What question did this study set out to answer?

This review focuses on the genetic mutations in EP300 and CREBBP, aiming to understand their frequency and impacts on cancer progression.

May 3, 2026

Genetic mutations and inhibitors of p300 and CBP.

Puntos clave

This review focuses on the genetic mutations in EP300 and CREBBP, aiming to understand their frequency and impacts on cancer progression.
Reviewed existing literature on mutations in EP300 and CREBBP.
Analyzed the relationship between these mutations and their influence on the efficacy of pharmacological agents.
Discussed the implications of dual inhibition strategies targeting HAT and bromodomain.
Identified significant frequencies of mutations in EP300 and CREBBP that are relevant for cancer.
Highlighted the potential for mutations to affect the outcomes of pharmacological agents targeting p300 and CBP.
Emphasized the role of these genetic alterations in altering the effectiveness of anticancer therapies.

Resumen

The p300 and CBP highly homologous acetyltransferases, are linked to malignant transformation and cancer progression. The longstanding attempts to find small molecules to block these enzymes in cancer have led to the identification of two inhibitor classes that target the acetyltransferase catalytic domain (HAT) or acetylated protein recognizing bromodomain (BRD), and related pharmacological agents such as dual BRD/BET inhibitors and PROTAC degraders. Although p300 and CBP behave as a synthetic lethal pair and their inhibition emerged promising in anticancer in vitro and in vivo studies, clinical approval has lagged. In this review we examine mutations in EP300 and CREBBP and describe their frequency and potential impacts. Particular attention is paid to genetic alterations in HAT and bromodomain simultaneously in EP300 and CREBBP, and we discuss how these mutations may influence efficacy of pharmacological agents.

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