Molecular biology and genetics: BCR-ABL fusion: practice question

A Biochemistry question in the style of the NEET PG paper. Answer it first, then read why the right option is right and why each of the others is wrong.

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Biochemistry · Molecular biology and genetics: BCR-ABL fusion

Sample item

A 45-year-old has splenomegaly, a leucocyte count of 150,000 per microlitre with myeloid cells at all stages of maturation, and t(9;22) on karyotype. What is the functional consequence of this translocation?

Original practice item, not a recalled exam question. Nothing here is recorded.

The answer and the reasoning

A. A fusion protein with constitutive tyrosine kinase activity

The Philadelphia chromosome fuses BCR to ABL1, producing a constitutively active tyrosine kinase that drives proliferation in chronic myeloid leukaemia. Imatinib inhibits this kinase. The other options belong to different lesions.

Option by option

  • A. A fusion protein with constitutive tyrosine kinase activity (correct)

    Correct. BCR-ABL is a constitutively active kinase and the target of imatinib.

  • B. Loss of the tumour suppressor p53

    p53 loss is not caused by this translocation.

  • C. Overexpression of cyclin D1

    Cyclin D1 overexpression results from t(11;14) in mantle cell lymphoma.

  • D. Overexpression of BCL2 from an immunoglobulin enhancer

    BCL2 overexpression results from t(14;18) in follicular lymphoma.

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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Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is A, A fusion protein with constitutive tyrosine kinase activity. The Philadelphia chromosome fuses BCR to ABL1, producing a constitutively active tyrosine kinase that drives proliferation in chronic myeloid leukaemia.

Why is "Loss of the tumour suppressor p53" not the answer?

p53 loss is not caused by this translocation.

Why is "Overexpression of cyclin D1" not the answer?

Cyclin D1 overexpression results from t(11;14) in mantle cell lymphoma.

Why is "Overexpression of BCL2 from an immunoglobulin enhancer" not the answer?

BCL2 overexpression results from t(14;18) in follicular lymphoma.

What concept does this question test?

It tests Molecular biology and genetics: BCR-ABL fusion in Biochemistry. Imatinib inhibits this kinase. The other options belong to different lesions.

How hard is this question?

We tag it as an application question: it asks you to use a fact on a patient or a finding. The tag is our own editorial judgement, not an official difficulty rating, so read the reason for every option, not only the answer.

How should I study Molecular biology and genetics: BCR-ABL fusion?

Build one table of enzyme deficiency, disease, inheritance and key finding, then revise it by spaced recall. Then use the flashcards and the other Biochemistry questions on this site to test what stuck.

Is this a real NEET PG question?

No. It is an original practice item (editorial status: sample, version 1). NextPrep does not publish recalled or leaked questions, and independent faculty review of this item has not been completed yet, so confirm important facts in a standard textbook.