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Key clinical point: Presence of non-breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) mutations in patients with chronic myeloid leukemia (CML) was not associated with clinical outcomes.
Major finding: Non-BCR-ABL1 mutations were observed in 18% of patients with CML at diagnosis and were mostly cleared with TKI therapy, indicating an origin in the Philadelphia chromosome-positive clone. However, no difference was observed in overall survival, progression-free survival, failure-free survival, and adverse events between patients with vs without non-BCR-ABL1 mutations.
Study details: Findings are from next-generation sequencing analysis of BCR-ABL1 kinase domain and 18 myeloid neoplasm-associated genes in 49 patients with de novo chronic phase-CML and 6 healthy controls.
Disclosures: This study was supported by grants from the Ministry of Health of the Czech Republic, the Ministry of Education, and Bristol-Myers Squibb. D Zackova and J Mayer reported ties with various pharmaceutical companies including Bristol-Myers Squibb. Other authors declared no competing interests.
Source: Romzova M et al. Br J Haematol. 2021 Jul 1. doi: 10.1111/bjh.17659.
Key clinical point: Presence of non-breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) mutations in patients with chronic myeloid leukemia (CML) was not associated with clinical outcomes.
Major finding: Non-BCR-ABL1 mutations were observed in 18% of patients with CML at diagnosis and were mostly cleared with TKI therapy, indicating an origin in the Philadelphia chromosome-positive clone. However, no difference was observed in overall survival, progression-free survival, failure-free survival, and adverse events between patients with vs without non-BCR-ABL1 mutations.
Study details: Findings are from next-generation sequencing analysis of BCR-ABL1 kinase domain and 18 myeloid neoplasm-associated genes in 49 patients with de novo chronic phase-CML and 6 healthy controls.
Disclosures: This study was supported by grants from the Ministry of Health of the Czech Republic, the Ministry of Education, and Bristol-Myers Squibb. D Zackova and J Mayer reported ties with various pharmaceutical companies including Bristol-Myers Squibb. Other authors declared no competing interests.
Source: Romzova M et al. Br J Haematol. 2021 Jul 1. doi: 10.1111/bjh.17659.
Key clinical point: Presence of non-breakpoint cluster region-Abelson murine leukemia viral oncogene homolog 1 (BCR-ABL1) mutations in patients with chronic myeloid leukemia (CML) was not associated with clinical outcomes.
Major finding: Non-BCR-ABL1 mutations were observed in 18% of patients with CML at diagnosis and were mostly cleared with TKI therapy, indicating an origin in the Philadelphia chromosome-positive clone. However, no difference was observed in overall survival, progression-free survival, failure-free survival, and adverse events between patients with vs without non-BCR-ABL1 mutations.
Study details: Findings are from next-generation sequencing analysis of BCR-ABL1 kinase domain and 18 myeloid neoplasm-associated genes in 49 patients with de novo chronic phase-CML and 6 healthy controls.
Disclosures: This study was supported by grants from the Ministry of Health of the Czech Republic, the Ministry of Education, and Bristol-Myers Squibb. D Zackova and J Mayer reported ties with various pharmaceutical companies including Bristol-Myers Squibb. Other authors declared no competing interests.
Source: Romzova M et al. Br J Haematol. 2021 Jul 1. doi: 10.1111/bjh.17659.