In chronic myeloid leukemia (CML), the BCR-ABL1 fusion protein on the Philadelphia chromosome results from which translocation, and its primary oncogenic mechanism is:

• A t(8;14)(q24;q32); MYC overexpression
• B t(9;22)(q34;q11.2); constitutively active tyrosine kinase ✓
• C t(15;17)(q22;q12); PML-RARA fusion blocking differentiation
• D t(11;14)(q13;q32); cyclin D1 overexpression

Explanation

CML is defined by t(9;22)(q34;q11.2) creating the Philadelphia chromosome with BCR-ABL1 fusion. The resulting p210 fusion protein is a constitutively active tyrosine kinase that drives uncontrolled myeloid proliferation by activating RAS, PI3K/AKT, and STAT5 pathways. The other translocations are characteristic of Burkitt lymphoma, APL, and mantle cell lymphoma respectively.

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.