ArticleCell reports. Medicine2025
Combined inhibition of KAT6A/B and Menin reverses estrogen receptor-driven gene expression programs in breast cancer.
Article in Cell reports. Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- KAT6A-inhibitor co-crystal structures: tackling a challenging crystallization target via two alternative approaches.Acta crystallographica. Section D, Structural biology · 2026Article
- Menin inhibitors as a treatment for acute leukemia: from bench to the clinic.Blood neoplasia · 2026Review
- Spatial transcriptome revealed associated biomarkers for endocrine therapy response in HR-positive/HER2-negative early breast cancer.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2026Article
- The roles of the acetyltransferase domains of the chromatin regulators KAT6A and KAT6B in vivo.Development (Cambridge, England) · 2026Article
- A Perturb-seq map of a differentiation hub reveals synergistic vulnerabilities in KMT2A-rearranged acute myeloid leukemia.Leukemia · 2026Article
- LncRNA FAM30A as a potential biomarker associated with periodontitis and its role in inflammatory responses and osteogenesis.BMC oral health · 2026Article
- Synthetic lethality in cancer therapy: Mechanisms, models and clinical translation for overcoming therapeutic resistance.Clinical and translational medicine · 2026Review
- Lysine Acetyltransferase 6 in Health and Disease.MedComm · 2025Review
- Co-targeting menin and LSD1 dismantles oncogenic programs and restores differentiation in MLL-rearranged AML.bioRxiv : the preprint server for biology · 2025Article
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Authors and funding
13 authors.
Funding
Abstract
KAT6A is a histone acetyltransferase that is emerging as a therapeutic target in cancer, including estrogen receptor-positive (ER+) breast cancer. Here, we perform CRISPR screens to identify the chromatin adaptor Menin as a regulator of KAT6A/B inhibitor response. Co-treatment with KAT6A/B and Menin inhibitors has synergistic anti-proliferative effects in ER+, but not ER-, breast cancer lines. Our data reveal that KAT6A and Menin-KMT2A cooperatively regulate ER-driven gene expression via direct effects on ESR1 expression and co-localization at ER target genes. Combined KAT6A/B and Menin inhibition displaces KAT6A and Menin-KMT2A from promoters of ER-driven genes leading to selective RNA polymerase II chromatin loss at these loci. Importantly, combined KAT6A/B and Menin inhibition is effective in ER+ patient-derived xenograft models and in multiple models of endocrine resistance. KAT6A/B and Menin inhibitors are currently in clinical trials and have shown manageable toxicity profiles, underscoring the potential therapeutic relevance for ER+ breast cancer.
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