ArticleProceedings of the National Academy of Sciences of the United States of America2001
AML1-ETO expression is directly involved in the development of acute myeloid leukemia in the presence of additional mutations.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 189 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
189 citing papers in PubMed, 430 citations in OpenAlex.
- Adding dasatinib to intensive treatment in core-binding factor acute myeloid leukemia-results of the AMLSG 11-08 trial.Leukemia · 2018Trial
- DHX15 affects AML1-ETO9a splicing together with HNRNPL, RBM33 in AML1-ETO-positive acute myeloid leukaemia.British journal of haematology · 2026Article
- Monitoring of measurable residual disease by next-generation sequencing in patients with acute myeloid leukaemia.British journal of haematology · 2025Article
- PredictingiScience · 2025Article
- Multiplex gene editing models of del(7q) reveal combinedBlood neoplasia · 2025Article
- Article
- Mutational cooperativity of RUNX1::RUNX1T1 isoform 9a and oncogenic NRAS in zebrafish myeloid leukaemia.Biology open · 2024Article
- Review
- Review
- [The study of clinical characteristics and prognosis of RUNX1-RUNX1T1 positive acute myeloid leukemia based on next-generation sequencing].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- CSF3R T618I Collaborates With RUNX1-RUNX1T1 to Expand Hematopoietic Progenitors and Sensitizes to GLI Inhibition.HemaSphere · 2023Article
- Article
- Children's Oncology Group's 2023 blueprint for research: Myeloid neoplasms.Pediatric blood & cancer · 2023Article
- Childhood hematopoietic stem cells constitute the permissive window for RUNX1-ETO leukemogenesis.International journal of hematology · 2023Review
- [Establishment of leukemia cell model with inducible AML1-ETO expression and its effect on fatty acid metabolism in leukemia cells].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- Review
- Repurposing cabozantinib with therapeutic potential in KIT-driven t(8;21) acute myeloid leukaemias.Cancer gene therapy · 2022Article
- Murine Models of Acute Myeloid Leukemia.Frontiers in oncology · 2022Review
- The Ups and Downs of STAT Inhibition in Acute Myeloid Leukemia.Biomedicines · 2021Review
- Profiling of somatic mutations and fusion genes in acute myeloid leukemia patients with FLT3-ITD or FLT3-TKD mutation at diagnosis reveals distinct evolutionary patterns.Experimental hematology & oncology · 2021Article
129 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
The t(8;21) is one of the most frequent chromosomal abnormalities associated with acute myeloid leukemia (AML). The translocation, which involves the AML1 gene on chromosome 21 and the ETO gene on chromosome 8, generates an AML1-ETO fusion transcription factor. To examine the effect of the AML1-ETO fusion protein on leukemogenesis, we made transgenic mice in which expression of AML1-ETO is under the control of the human MRP8 promoter (hMRP8-AML1-ETO). AML1-ETO is specifically expressed in myeloid cells, including common myeloid progenitors of hMRP8-AML1-ETO transgenic mice. The transgenic mice were healthy during their life spans, suggesting that AML1-ETO alone is not sufficient for leukemogenesis. However, after treatment of newborn hMRP8-AML1-ETO transgenic mice and their wild-type littermates with a strong DNA-alkylating mutagen, N-ethyl-N-nitrosourea, 55% of transgenic mice developed AML and the other 45% of transgenic mice and all of the wild-type littermates developed acute T lymphoblastic leukemia. Our results provide direct evidence that AML1-ETO is critical for causing myeloid leukemia, but one or more additional mutations are required for leukemogenesis. The hMRP8-AML1-ETO-transgenic mice provide an excellent model that can be used to isolate additional genetic events and to further understand the molecular pathogenesis of AML1-ETO-related leukemia.
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.