What chromosomal rearrangement is associated with chronic myeloid leukemia (CML)?

Chronic myeloid leukemia (CML) is primarily associated with a specific chromosomal rearrangement known as the Philadelphia chromosome, which results from a translocation between chromosomes 9 and 22. This translocation creates a hybrid gene, BCR-ABL, which encodes an active tyrosine kinase that promotes cell proliferation and inhibits apoptosis, thereby contributing to the development of leukemia.

The significance of the BCR-ABL fusion protein in CML is profound, as it serves as a target for specific therapies, particularly tyrosine kinase inhibitors like imatinib (Gleevec). The presence of this particular chromosomal change is a hallmark of CML and is commonly used in diagnosis and monitoring treatment response in affected patients.

Overall, the translocation between chromosomes 9 and 22 is directly linked to the pathophysiology of CML, making it the correct answer for the associated chromosomal rearrangement in this disease.