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Related Experiment Video

Updated: Jan 19, 2026

Bioluminescence-Based Tumor Quantification Method for Monitoring Tumor Progression and Treatment Effects in Mouse Lymphoma Models

Bioluminescence-Based Tumor Quantification Method for Monitoring Tumor Progression and Treatment Effects in Mouse Lymphoma Models

Published on: July 7, 2016

Scoring a HAT-Trick against Lymphoma.

Oliver Bannard¹

¹MRC Human Immunology Unit, Nuffield Department of Medicine, Weatherall Institute of Molecular Medicine, University of Oxford, OX3 9DS, UK.

|September 19, 2019

Summary

This summary is machine-generated.

Mutations in histone acetyltransferase genes CREBBP and EP300 are common in lymphomas. Inactivating one gene may make lymphomas vulnerable to drugs targeting the other, offering new therapeutic strategies.

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Area of Science:

Epigenetics
Cancer Biology
Lymphoma Pathogenesis

Background:

Histone acetyltransferases (HATs) CREBBP and EP300 are frequently mutated in germinal-center-derived B cell lymphomas.
Inactivation of these HATs is implicated in the development of lymphomas.

Purpose of the Study:

To investigate the functional consequences of somatic inactivation of CREBBP or EP300 in B cell lymphomas.
To determine if lymphomas with inactivated HATs exhibit unique sensitivities to specific therapeutic agents.

Main Methods:

Utilizing mouse models and cell lines representing germinal-center-derived B cell lymphomas.
Assessing the impact of genetic inactivation of CREBBP and EP300 on lymphoma cell growth and survival.
Evaluating the sensitivity of these lymphomas to antagonists targeting the remaining functional HAT.

Main Results:

Somatic inactivation of either CREBBP or EP300 leads to distinct epigenetic landscapes in lymphomas.
Lymphomas with inactivated CREBBP show increased sensitivity to EP300 antagonists, and vice versa.
This reciprocal sensitivity highlights a dependency on the remaining histone acetyltransferase activity.

Conclusions:

The study reveals a novel therapeutic vulnerability in lymphomas with mutations in HAT genes.
Targeting the remaining functional histone acetyltransferase (CREBBP or EP300) presents a promising strategy for treating these lymphomas.
These findings open new avenues for developing targeted therapies in B cell malignancies.