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In the realm of cancer treatment, personalized medicine has emerged as a promising approach to improving patient outcomes. One crucial aspect of personalized oncology revolves around the identification of genetic variations that can influence an individual’s response to specific medications. Among these medications, 5-fluorouracil (5FU), a widely used chemotherapy drug, has gained significant attention due to its connection with the DPYD gene.

The dihydropyrimidine dehydrogenase (DPD) enzyme, encoded by the DPYD gene, plays a crucial role in the metabolism of 5FU. DPD is responsible for breaking down 5FU into inactive metabolites, allowing the body to eliminate the drug effectively. However, some individuals possess genetic variations or polymorphisms in the DPYD gene that can result in reduced or absent DPD activity.

Patients with DPYD variants experience difficulty in metabolizing 5FU, leading to an increased risk of severe and potentially life-threatening side effects. These side effects may include severe neutropenia (low white blood cell count), mucositis (inflammation of the digestive tract lining), and hand-foot syndrome (skin rash on the palms and soles). Identifying patients with DPYD variants before initiating 5FU treatment is crucial to avoid such adverse reactions.

In conclusion, the relationship between 5FU and DPYD highlights the significance of pharmacogenomics in personalized cancer care. Identifying patients with DPYD variants before administering 5FU can significantly reduce the risk of adverse reactions and improve treatment efficacy. As researchers and clinicians delve deeper into the intricacies of drug-gene interactions, personalized medicine is expected to play an increasingly pivotal role in the fight against cancer.

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