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Pathology · Haematology: chronic myeloid leukaemia
Sample itemThe BCR-ABL fusion in chronic myeloid leukaemia encodes a constitutively active what?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
B. Tyrosine kinase
The t(9;22) Philadelphia chromosome creates BCR-ABL, an always-active tyrosine kinase that drives myeloid proliferation. Tyrosine-kinase inhibitors such as imatinib target this abnormal protein.
Option by option
A. Tumour-suppressor phosphatase
BCR-ABL is oncogenic, not a tumour suppressor.
B. Tyrosine kinase (correct)
Correct. BCR-ABL signalling is tyrosine-kinase dependent.
C. Serine protease
A serine protease does not explain the Philadelphia chromosome effect.
D. DNA helicase
Helicase defects are not the core lesion in CML.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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