Neoplasia: p16 as HPV surrogate: 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 · Neoplasia: p16 as HPV surrogate

Sample item

A biopsy from a tonsillar squamous carcinoma in a non-smoker shows strong, diffuse nuclear and cytoplasmic p16 staining. What is the molecular explanation for this overexpression?

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

The answer and the reasoning

A. E7 inactivates Rb, removing feedback inhibition of p16

HPV E7 binds and inactivates Rb. Because p16 normally acts upstream to keep Rb active, and Rb loss removes negative feedback, p16 accumulates. Diffuse p16 staining is therefore used as a surrogate marker of high-risk HPV in oropharyngeal and cervical carcinoma.

Option by option

  • A. E7 inactivates Rb, removing feedback inhibition of p16 (correct)

    Correct. Functional loss of Rb through E7 causes compensatory p16 overexpression.

  • B. Amplification of the CDKN2A gene on chromosome 9p

    CDKN2A is usually deleted or methylated in tumours, not amplified.

  • C. E6 degrades p53, so p16 is no longer degraded

    E6 degrades p53 but does not control p16 stability.

  • D. A germline mutation of the CDKN2A promoter silences p16

    Silencing of p16 would reduce, not increase, staining.

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.

More Pathology questions

Questions about this Pathology question

What is the answer to this Pathology question?

The best answer is A, E7 inactivates Rb, removing feedback inhibition of p16. HPV E7 binds and inactivates Rb.

Why is "Amplification of the CDKN2A gene on chromosome 9p" not the answer?

CDKN2A is usually deleted or methylated in tumours, not amplified.

Why is "E6 degrades p53, so p16 is no longer degraded" not the answer?

E6 degrades p53 but does not control p16 stability.

Why is "A germline mutation of the CDKN2A promoter silences p16" not the answer?

Silencing of p16 would reduce, not increase, staining.

What concept does this question test?

It tests Neoplasia: p16 as HPV surrogate in Pathology. Because p16 normally acts upstream to keep Rb active, and Rb loss removes negative feedback, p16 accumulates. Diffuse p16 staining is therefore used as a surrogate marker of high-risk HPV in oropharyngeal and cervical carcinoma.

How hard is this question?

We tag it as a multi-step question: it asks you to combine more than one idea. 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 Neoplasia: p16 as HPV surrogate?

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.