For example, M-type BCR-ABL1 fusion protein encoding 210KD relative molecular weight exists in more than 90 to 95% of CML patients, 1/3 of ALL patients and 1 to 2% of AML patients. The M-type BCR-ABL1 fusion protein, encoding a relative molecular mass of 190KD, is present in two-thirds of ALL patients and 3% of atypical CML patients. With the development of the process, the occurrence of drug resistance is closely related to the mutation of BCR-ABL1 gene , in which patients with T315I point mutation are resistant to Imatinib and all second-generation drugs, and the detection of the mutation status of this site also provides a theoretical basis for third-generation TKI drug use ^[1].  To ensure optimal outcomes, regular, high-quality molecular biological monitoring minimizes the risk of disease progression and maximizes the chance of achieving treatment-free remission (TFR).

If elevated BCR-ABL1 values are detected early or a predetermined response goal is not achieved, mutation analysis may be required, and if the patient fails treatment, a more effective TKI treatment may be replaced.  Continuing to maintain deep molecular response ( DMR ) is associated with the success of TFR, and maximizing the likelihood of reaching DMR ( 3 years for patients with MR4.0 , 2 years for patients with MR4.5 ) through appropriate treatment options has become an increasingly important therapeutic target for CML.  Quantitative monitoring of BCR-ABL1 fusion gene is a means to guide prognosis, monitor relapse and drug resistance. The gradual increase of its expression level is indicative of disease recurrence ^[2].

[1] Blood Cancer J . 2023 Apr 24;13(1):58.

[2] NCCN. Clinical Practice Guidelines in Oncology. Chronic myeloid leukemia.