ReviewLeukemia2003
New mechanisms of AML1 gene alteration in hematological malignancies.
Review in Leukemia, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 137 citations in OpenAlex.
- Review
- iAMP21 in acute myeloid leukemia is associated with complex karyotype, TP53 mutation and dismal outcome.Modern pathology : an official journal of the United States and Canadian Academy of Pathology, Inc · 2020Article
- Laying the foundation for genomically-based risk assessment in chronic myeloid leukemia.Leukemia · 2019Review
- Tetrasomy 8 Associated with a Poor Prognosis in Acute Monoblastic Leukemia: A Case Report.Cureus · 2019Article
- Thermodynamic investigation of DNA-binding affinity of wild-type and mutant transcription factor RUNX1.PloS one · 2019Article
- Trisomy 21 with t(5; 11) chromosomal translocation as new unfavorable cytogenetic abnormalities in pediatric acute myeloid leukemia type M2: One case report of nine-year follow-up and literature review.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2017Review
- Targeting binding partners of the CBFβ-SMMHC fusion protein for the treatment of inversion 16 acute myeloid leukemia.Oncotarget · 2016Review
- Internal tandem duplication of FLT3 deregulates proliferation and differentiation and confers resistance to the FLT3 inhibitor AC220 by Up-regulating RUNX1 expression in hematopoietic cells.International journal of hematology · 2016Article
- [Acute myelomonocytic leukemia eosinophilic revealed by acute pancreatitis].The Pan African medical journal · 2015Article
- Screening of Transcription Factors Involved in Fetal Hemoglobin Regulation Using Phylogenetic Footprinting.Evolutionary bioinformatics online · 2015Article
- RUNX1 mutation associated with clonal evolution in relapsed pediatric acute myeloid leukemia with t(16;21)(p11;q22).International journal of hematology · 2014Article
- Review
- The RUNX1 transcription factor is expressed in serous epithelial ovarian carcinoma and contributes to cell proliferation, migration and invasion.Cell cycle (Georgetown, Tex.) · 2013Article
- PIBiophysical reviews · 2013Article
- Runt-related transcription factor 1 (RUNX1) stimulates tumor suppressor p53 protein in response to DNA damage through complex formation and acetylation.The Journal of biological chemistry · 2013Article
- Molecular genetics of B-precursor acute lymphoblastic leukemia.The Journal of clinical investigation · 2012Review
- Article
- Activation of Notch signal pathway is associated with a poorer prognosis in acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2011Article
- CD56 antigen expression and hemophagocytosis of leukemic cells in acute myeloid leukemia with t(16;21)(p11;q22).International journal of hematology · 2010Article
- RUNX1 repression-independent mechanisms of leukemogenesis by fusion genes CBFB-MYH11 and AML1-ETO (RUNX1-RUNX1T1).Journal of cellular biochemistry · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human AML1 gene (also named CBFA2 or RUNX1), located in the 21q22 chromosomal band, encodes for one of the two subunits forming a heterodimeric transcription factor, the human core binding factor (CBF). AML1 protein contains a highly evolutionary conserved domain of 128 amino acids called runt domain, responsible for both heterodimerization with the beta subunit of CBF and for DNA binding. AML1 is normally expressed in all hematopoietic lineages and acts to regulate the expression of various genes specific to hematopoiesis playing a pivotal role in myeloid differentiation. AML1 is one of the genes most frequently deregulated in leukemia through different mechanisms including translocation, mutation and amplification. Translocations lead to the formation of fusion genes encoding for chimerical proteins such as AML1-ETO which induces leukemogenesis. Recently, new mechanisms of AML1 deregulation by point mutations or amplification have been reported. To our knowledge, 51 patients (among 805 studied) with AML1 point mutations have been described. Forty of them have acute myeloid leukemia (AML) most often M0 AML. In this subtype of AML, the frequency of AML1 mutation is significantly higher; 21.5% of patients mutated (34/158). Mutations have also been found with lower frequency in other FAB subtype AML (6 cases), in myeloproliferative disorders (6 cases), in myelodysplastic syndrome (3 cases) and rarely in acute lymphoblastic leukemia (1 case). AML1 gene amplification has been found essentially in childhood ALL (12 cases) and more rarely in myeloid malignancies (4 cases). Here, we reviewed all these cases of AML1 point mutations and amplification and focused on the mechanisms of AML1 deregulation induced by these alterations.
Indexed as
Identifiers
What 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.