ArticleCancer gene therapy2020
Companion gene mutations and their clinical significance in AML with double mutant CEBPA.
Article in Cancer gene therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed.
- More precise risk stratification for de novo acute myeloid leukemia with double-mutation CEBPA.Therapeutic advances in hematology · 2026Article
- CEBPA bZIP in-frame mutations in acute myeloid leukemia: prognostic and therapeutic implications.Blood cancer journal · 2024Article
- Germline predisposition to myeloid neoplasms: Characteristics and management of high versus variable penetrance disorders.Best practice & research. Clinical haematology · 2024Review
- Article
- Article
- Sporadic and Familial Acute Myeloid Leukemia with CEBPA Mutations.Current hematologic malignancy reports · 2023Review
- Hereditary acute myeloid leukemia associated with C-terminal CEBPA germline variants.Familial cancer · 2023Review
- Acute Myeloid Leukemia WithFrontiers in oncology · 2022Review
- Mutational Landscape ofFrontiers in pediatrics · 2022Article
- Risk Stratification of Cytogenetically Normal Acute Myeloid Leukemia With BiallelicFrontiers in oncology · 2021Article
- CCAAT enhancer binding protein alpha (CEBPA) biallelic acute myeloid leukaemia: cooperating lesions, molecular mechanisms and clinical relevance.British journal of haematology · 2020Review
- Secondary leukemia in patients with germline transcription factor mutations (RUNX1, GATA2, CEBPA).Blood · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute myeloid leukemia (AML) with double mutant CEBPA (CEBPAdm) is generally associated with favorable prognosis, but the heterogeneity still blatant and needs further exploration. We aimed to comprehensively analyze the companion genetic abnormalities and their clinical significance in AML patients with CEBPAdm. By performed targeted amplicon sequencing of 58 genes in specimens at the time of initial diagnosis of 609 AML patients, we identified 76 cases (12.5%) were CEBPAdm, and 88.2% of them also carry other gene mutations. There were more additional gene mutations, especially more epigenetic modifiers gene mutations in CEBPAsm than CEBPAdm cases, while GATA2, CSF3R, JAK3, and KIT mutations were exclusively betide in CEBPAdm but not CEBPAsm. Mutations of tyrosine kinase genes confer to adverse prognostic in karyotype normal CEBPAdm AML and provide potential therapeutic targets. The incidence of germline CEBPA mutation in CEBPAdm cases was 5.3% (4/76), including one C-terminal mutation. Deciphering the mutation spectrum of CEBPAdm AML could facilitate an in-depth understanding of the pathogenesis and refine the prognostic classification of this disease entity.
Indexed as
Identifiers
31477806What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.