Medical genetics: BRCA and PARP inhibition: practice question

A Anatomy 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.

Try it

Anatomy · Medical genetics: BRCA and PARP inhibition

Sample item

A woman with BRCA1-mutated ovarian cancer responds to a PARP inhibitor. Why does the drug kill tumour cells but spare normal cells?

AThe drug directly cross-links the DNA of dividing cellsBSynthetic lethality: loss of homologous recombination plus blocked single-strand repairCThe tumour cells lack the target enzyme completelyDThe drug restores the function of the mutated BRCA1 protein

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

The answer and the reasoning

B. Synthetic lethality: loss of homologous recombination plus blocked single-strand repair

BRCA1-mutated cells cannot repair double-strand breaks by homologous recombination. PARP inhibition blocks single-strand break repair, which becomes double-strand breaks that cannot be repaired, a synthetic lethal interaction, whereas normal cells retain homologous recombination.

Option by option

A. The drug directly cross-links the DNA of dividing cells
Cross-linking is the mechanism of platinum drugs.
B. Synthetic lethality: loss of homologous recombination plus blocked single-strand repair (correct)
Correct. Two pathways are lost together, which is lethal only to tumour cells.
C. The tumour cells lack the target enzyme completely
The tumour cells have the enzyme, which is why it can be inhibited.
D. The drug restores the function of the mutated BRCA1 protein
PARP inhibitors do not restore BRCA1 function.

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 Anatomy question

What is the answer to this Anatomy question?

The best answer is B, Synthetic lethality: loss of homologous recombination plus blocked single-strand repair. BRCA1-mutated cells cannot repair double-strand breaks by homologous recombination.

Why is "The drug directly cross-links the DNA of dividing cells" not the answer?

Cross-linking is the mechanism of platinum drugs.

Why is "The tumour cells lack the target enzyme completely" not the answer?

The tumour cells have the enzyme, which is why it can be inhibited.

Why is "The drug restores the function of the mutated BRCA1 protein" not the answer?

PARP inhibitors do not restore BRCA1 function.

What concept does this question test?

It tests Medical genetics: BRCA and PARP inhibition in Anatomy. PARP inhibition blocks single-strand break repair, which becomes double-strand breaks that cannot be repaired, a synthetic lethal interaction, whereas normal cells retain homologous recombination.

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 Medical genetics: BRCA and PARP inhibition?

Learn every nerve by its route, its muscles and what a lesion looks like at the bedside. That one habit answers a large share of questions. Then use the flashcards and the other Anatomy 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.