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Updated: May 4, 2026
09:49
Oncogenic Gene Fusion Detection Using Anchored Multiplex Polymerase Chain Reaction Followed by Next Generation Sequencing
Published on: July 5, 2019
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Genetic events other than BCR-ABL1.
1Comprehensive Cancer Center, The Ohio State University, Columbus, OH, USA, paolo.neviani@osumc.edu.
Current Hematologic Malignancy Reports
|January 11, 2014
Summary
Chronic myeloid leukemia (CML) is caused by the BCR-ABL1 oncoprotein. Understanding secondary genetic events in CML is crucial for developing new therapies against resistance.
Area of Science:
- Hematology
- Oncology
- Genetics
Background:
- The BCR-ABL1 oncoprotein, resulting from the t(9;22) translocation and Philadelphia chromosome formation, drives chronic myeloid leukemia (CML).
- CML progression involves clonal evolution and accumulation of secondary genetic alterations, leading to genomic instability.
- Understanding these genetic events is key to addressing blastic transformation and resistance to tyrosine kinase inhibitors.
Purpose of the Study:
- To investigate the frequency and nature of genomic events in CML at diagnosis and during disease progression.
- To identify novel therapeutic targets beyond BCR-ABL1 for resistant or intolerant CML patients.
Main Methods:
- Analysis of genomic alterations in CML patient samples at various disease stages.
- Investigation of BCR-ABL1-dependent and independent pathways sustaining leukemic cell survival.
Main Results:
- Genomic instability contributes to CML evolution and blastic transformation.
- Secondary genetic events play a significant role in CML pathogenesis and treatment resistance.
Conclusions:
- Dissecting genomic events in CML provides insights into disease mechanisms.
- Identifying alternative targets is essential for developing new therapies for CML patients resistant to current treatments.
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