ArticleCancer science2024
Enhancer-activated RET confers protection against oxidative stress to KMT2A-rearranged acute myeloid leukemia.
Article in Cancer science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Review
- DNMT3B Controls Enhancer-Linked Chromatin and Cell Cycle Networks in Acute Myeloid Leukemia.Cancers · 2026Article
- Transcriptional rewiring by enhancer methylation in CBFA2T3-GLIS2-driven pediatric acute megakaryoblastic leukemia.Genes & diseases · 2026Article
- Epigenetic dysregulation and therapeutic targeting of RET receptor tyrosine kinase in high-risk KMT2A-rearranged acute myeloid leukaemia.British journal of haematology · 2025Article
- Epigenetic regulation of MED12: a key contributor to the leukemic chromatin landscape and transcriptional dysregulation.Epigenetics & chromatin · 2025Article
- Enhancer-activated RET confers protection against oxidative stress to KMT2A-rearranged acute myeloid leukemia.Cancer science · 2024Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Ectopic activation of rearranged during transfection (RET) has been reported to facilitate lineage differentiation and cell proliferation in different cytogenetic subtypes of acute myeloid leukemia (AML). Herein, we demonstrate that RET is significantly (p < 0.01) upregulated in AML subtypes containing rearrangements of the lysine methyltransferase 2A gene (KMT2A), commonly referred to as KMT2A-rearranged (KMT2A-r) AML. Integrating multi-epigenomics data, we show that the KMT2A-MLLT3 fusion induces the development of CCCTC-binding (CTCF)-guided de novo extrusion enhancer loop to upregulate RET expression in KMT2A-r AML. Based on the finding that RET expression is tightly correlated with the selective chromatin remodeler and mediator (MED) proteins, we used a small-molecule inhibitor having dual inhibition against RET and MED12-associated cyclin-dependent kinase 8 (CDK8) in KMT2A-r AML cells. Dual inhibition of RET and CDK8 restricted cell proliferation by producing multimodal oxidative stress responses in treated cells. Our data suggest that epigenetically enhanced RET protects KMT2A-r AML cells from oxidative stresses, which could be exploited as a potential therapeutic strategy.
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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.