinophil lineage commitment and maturation.
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PMID 9694805
 
Expression of CCAAT/enhancer binding proteins (C/EBP) is associated with squamous differentiation in epidermis and isolated primary keratinocytes and is altered in skin neoplasms.
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PMID 9620302
 
CCAAT/enhancer binding protein alpha is a regulatory switch sufficient for induction of granulocytic development from bipotential myeloid progenitors.
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PMID 10438731
 
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PMID 10921906
 
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PMID 11193765
 
Genome-wide allelotyping of lung cancer identifies new regions of allelic loss, differences between small cell lung cancer and non-small cell lung cancer, and loci clustering.
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Cancer Res. 2000 Sep 1;60(17):4894-906.
PMID 10987304
 
AML1-ETO downregulates the granulocytic differentiation factor C/EBPalpha in t(8;21) myeloid leukemia.
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PMID 11731483
 
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J Biol Chem. 2002 Oct 4;277(40):36970-7. Epub 2002 Aug 2.
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Biallelic mutations in the CEBPA gene and low CEBPA expression levels as prognostic markers in intermediate-risk AML.
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Blood. 2003 Oct 1;102(7):2705-6.
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CCAAT/enhancer-binding protein family members recruit the coactivator CREB-binding protein and trigger its phosphorylation.
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J Biol Chem. 2003 Sep 19;278(38):36959-65. Epub 2003 Jul 11.
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Recruitment of p300 by C/EBPbeta triggers phosphorylation of p300 and modulates coactivator activity.
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Genes Chromosomes Cancer. 2003 May;37(1):72-8.
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Down-regulated expression of the CCAAT/enhancer binding protein alpha and beta genes in human hepatocellular carcinoma: a possible prognostic marker.
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CCAAT/Enhancer binding proteins repress the leukemic phenotype of acute myeloid leukemia.
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Blood. 2003 Feb 1;101(3):1141-8. Epub 2002 Oct 3.
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CEBPA mutations in younger adults with acute myeloid leukemia and normal cytogenetics: prognostic relevance and analysis of cooperating mutations.
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A transcriptional profiling study of CCAAT/enhancer binding protein targets identifies hepatocyte nuclear factor 3 beta as a novel tumor suppressor in lung cancer.
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Cancer Res. 2004 Jun 15;64(12):4137-47.
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C/EBPalpha deficiency results in hyperproliferation of hematopoietic progenitor cells and disrupts macrophage development in vitro and in vivo.
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Blood. 2004 Sep 15;104(6):1639-47. Epub 2004 Apr 8.
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C/EBPalpha mutations in acute myeloid leukaemias.
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Cell. 2004 May 28;117(5):663-76.
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Role of transcription factors C/EBPalpha and PU.1 in normal hematopoiesis and leukemia.
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Int J Hematol. 2005 Jun;81(5):368-77.(REVIEW)
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CEBPA point mutations in hematological malignancies.
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Leukemia. 2005 Mar;19(3):329-34. (REVIEW)
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Characterization of CEBPA mutations in acute myeloid leukemia: most patients with CEBPA mutations have biallelic mutations and show a distinct immunophenotype of the leukemic cells.
Lin LI, Chen CY, Lin DT, Tsay W, Tang JL, Yeh YC, Shen HL, Su FH, Yao M, Huang SY, Tien HF.
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Heterogeneous patterns of CEBPalpha mutation status in the progression of myelodysplastic syndrome and chronic myelomonocytic leukemia to acute myelogenous leukemia.
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Clin Cancer Res. 2005 Mar 1;11(5):1821-6.
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Diminished expression of C/EBPalpha in skin carcinomas is linked to oncogenic Ras and reexpression of C/EBPalpha in carcinoma cells inhibits proliferation.
Shim M, Powers KL, Ewing SJ, Zhu S, Smart RC.
Cancer Res. 2005 Feb 1;65(3):861-7.
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CCAAT/enhancer binding protein alpha knock-in mice exhibit early liver glycogen storage and reduced susceptibility to hepatocellular carcinoma.
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Respiratory failure due to differentiation arrest and expansion of alveolar cells following lung-specific loss of the transcription factor C/EBPalpha in mice.
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Mol Cell Biol. 2006 Feb;26(3):1109-23.
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Overexpression of CEBPA resulting from the translocation t(14;19)(q32;q13) of human precursor B acute lymphoblastic leukemia.
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The CCAAT enhancer-binding protein-alpha negatively regulates the transactivation of androgen receptor in prostate cancer cells.
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Mol Endocrinol. 2006 May;20(5):984-95. Epub 2006 Feb 2.
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Reprogramming of committed T cell progenitors to macrophages and dendritic cells by C/EBP alpha and PU.1 transcription factors.
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Immunity. 2006 Nov;25(5):731-44.
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C/EBPalpha is required for lung maturation at birth.
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Development. 2006 Mar;133(6):1155-64. Epub 2006 Feb 8.
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The proline-histidine-rich CDK2/CDK4 interaction region of C/EBPalpha is dispensable for C/EBPalpha-mediated growth regulation in vivo.
Porse BT, Pedersen TA, Hasemann MS, Schuster MB, Kirstetter P, Luedde T, Damgaard I, Kurz E, Schjerling CK, Nerlov C.
Mol Cell Biol. 2006 Feb;26(3):1028-37.
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J Natl Cancer Inst. 2006 Mar 15;98(6):396-406.
PMID 16537832
 
In prostate cancer cells the interaction of C/EBPalpha with Ku70, Ku80, and poly(ADP-ribose) polymerase-1 increases sensitivity to DNA damage.
Yin H, Glass J.
J Biol Chem. 2006 Apr 28;281(17):11496-505. Epub 2006 Feb 20.
PMID 16490787
 
Down regulation of PSA by C/EBPalpha is associated with loss of AR expression and inhibition of PSA promoter activity in the LNCaP cell line.
Yin H, Radomska HS, Tenen DG, Glass J.
BMC Cancer. 2006 Jun 14;6:158.
PMID 16774685
 
Five members of the CEBP transcription factor family are targeted by recurrent IGH translocations in B-cell precursor acute lymphoblastic leukemia (BCP-ALL).
Akasaka T, Balasas T, Russell LJ, Sugimoto KJ, Majid A, Walewska R, Karran EL, Brown DG, Cain K, Harder L, Gesk S, Martin-Subero JI, Atherton MG, Bruggemann M, Calasanz MJ, Davies T, Haas OA, Hagemeijer A, Kempski H, Lessard M, Lillington DM, Moore S, Nguyen-Khac F, Radford-Weiss I, Schoch C, Struski S, Talley P, Welham MJ, Worley H, Strefford JC, Harrison CJ, Siebert R, Dyer MJ.
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Tumor suppressor activity of CCAAT/enhancer binding protein alpha is epigenetically down-regulated in head and neck squamous cell carcinoma.
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Lung Cancer. 2007 Apr;56(1):97-103. Epub 2007 Jan 18.
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Genetic ablation of CCAAT/enhancer binding protein alpha in epidermis reveals its role in suppression of epithelial tumorigenesis.
Loomis KD, Zhu S, Yoon K, Johnson PF, Smart RC.
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Modeling of C/EBPalpha mutant acute myeloid leukemia reveals a common expression signature of committed myeloid leukemia-initiating cells.
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Cancer Cell. 2008 Apr;13(4):299-310. doi: 10.1016/j.ccr.2008.02.008.
PMID 18394553
 
Expression and sub-cellular localization of the CCAAT/enhancer binding protein alpha in relation to postnatal development and malignancy of the prostate.
Zhang J, Wilkinson JE, Gonit M, Keck R, Selman S, Ratnam M.
Prostate. 2008 Aug 1;68(11):1206-14. doi: 10.1002/pros.20779.
PMID 18481268
 
Hematopoietic stem cell expansion precedes the generation of committed myeloid leukemia-initiating cells in C/EBPalpha mutant AML.
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Cancer Cell. 2009 Nov 6;16(5):390-400. doi: 10.1016/j.ccr.2009.09.036.
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A robust and highly efficient immune cell reprogramming system.
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Another pedigree with familial acute myeloid leukemia and germline CEBPA mutation.
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CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.
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C/EBPα expression is downregulated in human nonmelanoma skin cancers and inactivation of C/EBPα confers susceptibility to UVB-induced skin squamous cell carcinomas.
Thompson EA, Zhu S, Hall JR, House JS, Ranjan R, Burr JA, He YY, Owens DM, Smart RC.
J Invest Dermatol. 2011 Jun;131(6):1339-46. doi: 10.1038/jid.2011.31. Epub 2011 Feb 24.
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Tet2 facilitates the derepression of myeloid target genes during CEBPα-induced transdifferentiation of pre-B cells.
Kallin EM, Rodriguez-Ubreva J, Christensen J, Cimmino L, Aifantis I, Helin K, Ballestar E, Graf T.
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C/EBPα induces highly efficient macrophage transdifferentiation of B lymphoma and leukemia cell lines and impairs their tumorigenicity.
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CCAAT/enhancer-binding protein-α suppresses lung tumor development in mice through the p38α MAP kinase pathway.
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PLoS One. 2013;8(2):e57013. doi: 10.1371/journal.pone.0057013. Epub 2013 Feb 20.
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C/EBPα poises B cells for rapid reprogramming into induced pluripotent stem cells.
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Contributor(s)

Written05-2006Lan-Lan Smith
Cancer Research UK Medical Oncology Unit, Charterhouse Square, Barts and the London School of Medicine and Dentistry, London, UK
Updated07-2014Tian V Tian, Thomas Graf
Gene Regulation, Stem Cells and Cancer Programme, Centre for Genomic Regulation (CRG), Dr Aiguader 88, 08003 Barcelona, Spain (TVT, TG); Universitat Pompeu Fabra (UPF), Dr Aiguader 88, 08003 Barcelona, Spain (TVT, TG); Institucio Catalana de Recerca i Estudis Avancats (ICREA), Pg Lluis Companys 23, 08010 Barcelona, Spain (TG)

Citation

This paper should be referenced as such :
Tian TV, Graf T
CEBPA (CCAAT/enhancer binding protein (C/EBP), alpha);
Atlas Genet Cytogenet Oncol Haematol. July 2014
Free journal version : [ pdf ]   [ DOI ]
Atlas Genet Cytogenet Oncol Haematol. July 2014
URL : http://AtlasGeneticsOncology.org/Genes/CEBPAID40050ch19q13.html

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