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Cracking the histone code for prostate cancer therapy

In this study, we uncover the critical role of p300/CBP-mediated histone H2B N terminus multisite lysine acetylation (H2BNTac) in defining oncogenic enhanceosomes in prostate cancer. Degradation of p300/CBP rapidly disables H2BNTac-marked oncogenic enhancers and represents a promising therapeutic strategy for enhancer-driven malignancies, including prostate cancer.

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Fig. 1: Targeting p300/CBP to disrupt H2BNTac-marked hyperactive AR enhancers in prostate cancer.

References

  1. Dai, C., Dehm, S. M. & Sharifi, N. Targeting the androgen signalling axis in prostate cancer. J. Clin. Oncol. 41, 4267–4278 (2023). A review article discussing the role of AR in prostate cancer.

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This is a summary of: Luo, J. et al. Targeting histone H2B acetylated enhanceosomes via p300/CBP degradation in prostate cancer. Nat. Genet. https://doi.org/10.1038/s41588-025-02336-6 (2025).

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Cracking the histone code for prostate cancer therapy. Nat Genet 57, 2357–2358 (2025). https://doi.org/10.1038/s41588-025-02354-4

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