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Related Experiment Video

Updated: Jun 9, 2025

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

A Method for Screening and Validation of Resistant Mutations Against Kinase Inhibitors

Published on: December 7, 2014

New ABL1 Kinase Domain Mutations in BCR::ABL1-Positive Acute Lymphoblastic Leukemia.

Zixuan Li¹, Danyue Peng¹, Jun Deng¹

¹Institute of Hematology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Cancer Medicine

|October 23, 2024

Summary

New ABL1 kinase domain (ABL1 KD) mutations are prevalent in BCR::ABL1-positive acute lymphoblastic leukemia (ALL). These mutations impact Tyrosine Kinase Inhibitor (TKI) resistance, necessitating targeted therapies for improved patient outcomes.

Keywords:

ABL1 acute lymphoblastic leukemia mutation tyrosine kinase inhibitors

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Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Next Generation Sequencing for the Detection of Actionable Mutations in Solid and Liquid Tumors

Published on: September 20, 2016

Area of Science:

Hematology
Oncology
Molecular Biology

Background:

Tyrosine Kinase Inhibitors (TKIs) are vital for treating BCR::ABL1-positive leukemias.
ABL1 kinase domain (ABL1 KD) mutations can cause TKI resistance.
ABL1 KD mutations are less studied in BCR::ABL1-positive acute lymphoblastic leukemia (ALL) compared to chronic myeloid leukemia (CML).

Purpose of the Study:

To analyze ABL1 KD mutations in adults with BCR::ABL1-positive ALL.
To investigate the relationship between ABL1 KD mutations and TKI selection.
To identify novel mutations and their clinical implications.

Main Methods:

Next-generation sequencing (NGS) was used to analyze ABL1 KD mutations.
Samples were collected from 97 newly-diagnosed adults with BCR::ABL1-positive ALL.
Mutations were analyzed at pre-therapy, cytogenetic complete remission, and relapse stages.

Main Results:

Novel ABL1 KD mutations (R239G, F401V/L, R516L, K262T) were prevalent before therapy and in remission.
T315I/P and P-loop mutations were more common at relapse.
Novel mutations conferred imatinib resistance but were sensitive to olverembatinib, which improved molecular response.

Conclusions:

New ABL1 KD mutations are common in BCR::ABL1-positive ALL.
These mutations affect TKI efficacy and treatment strategies.
Targeted therapies are crucial for managing TKI-resistant ALL.