Oncogenes: BCR-ABL in chronic myeloid leukaemia: 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 · Oncogenes: BCR-ABL in chronic myeloid leukaemia

Sample item

A 45-year-old man has fatigue, splenomegaly, a total leucocyte count of 150,000/mm3 with myelocytes and basophils, and a low leucocyte alkaline phosphatase score. The marrow shows t(9;22). What is the molecular consequence of this translocation?

AOverexpression of BCL2 through juxtaposition with the immunoglobulin heavy chain locusBAmplification of N-mycCLoss of function of a tumour suppressor gene by deletionDA fusion gene encoding a constitutively active tyrosine kinase

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

The answer and the reasoning

D. A fusion gene encoding a constitutively active tyrosine kinase

The t(9;22) joins BCR on chromosome 22 to ABL on chromosome 9, making the Philadelphia chromosome. The BCR-ABL fusion protein is a tyrosine kinase that is always active, driving proliferation and resistance to apoptosis. Imatinib competes with ATP at the kinase site and is first-line therapy.

Option by option

A. Overexpression of BCL2 through juxtaposition with the immunoglobulin heavy chain locus
BCL2 juxtaposition with the heavy chain locus is the t(14;18) of follicular lymphoma.
B. Amplification of N-myc
N-myc amplification is characteristic of neuroblastoma.
C. Loss of function of a tumour suppressor gene by deletion
The translocation creates an oncogene and does not delete a tumour suppressor.
D. A fusion gene encoding a constitutively active tyrosine kinase (correct)
The fusion kinase is permanently active and is the target of imatinib.

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.

Questions about this Biochemistry question

What is the answer to this Biochemistry question?

The best answer is D, A fusion gene encoding a constitutively active tyrosine kinase. The t(9;22) joins BCR on chromosome 22 to ABL on chromosome 9, making the Philadelphia chromosome.

Why is "Overexpression of BCL2 through juxtaposition with the immunoglobulin…" not the answer?

BCL2 juxtaposition with the heavy chain locus is the t(14;18) of follicular lymphoma.

Why is "Amplification of N-myc" not the answer?

N-myc amplification is characteristic of neuroblastoma.

Why is "Loss of function of a tumour suppressor gene by deletion" not the answer?

The translocation creates an oncogene and does not delete a tumour suppressor.

What concept does this question test?

It tests Oncogenes: BCR-ABL in chronic myeloid leukaemia in Biochemistry. The BCR-ABL fusion protein is a tyrosine kinase that is always active, driving proliferation and resistance to apoptosis. Imatinib competes with ATP at the kinase site and is first-line therapy.

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 Oncogenes: BCR-ABL in chronic myeloid leukaemia?

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.