CREBBP histone acetyltransferase domain mutations predict response to mTOR inhibition in relapsed/refractory follicular lymphoma

Br J Haematol. 2024 Nov;205(5):1804-1809. doi: 10.1111/bjh.19671. Epub 2024 Aug 26.

Abstract

Despite the clinical and molecular heterogeneity of follicular lymphoma (FL), there remains a lack of biomarker-directed therapeutic approaches in routine clinical practice, with the notable exception of the EZH2 inhibitor tazemetostat in EZH2-mutant FL. Here we examined whether gene mutation status predicts response to clinical mTOR inhibitors (mTORi) in FL, by performing targeted mutational profiling of biopsies from 21 relapsed/refractory FL patients treated with mTORi everolimus or temsirolimus within clinical trials. We observed an enrichment of mutations within the catalytic histone acetyltransferase (HAT) domain of CREBBP in mTORi-responders, and describe distinct transcriptional characteristics and co-occurring mutations of FL harbouring these mutations; reinforcing the growing appreciation of CREBBPHAT mutation as a key biological determinant and its promise as a therapeutic biomarker in FL.

Keywords: CREBBP; follicular lymphoma; genetics; mTOR inhibition; mutation analysis.

MeSH terms

  • Aged
  • CREB-Binding Protein* / genetics
  • Everolimus / therapeutic use
  • Female
  • Humans
  • Lymphoma, Follicular* / drug therapy
  • Lymphoma, Follicular* / genetics
  • MTOR Inhibitors* / pharmacology
  • MTOR Inhibitors* / therapeutic use
  • Male
  • Middle Aged
  • Mutation*
  • Protein Domains
  • Recurrence
  • Sirolimus / analogs & derivatives
  • TOR Serine-Threonine Kinases / antagonists & inhibitors

Substances

  • CREB-Binding Protein
  • CREBBP protein, human
  • MTOR protein, human
  • MTOR Inhibitors
  • temsirolimus
  • Everolimus
  • TOR Serine-Threonine Kinases
  • Sirolimus