Apoptosis: BCL-2 family: practice question

A Pathology 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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Pathology · Apoptosis: BCL-2 family

Sample item

A 55-year-old man has painless generalised lymphadenopathy and a lymph node biopsy shows a nodular proliferation of small cleaved cells. Cytogenetics show t(14;18). What is the consequence of this translocation?

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

The answer and the reasoning

B. Overexpression of BCL-2, blocking mitochondrial apoptosis and prolonging B-cell survival

In follicular lymphoma, t(14;18) places the BCL2 gene next to the immunoglobulin heavy chain enhancer, causing overexpression of BCL-2. BCL-2 prevents BAX and BAK from permeabilising the mitochondrial membrane, so cytochrome c is not released and cells fail to undergo apoptosis. The tumour is therefore driven by survival rather than rapid proliferation.

Option by option

  • A. Constitutive tyrosine kinase activity from a fusion gene

    A constitutively active tyrosine kinase fusion is the mechanism of BCR-ABL in chronic myeloid leukaemia.

  • B. Overexpression of BCL-2, blocking mitochondrial apoptosis and prolonging B-cell survival (correct)

    Correct. BCL-2 is an anti-apoptotic protein that keeps lymphoma cells alive.

  • C. Overexpression of cyclin D1, driving cell cycle entry

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

  • D. Loss of p53 function, preventing DNA damage responses

    TP53 loss is a separate event and is not the product of t(14;18).

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 Pathology question

What is the answer to this Pathology question?

The best answer is B, Overexpression of BCL-2, blocking mitochondrial apoptosis and prolonging B-cell survival. In follicular lymphoma, t(14;18) places the BCL2 gene next to the immunoglobulin heavy chain enhancer, causing overexpression of BCL-2.

Why is "Constitutive tyrosine kinase activity from a fusion gene" not the answer?

A constitutively active tyrosine kinase fusion is the mechanism of BCR-ABL in chronic myeloid leukaemia.

Why is "Overexpression of cyclin D1, driving cell cycle entry" not the answer?

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

Why is "Loss of p53 function, preventing DNA damage responses" not the answer?

TP53 loss is a separate event and is not the product of t(14;18).

What concept does this question test?

It tests Apoptosis: BCL-2 family in Pathology. BCL-2 prevents BAX and BAK from permeabilising the mitochondrial membrane, so cytochrome c is not released and cells fail to undergo apoptosis. The tumour is therefore driven by survival rather than rapid proliferation.

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 Apoptosis: BCL-2 family?

Learn each disease as a bundle: cause, key histology, markers, and the clinical hallmark. Then use the flashcards and the other Pathology 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.