ArticleBlood2015
Mutational spectrum of myeloid malignancies with inv(3)/t(3;3) reveals a predominant involvement of RAS/RTK signaling pathways.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 102 citations in OpenAlex.
- Phase II Trial of Pembrolizumab after High-Dose Cytarabine in Relapsed/Refractory Acute Myeloid Leukemia.Blood cancer discovery · 2021Trial
- Genomic Classification and Prognosis in Acute Myeloid Leukemia.The New England journal of medicine · 2016Trial
- Defining a Subgroup of Myelodysplastic Syndrome Patients With Very Poor-Risk Cytogenetics Demonstrating a Relatively More Favorable Outcome After Allogeneic Hematopoietic Cell Transplantation.American journal of hematology · 2026Article
- Comparative effectiveness of HMA with venetoclax vs intensive chemotherapy in AML with very high-risk cytogenetics.Blood neoplasia · 2026Article
- Mechanisms of enhancer-driven oncogene activation.International journal of cancer · 2026Review
- A rare cytogenetically crypticFrontiers in oncology · 2026Article
- The oncogenic role of ecotropic viral integration site 1 in hematological malignancies: mechanisms of activation and leukemogenesis.Frontiers in immunology · 2026Review
- Molecular abnormalities and clinical features in adult patients with acute myeloid leukemia in Thailand.Diagnostic pathology · 2025Article
- BRD4 and MYB inhibition overcomes venetoclax resistance in EVI1-rearranged acute myeloid leukemia.Scientific reports · 2025Article
- PRC2-mediated apoptosis evasion is a therapeutic target of MDS/AML harboring inv(3)/t(3;3) and monosomy 7.HemaSphere · 2025Article
- Oncogenic Enhancers in Leukemia.Blood cancer discovery · 2024Review
- Preclinical efficacy of targeting epigenetic mechanisms in AML with 3q26 lesions and EVI1 overexpression.Leukemia · 2024Article
- Article
- Multi-omic analysis of longitudinal acute myeloid leukemia patient samples reveals potential prognostic markers linked to disease progression.Frontiers in genetics · 2024Article
- TET2 lesions enhance the aggressiveness of CEBPA-mutant acute myeloid leukemia by rebalancing GATA2 expression.Nature communications · 2023Article
- Characteristics and clinical outcomes of patients with acute myeloid leukemia with inv(3)(q21q26.2) or t(3;3)(q21;q26.2).Haematologica · 2023Article
- 3q26.2/Cancers · 2023Article
- Analysis of the clinical characteristics and prognosis of adultOpen medicine (Warsaw, Poland) · 2023Article
- Uncovering novel mutational signatures byCell genomics · 2022Article
- Article
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13 authors at 3 institutions in 2 countries.
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Abstract
Myeloid malignancies bearing chromosomal inv(3)/t(3;3) abnormalities are among the most therapy-resistant leukemias. Deregulated expression of EVI1 is the molecular hallmark of this disease; however, the genome-wide spectrum of cooperating mutations in this disease subset has not been systematically elucidated. Here, we show that 98% of inv(3)/t(3;3) myeloid malignancies harbor mutations in genes activating RAS/receptor tyrosine kinase (RTK) signaling pathways. In addition, hemizygous mutations in GATA2, as well as heterozygous alterations in RUNX1, SF3B1, and genes encoding epigenetic modifiers, frequently co-occur with the inv(3)/t(3;3) aberration. Notably, neither mutational patterns nor gene expression profiles differ across inv(3)/t(3;3) acute myeloid leukemia, chronic myeloid leukemia, and myelodysplastic syndrome cases, suggesting recognition of inv(3)/t(3;3) myeloid malignancies as a single disease entity irrespective of blast count. The high incidence of activating RAS/RTK signaling mutations may provide a target for a rational treatment strategy in this high-risk patient group.
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