The enzyme DPD (full name: dihydropyrimidine dehydrogenase) is coded by the DPYD gene and is responsible for breaking down excess pyrimidines such as thymine and uracil (building blocks of DNA).
The enzyme is also involved in breaking down drugs that are similar to pyrimidines, such as cytostatics from the fluoropyrimidine group.
Fluoropyrimidines (such as fluorouracil, tegafur and capecitabine) are frequently used as a standard treatment for various types of cancer, including bowel, stomach and breast cancer. The enzyme DPD accounts for over 80% of the metabolisation of these drugs.
Drugs that can be metabolised by the enzyme DPD include the cytostatics fluorouracil, tegafur and capecitabine. These cytostatics are used in the treatment of bowel, breast, stomach, liver and oesophageal cancer.
Genetic predisposition
The activity of the enzyme DPD varies from one individual to another.
This variation can be explained in part by genetic variations in the DPYD gene.
Consequently, the side effects of drugs broken down by the enzyme DPD can also vary from person to person.
When a genotype is determined variations in the DPYD gene are indicated by two so-called alleles. Each allele has a name consisting of an asterisk (*) and a number (this may also be an rs number).
An example of a possible DPYD genotype is DPYD*1/*2A.
At iGene we determine the following variants (alleles) of the DPYD gene:
DPYD*2A, DPYD*3, DPYD*6, DPYD*7, DPYD*8, DPYD*10, DPYD*12, DPYD*13, DPYD 1236A, DPYD 2846T and other (classified as DPYD*1).