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Targeted Cancer Therapies

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Related Experiment Video

Updated: Mar 2, 2026

Genome Engineering of Primary Human B Cells Using CRISPR/Cas9

Genome Engineering of Primary Human B Cells Using CRISPR/Cas9

Published on: November 3, 2020

BCR::ABL1-Induced Enhancer Reprogramming Uncovers Hypersensitivity of Ph+B-ALL Cells to Enhancer-Targeting Drugs.

Han Leng Ng¹, Trudy Lee Glaser¹, Jintao Zhu¹

¹Centre for Haematology, Department of Immunology and Inflammation, Faculty of Medicine, Imperial College London, London, UK.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|March 1, 2026

Summary

Philadelphia chromosome-positive B-lineage acute lymphoblastic leukemia (B-ALL) relies on enhancer reprogramming for malignant transformation. Enhancer-targeting drugs show promise as a new therapy, especially for relapsed cases.

Keywords:

BCR::ABL1 CBP/P300 inhibitors Ph+B‐ALL enhancer reprogramming leukemia

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Area of Science:

Oncology
Molecular Biology
Genomics

Background:

Cancer pathogenesis involves genomic lesions and transcriptional dysregulation.
Enhancer deregulation is a known driver in some cancers, leading to targeted therapies.
The role of enhancers in Philadelphia chromosome-positive B-lineage acute lymphoblastic leukemia (Ph+ B-ALL), driven by BCR::ABL1, remains unclear.

Purpose of the Study:

To investigate enhancer reprogramming in Ph+ B-ALL.
To determine if Ph+ B-ALL is sensitive to enhancer-targeting therapies.
To explore enhancer-targeting as an adjunct to existing treatments.

Main Methods:

Analysis of enhancer signatures in Ph+ B-ALL.
Investigating BCR::ABL1-mediated enhancer activation mechanisms.
Assessing sensitivity of Ph+ B-ALL cells to enhancer inhibitors.
Evaluating combination therapy with BCR::ABL1 kinase inhibitors.

Main Results:

BCR::ABL1 drives malignant transformation through enhancer reprogramming, distinct from TF-related lesions.
Enhancer signatures effectively differentiate Ph+ B-ALL from other leukemias.
BCR::ABL1 activates enhancers via its kinase activity and STAT5, ETV5, and MYC.
Ph+ B-ALL cells exhibit hypersensitivity to enhancer inhibition and enhancer-targeting drugs.
Combination therapy enhances efficacy, particularly in IKZF1^PLUS patients.

Conclusions:

Enhancer reprogramming is a critical mechanism in BCR::ABL1-driven Ph+ B-ALL.
Enhancer-targeting agents represent a promising therapeutic strategy for Ph+ B-ALL.
Combination of enhancer-targeting and kinase inhibitors may overcome treatment resistance, especially in IKZF1^PLUS cases.