Apoptosis: BCL-2 in follicular lymphoma: 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 · Apoptosis: BCL-2 in follicular lymphoma

Sample item

A 55-year-old man has painless lymphadenopathy and a biopsy diagnosis of follicular lymphoma with t(14;18). How does the translocation promote tumour cell accumulation?

AInactivation of caspase-3 through p53 mutationBBCL-2 overexpression blocks cytochrome c release, so caspase-9 activation by the apoptosome is preventedCConstitutive Fas receptor signalling drives proliferationDLoss of BAX increases cell division directly

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

The answer and the reasoning

B. BCL-2 overexpression blocks cytochrome c release, so caspase-9 activation by the apoptosome is prevented

The t(14;18) juxtaposes BCL-2 with the immunoglobulin heavy chain enhancer. BCL-2 protects mitochondrial membrane integrity and prevents cytochrome c release, so Apaf-1 and caspase-9 are not activated. The cells survive rather than proliferate faster, which explains the indolent course.

Option by option

A. Inactivation of caspase-3 through p53 mutation
p53 mutation is not the defining lesion of follicular lymphoma.
B. BCL-2 overexpression blocks cytochrome c release, so caspase-9 activation by the apoptosome is prevented (correct)
Correct. Excess BCL-2 prevents the intrinsic pathway of apoptosis.
C. Constitutive Fas receptor signalling drives proliferation
Fas signalling promotes apoptosis through caspase-8 and is not constitutively mitogenic.
D. Loss of BAX increases cell division directly
The translocation involves BCL-2, not loss of BAX, and acts by blocking death rather than driving division.

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 B, BCL-2 overexpression blocks cytochrome c release, so caspase-9 activation by the apoptosome is prevented. The t(14;18) juxtaposes BCL-2 with the immunoglobulin heavy chain enhancer.

Why is "Inactivation of caspase-3 through p53 mutation" not the answer?

p53 mutation is not the defining lesion of follicular lymphoma.

Why is "Constitutive Fas receptor signalling drives proliferation" not the answer?

Fas signalling promotes apoptosis through caspase-8 and is not constitutively mitogenic.

Why is "Loss of BAX increases cell division directly" not the answer?

The translocation involves BCL-2, not loss of BAX, and acts by blocking death rather than driving division.

What concept does this question test?

It tests Apoptosis: BCL-2 in follicular lymphoma in Biochemistry. BCL-2 protects mitochondrial membrane integrity and prevents cytochrome c release, so Apaf-1 and caspase-9 are not activated. The cells survive rather than proliferate faster, which explains the indolent course.

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 in follicular lymphoma?

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.