Molecular biology and genetics: APC and beta-catenin: 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: APC and beta-catenin

Sample item

A 19-year-old has hundreds of adenomatous polyps in the colon and a family history of colorectal cancer. A germline mutation of the APC gene is found. Which molecular consequence of APC loss promotes tumour growth?

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

The answer and the reasoning

D. Accumulation of beta-catenin, which activates transcription of growth-promoting genes

APC is part of the destruction complex that marks beta-catenin for degradation. Without functional APC, beta-catenin accumulates, enters the nucleus and activates MYC and cyclin D1 transcription through the Wnt pathway. This is the basis of familial adenomatous polyposis.

Option by option

  • A. Loss of DNA mismatch repair

    Loss of mismatch repair underlies Lynch syndrome, not adenomatous polyposis.

  • B. Activation of BCL-2 and resistance to apoptosis

    BCL-2 overexpression is typical of follicular lymphoma and not the APC mechanism.

  • C. Constitutive activation of the RET receptor

    Activated RET causes medullary thyroid carcinoma in MEN 2.

  • D. Accumulation of beta-catenin, which activates transcription of growth-promoting genes (correct)

    Correct. Loss of APC lets beta-catenin escape degradation and drive proliferative genes.

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 D, Accumulation of beta-catenin, which activates transcription of growth-promoting genes. APC is part of the destruction complex that marks beta-catenin for degradation.

Why is "Loss of DNA mismatch repair" not the answer?

Loss of mismatch repair underlies Lynch syndrome, not adenomatous polyposis.

Why is "Activation of BCL-2 and resistance to apoptosis" not the answer?

BCL-2 overexpression is typical of follicular lymphoma and not the APC mechanism.

Why is "Constitutive activation of the RET receptor" not the answer?

Activated RET causes medullary thyroid carcinoma in MEN 2.

What concept does this question test?

It tests Molecular biology and genetics: APC and beta-catenin in Biochemistry. Without functional APC, beta-catenin accumulates, enters the nucleus and activates MYC and cyclin D1 transcription through the Wnt pathway. This is the basis of familial adenomatous polyposis.

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: APC and beta-catenin?

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.