ArticleLeukemia2005
Mutations of genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal transduction pathway in therapy-related myelodysplasia and acute myeloid leukemia.
Article in Leukemia, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed.
- Phase II Trial of MEK Inhibitor Binimetinib (MEK162) in RAS-mutant Acute Myeloid Leukemia.Clinical lymphoma, myeloma & leukemia · 2019Trial
- Trial
- BRAF Mutations in Myeloid Neoplasms: Prevalence, Co-Mutation Landscape, and Clinical Outcomes-A Comprehensive Review.Biomedicines · 2026Review
- Therapy-Related Myeloid Neoplasms: Complex Interactions among Cytotoxic Therapies, Genetic Factors, and Aberrant Microenvironment.Blood cancer discovery · 2024Review
- Review
- Article
- Vemurafenib induces senescence in acute myeloid leukemia and myelodysplastic syndrome by activating the HIPPO signaling pathway: implications for potential targeted therapy.Biology direct · 2024Article
- A gain-of-function p53 mutant synergizes with oncogenic NRAS to promote acute myeloid leukemia in mice.The Journal of clinical investigation · 2023Article
- CPX-351 and allogeneic stem cell transplant for a therapy-related acute myeloid leukemia that developed after treatment of acute promyelocytic leukemia: a case report and review of the literature.Frontiers in oncology · 2023Article
- A somatic mutation in moesin drives progression into acute myeloid leukemia.Science advances · 2022Article
- The genetics of myelodysplastic syndromes and the opportunities for tailored treatments.Frontiers in oncology · 2022Review
- Genetic Pathway in the Pathogenesis of Therapy-Related Myeloid Neoplasms: A Literature Review.Oncology and therapy · 2020Review
- Review
- Binimetinib, a novel MEK1/2 inhibitor, exerts anti-leukemic effects under inactive status of PI3Kinase/Akt pathway.International journal of hematology · 2019Article
- Pre-clinical evaluation of Minnelide as a therapy for acute myeloid leukemia.Journal of translational medicine · 2019Article
- Ocular infiltration as initial presentation of acute monocytic leukaemia transformed from chronic myelomonocytic leukaemia associated withBMJ case reports · 2019Article
- JNK1 as a signaling node in VDR-BRAF induction of cell death in AML.The Journal of steroid biochemistry and molecular biology · 2018Article
- Development of Secondary Acute Myeloid Leukemia in a Pediatric Patient Concurrently Receiving Primary Therapy for Ewing Sarcoma.Journal of pediatric hematology/oncology · 2017Article
- RKTG overexpression inhibits proliferation and induces apoptosis of human leukemia cells via suppression of the ERK and PI3K/AKT signaling pathways.Oncology letters · 2017Article
- Therapy-related myeloid neoplasms: does knowing the origin help to guide treatment?Hematology. American Society of Hematology. Education Program · 2016Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors.
Funding
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Abstract
Mutations of the FLT3, c-KIT, c-FMS, KRAS, NRAS, BRAF and CEBPA genes in the receptor tyrosine kinase (RTK)/RAS-BRAF signal-transduction pathway are frequent in acute myeloid leukemia (AML). We examined 140 patients with therapy-related myelodysplasia or AML (t-MDS/t-AML) for point mutations of these seven genes. In all, 11 FLT3, two c-KIT, seven KRAS, eight NRAS and three BRAF mutations were identified in 29 patients (21%). All but one patient with a FLT3 mutation presented with t-AML (P=0.0002). Furthermore, FLT3 mutations were significantly associated with previous radiotherapy without chemotherapy (P=0.03), and with a normal karyotype (P=0.004), but inversely associated with previous therapy with alkylating agents (P=0.003) and with -7/7q- (P=0.001). RAS mutations were associated with AML1 point mutations (P=0.046) and with progression from t-MDS to t-AML (P=0.008). Noteworthy, all three patients with BRAF mutations presented as t-AML of M5 subtype with t(9;11)(p22;q23) and MLL-rearrangement (P=0.01). In t-AML RAS/BRAF mutations were significantly associated with a very short survival (P=0.017). Half of the patients with a mutation in the RTK/RAS-BRAF signal-transduction pathway (denoted 'class-I' mutations) simultaneously disclosed mutation of a hematopoietic transcription factor (denoted 'class-II' mutations) (P=0.046) suggesting their cooperation in leukemogenesis.
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