What is the first-line management for CML involving the 9;22 translocation?

Chronic myeloid leukemia (CML) is commonly associated with the Philadelphia chromosome, a genetic abnormality resulting from the translocation of chromosomes 9 and 22. This genetic change leads to the formation of the BCR-ABL fusion protein, which is a constitutively active tyrosine kinase that plays a critical role in the pathogenesis of CML by driving cell proliferation and inhibiting apoptosis.

Imatinib is a targeted therapy that specifically inhibits the activity of the BCR-ABL fusion protein. As a first-line treatment, it has significantly improved the outcomes for patients with CML, leading to long-term remission and a better quality of life. In contrast to other treatments, imatinib directly addresses the dysregulated signaling that contributes to the disease's progression.

Other treatment options may have a role in specific scenarios, such as hydroxyurea, which can be used in the acute setting to control high white blood cell counts but does not target the underlying cause of CML. Allogeneic bone marrow transplant is considered for younger patients with advanced disease or those who are resistant to imatinib, but it is not typically the first-line approach due to its associated risks and potential complications. Interferon therapy has been largely