Which oncogene is involved in chronic myeloid leukemia?

Chronic myeloid leukemia (CML) is primarily characterized by the presence of a specific genetic abnormality known as the Philadelphia chromosome. This chromosome results from a translocation between chromosome 9 and chromosome 22, leading to the fusion of two genes: BCR (Breakpoint Cluster Region) and ABL (Abelson Murine Leukemia Viral Oncogene Homolog). The resultant fusion protein, BCR-Abl, acts as a tyrosine kinase that promotes cell proliferation and inhibits apoptosis, contributing to the development of leukemia.

Understanding the role of BCR-Abl in CML is crucial because it serves as both a diagnostic marker and a therapeutic target. Treatments such as tyrosine kinase inhibitors (e.g., imatinib) have been developed specifically to inhibit the activity of the BCR-Abl protein, significantly improving outcomes for patients with CML.

Other options listed represent oncogenes associated with different cancers or pathways but are not specifically linked to CML. HER2 is predominantly related to breast cancer, KRAS is involved in various solid tumors, and EGFR is associated with lung and head and neck cancers. None of these contribute to the pathogenesis of chronic myeloid leukemia in the way that BCR-A