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GENE:

CEBPA (CCAAT Enhancer Binding Protein Alpha)

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Other names: CEBPA, CCAAT Enhancer Binding Protein Alpha, CCAAT/Enhancer Binding Protein (C/EBP), Alpha, CCAAT/Enhancer-Binding Protein Alpha, CEBP, CCAAT/Enhancer Binding Protein Alpha, C/EBP-Alpha, C/EBP Alpha
2d
Validation and Refinement of the European LeukemiaNet 2022 Genetic Risk Stratification of AML. (PubMed, JCO Glob Oncol)
We conclude that ELN22 is prognostically valid in intensively treated younger patients with AML. Incorporation of WT1 mutation status, triple-mutated NPM1, and LSC burden may improve risk stratification, particularly within the heterogeneous intermediate-risk category.
Retrospective data • Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • DNMT3A (DNA methyltransferase 1) • WT1 (WT1 Transcription Factor) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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FLT3-ITD mutation • NPM1 mutation
6d
Pan-cancer multi-omics profiling of OAS3 reveals its immunological and prognostic associations across human cancers. (PubMed, PeerJ)
Functional validation through RNA interference demonstrated that OAS3 knockdown significantly induced apoptosis in THP-1 cells. This study demonstrates that OAS3 acts as a pivotal modulator in the complex network of cancer progression, highlighting its dual role in both tumorigenesis and immune response regulation.
Journal • Tumor mutational burden • Pan tumor
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TMB (Tumor Mutational Burden) • FLT3 (Fms-related tyrosine kinase 3) • NRAS (Neuroblastoma RAS viral oncogene homolog) • HRD (Homologous Recombination Deficiency) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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HRD
11d
M6A demethylase FTO in leukemia: Function, molecular mechanisms, and therapeutic implications. (PubMed, Pathol Res Pract)
Preclinical studies show that genetic depletion, small-molecule inhibition, or targeted degradation of FTO increases m6A on key targets, suppresses leukemic growth, and can sensitize cells to standard therapies, supporting FTO as a druggable epitranscriptomic vulnerability. This review summarizes FTO structure and function, highlights subtype-specific mechanisms in AML and ALL, and discusses emerging therapeutic strategies and translational challenges.
Review • Journal
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CEBPA (CCAAT Enhancer Binding Protein Alpha) • IRF8 (Interferon Regulatory Factor 8) • FTO (Alpha-Ketoglutarate-Dependent Dioxygenase FTO)
14d
Single-cell RNA sequencing unveils CCDC86-driven immune modulation and antigen-presenting cell dynamics in head and neck squamous cell carcinoma. (PubMed, Discov Oncol)
CCDC86 acts as a key regulator of immune communication in HNSCC, orchestrating APC-T cell interactions and shaping an immunoregulatory niche. By linking antigen presentation with checkpoint signaling, CCDC86 contributes to immune evasion while maintaining local immune activation. These findings highlight CCDC86 as a promising prognostic biomarker and potential immunotherapeutic target in HNSCC.
Journal • PD(L)-1 Biomarker • IO biomarker
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PD-1 (Programmed cell death 1) • CCDC6 (Coiled-Coil Domain Containing 6) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • SPI1 (Spi-1 Proto-Oncogene) • CCDC86 (Coiled-Coil Domain Containing 86) • CD86 (CD86 Molecule)
16d
LEAH: Cohort Evaluation of Body Fluids Early Detection of Cancer in High-risk Individuals (clinicaltrials.gov)
P=N/A, N=5909, Not yet recruiting, Gustave Roussy, Cancer Campus, Grand Paris | Initiation date: Jun 2025 --> Feb 2026
Trial initiation date
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TP53 (Tumor protein P53) • BRCA1 (Breast cancer 1, early onset) • BRCA2 (Breast cancer 2, early onset) • PTEN (Phosphatase and tensin homolog) • STK11 (Serine/threonine kinase 11) • CDKN2A (Cyclin Dependent Kinase Inhibitor 2A) • POLE (DNA Polymerase Epsilon) • RUNX1 (RUNX Family Transcription Factor 1) • BAP1 (BRCA1 Associated Protein 1) • ETV6 (ETS Variant Transcription Factor 6) • MLH1 (MutL homolog 1) • CDK4 (Cyclin-dependent kinase 4) • MSH2 (MutS Homolog 2) • SMAD4 (SMAD family member 4) • CDH1 (Cadherin 1) • SDHB (Succinate Dehydrogenase Complex Iron Sulfur Subunit B) • POLD1 (DNA Polymerase Delta 1) • RAD51C (RAD51 paralog C) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • RAD51D (RAD51 paralog D) • DDX41 (DEAD-Box Helicase 41) • GATA2 (GATA Binding Protein 2) • DICER1 (Dicer 1 Ribonuclease III) • FLCN (Folliculin) • PRSS1 (Serine Protease 1) • SDHD (Succinate Dehydrogenase Complex Subunit D) • TXNIP (Thioredoxin Interacting Protein) • ANKRD26 (Ankyrin Repeat Domain Containing 26) • BMPR1A (Bone Morphogenetic Protein Receptor Type 1A) • HOXB13 (Homeobox B13)
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TP53 mutation • PTEN deletion
20d
Identification of cellular hierarchy in paediatric acute myeloid leukaemia: The Japan Children's Cancer Group trial (JCCG AML-12). (PubMed, Br J Haematol)
LSPC-Cycle, FLT3-ITD and NUP98::KDM5A were considered independent prognostic factors in multivariate analysis. Findings indicate the prognostic relevance of cellular hierarchy and the importance of integrating hierarchy-specific molecular profiles for improved risk stratification and treatment formulation.
Journal
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FLT3 (Fms-related tyrosine kinase 3) • NPM1 (Nucleophosmin 1) • RUNX1 (RUNX Family Transcription Factor 1) • KMT2A (Lysine Methyltransferase 2A) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • NUP98 (Nucleoporin 98 And 96 Precursor 2) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • MECOM (MDS1 And EVI1 Complex Locus) • NSD1 (Nuclear Receptor Binding SET Domain Protein 1) • NUP214 (Nucleoporin 214) • CBFA2T3 (CBFA2/RUNX1 Partner Transcriptional Co-Repressor 3) • GATA1 (GATA Binding Protein 1) • GLIS2 (GLIS Family Zinc Finger 2) • KDM5A (Lysine Demethylase 5A) • MLLT3 (MLLT3 Super Elongation Complex Subunit)
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FLT3-ITD mutation
22d
Augmenting Nrf2 signaling pathway promotes adipocyte differentiation from human embryonic stem cells. (PubMed, Exp Cell Res)
Notably, we identified PAX3 as a transcriptional target associated with Nrf2 activation, suggesting a potential link between Nrf2 signaling and adipogenic regulation. Together, these findings reveal a previously underappreciated role for Nrf2 in human adipogenesis.
Journal
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KEAP1 (Kelch Like ECH Associated Protein 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha) • PPARG (Peroxisome Proliferator Activated Receptor Gamma) • FABP4 (Fatty Acid Binding Protein 4) • PAX3 (Paired Box 3)
26d
bZIP-Domain Variant Allele Frequency Helps to Refine Risk Stratification in CEBPA-Mutated AML. (PubMed, Biomedicines)
Multivariate analysis confirmed high bZIP-domain VAF and DNMT3A mutation as independent risk factors. Our results confirm that the bZIP-domain VAF of CEBPA mutations is a more effective predictor of relapse than the maximum VAF, offering a valuable tool for the early identification of patients at high risk of relapse.
Journal
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DNMT3A (DNA methyltransferase 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
26d
Moving Beyond Somatic Alterations: Uncovering the Germline Basis of Myeloid Malignancies. (PubMed, Cancers (Basel))
Identification of these germline mutations is critical as MNs with germline predisposition dictate specific therapeutic strategies-particularly for hematopoietic stem cell transplantation (HSCT)-and require genetic counseling and surveillance for at-risk relatives. Accurate diagnosis often requires non-hematopoietic germline DNA testing, which provides important biological insights into the development of different myeloid neoplasms and directs personalized patient care.
Review • Journal
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RUNX1 (RUNX Family Transcription Factor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
27d
The C/EBPα-(PU.1-LOUP) regulatory circuit regulates monocyte/macrophage development and immune functions. (PubMed, Blood)
Collectively, our findings reveal that PU.1 and the enhancer RNA LOUP form a previously unrecognized feed-forward loop, induced by C/EBPα, that drives their mutual expression and establishes a regulatory circuit. This circuit programs monocyte to macrophage differentiation as well as innate immune function, providing important implications for inflammatory diseases and myeloid malignancies.
Journal
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CEBPA (CCAAT Enhancer Binding Protein Alpha)
27d
Age-dependent clinical, molecular, and prognostic differences in patients with AML: a retrospective study. (PubMed, Hematology)
This study revealed that patients aged ≥50 years displayed more complex genetic aberration profiles and experienced significantly poorer prognoses compared to their younger counterparts. These findings provided novel insights for optimizing treatment strategies for middle-aged and elderly AML patients in the Chinese population.
Retrospective data • Journal
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TP53 (Tumor protein P53) • NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • IDH2 (Isocitrate Dehydrogenase (NADP(+)) 2) • DNMT3A (DNA methyltransferase 1) • RUNX1 (RUNX Family Transcription Factor 1) • WT1 (WT1 Transcription Factor) • RUNX1T1 (RUNX1 Partner Transcriptional Co-Repressor 1) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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TP53 mutation • KIT mutation • Chr del(5q) • CBFB-MYH11 fusion
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Venclexta (venetoclax)
1m
KIT Mutant/Core binding factor-negative acute myeloid leukemia might be a complex subgroup with dismal prognosis: a single-center retrospective analysis. (PubMed, Ann Hematol)
Patients with KIT exon 17 mutations tended to harbor an inferior EFS and OS. In conclusion, KIT mutant/CBF-neg AML was a complex subgroup with dismal prognosis and NIT might bring benefits for those patients.
Retrospective data • Journal
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NRAS (Neuroblastoma RAS viral oncogene homolog) • KIT (KIT proto-oncogene, receptor tyrosine kinase) • WT1 (WT1 Transcription Factor) • CEBPA (CCAAT Enhancer Binding Protein Alpha)
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Venclexta (venetoclax)