What is the clinical utility of pharmacogenomics in the context of antidepressants or oncology?

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Multiple Choice

What is the clinical utility of pharmacogenomics in the context of antidepressants or oncology?

Explanation:
Genetic differences in drug-metabolizing enzymes and drug targets shape both how antidepressants are processed and how effective they are, as well as how cancer therapies work and what toxicities they cause. In antidepressants, variants in enzymes like CYP2D6 and CYP2C19 create different metabolizer categories. Poor metabolizers can have higher drug exposure and more side effects, while ultrarapid metabolizers may have low drug levels and reduced efficacy. Pharmacogenomic testing can guide which antidepressant to choose and what dose to start and adjust, aiming for safer, more effective treatment. In oncology, the same idea applies to how patients metabolize therapies and how tumors respond. Germline variants like TPMT or NUDT15 increase risk of bone marrow suppression with thiopurines; DPYD variants raise the risk of severe toxicity with 5-FU; other genetic biomarkers guide the use of targeted drugs (for example, HER2 status guiding trastuzumab). By predicting who will benefit and who may be harmed, pharmacogenomics helps tailor therapy to maximize efficacy and minimize toxicity.

Genetic differences in drug-metabolizing enzymes and drug targets shape both how antidepressants are processed and how effective they are, as well as how cancer therapies work and what toxicities they cause. In antidepressants, variants in enzymes like CYP2D6 and CYP2C19 create different metabolizer categories. Poor metabolizers can have higher drug exposure and more side effects, while ultrarapid metabolizers may have low drug levels and reduced efficacy. Pharmacogenomic testing can guide which antidepressant to choose and what dose to start and adjust, aiming for safer, more effective treatment.

In oncology, the same idea applies to how patients metabolize therapies and how tumors respond. Germline variants like TPMT or NUDT15 increase risk of bone marrow suppression with thiopurines; DPYD variants raise the risk of severe toxicity with 5-FU; other genetic biomarkers guide the use of targeted drugs (for example, HER2 status guiding trastuzumab). By predicting who will benefit and who may be harmed, pharmacogenomics helps tailor therapy to maximize efficacy and minimize toxicity.

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