What you carry at this position in your DNA and what research says about it.
Chemotherapy Toxicity Risk: 8/10 evidence, 17 publications.
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Sample genotype (not yours): C/C
Typical Chemotherapy Toxicity Risk
Two copies of the normal gene allele are present. This genotype is associated with standard dihydropyrimidine dehydrogenase enzyme activity and normal drug clearance.
What this genotype means: Normal clearance of fluoropyrimidine drugs; Standard risk of chemotherapy-related side effects.
Sample genotype (not yours): C/T
Increased Chemotherapy Toxicity Risk
One copy of the variant allele is present. This genotype is linked to a higher risk of severe side effects from certain chemotherapy drugs.
What this genotype means: Slower metabolism of fluorouracil and capecitabine; Increased risk of severe neutropenia and diarrhea during treatment.
Sample genotype (not yours): T/T
High Chemotherapy Toxicity Risk
Two copies of the variant allele are present. This genotype is associated with significantly reduced enzyme activity and a high risk of drug toxicity.
What this genotype means: Significantly impaired clearance of fluoropyrimidine chemotherapy; High risk of severe, life-threatening drug toxicity.
Gene function and biological role
Gene Function: The DPYD gene encodes dihydropyrimidine dehydrogenase, which is the primary enzyme responsible for breaking down pyrimidines [1]. This enzyme plays a critical role in metabolizing more than eighty percent of administered fluoropyrimidine chemotherapy drugs [2]. When the enzyme is fully functional, these toxic chemotherapy agents are rapidly cleared from the body, preventing severe systemic damage [2]. However, genetic variations that reduce enzyme activity can lead to a dangerous buildup of active drug metabolites in the bloodstream [1]. This accumulation can result in life-threatening toxicities, including severe bone marrow suppression, diarrhea, and hand-foot syndrome [2].
Variant Impact: The rs1801160 variant, also known as p.Val732Ile or DPYD*6, is a missense mutation in the DPYD gene [1]. This genetic change replaces the amino acid valine with isoleucine at position 732 of the enzyme [1]. While some major pharmacogenetic consortia classify this variant as having normal function, clinical studies have repeatedly linked it to reduced enzyme activity [3]. Patients carrying this variant often exhibit a slower clearance rate of fluoropyrimidine-based drugs [4]. Consequently, carriers are at a significantly higher risk of experiencing severe adverse reactions during standard chemotherapy regimens [4].
Key Insight: Although some international databases classify this variant as normal, real-world clinical studies show it can double the risk of severe chemotherapy side effects like extreme white blood cell depletion.
Location: DPYD. Chromosome 1 · 1p21.3 · 97.3 Mb
Estimated prevalence by population
Global 92.2%; European 91.2%; African 95.2%; East Asian 96.9%; South Asian 82.3%; Americas 91.0%; Ashkenazi 79.8%; Finnish 95.6%; Middle Eastern 80.0%; Amish 96.5%.
Estimated CC genotype frequency.
Global 7.6%; European 8.6%; African 4.8%; East Asian 3.0%; South Asian 16.9%; Americas 8.8%; Ashkenazi 19.1%; Finnish 4.3%; Middle Eastern 18.9%; Amish 3.4%.
Estimated CT genotype frequency.
Global 0.2%; European 0.2%; African 0.1%; East Asian < 0.1%; South Asian 0.9%; Americas 0.2%; Ashkenazi 1.1%; Finnish < 0.1%; Middle Eastern 1.1%; Amish < 0.1%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Chemotherapy Response
Fluorouracil Toxicity. Evidence: 8/10. Source: PMID 26794347. Typical Risk.
Capecitabine Toxicity. Evidence: 8/10. Source: PMID 28745575. Typical Risk.
Pyrimidine Drug Toxicity. Evidence: 5/10. Source: PMID 35207713. Typical Risk.
Drug Metabolism Enzyme Activity
DPD Enzyme Activity. Evidence: 8/10. Source: PMID 23328581. Normal Activity.
Showing effects for C/T genotype
Fluorouracil Toxicity. Evidence: 8/10. Source: PMID 26794347. ~2x Higher Risk.
Capecitabine Toxicity. Evidence: 8/10. Source: PMID 28745575. Increased Risk.
Pyrimidine Drug Toxicity. Evidence: 5/10. Source: PMID 35207713. Increased Risk.
DPD Enzyme Activity. Evidence: 8/10. Source: PMID 23328581. Decreased Activity.
Showing effects for T/T genotype
Fluorouracil Toxicity. Evidence: 8/10. Source: PMID 26794347. Elevated Risk.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having the C/C genotype means the body produces the standard, fully functional version of the dihydropyrimidine dehydrogenase enzyme [1]. This enzyme is responsible for breaking down and clearing fluoropyrimidine chemotherapy drugs like fluorouracil and capecitabine [2]. Because the enzyme functions at a normal rate, the risk of experiencing severe, unexpected toxicities from these medications is not elevated [2]. Standard clinical dosing guidelines typically apply to individuals with this genetic profile [3]. However, other genetic variants or clinical factors can still influence how a person responds to chemotherapy [3]. It is always important to discuss any treatment plans and potential side effects with a healthcare provider [2].
Normal clearance of fluoropyrimidine drugs; Standard risk of chemotherapy-related side effects.
Sample genotype: CT (Heterozygous)
Carrying one copy of the T allele means the body may produce a mixture of normal and less active dihydropyrimidine dehydrogenase enzymes [1]. Clinical studies have shown that individuals with this genotype have a roughly two-fold higher risk of experiencing severe adverse reactions when treated with fluorouracil or capecitabine [2]. These adverse reactions can include severe neutropenia, which is a dangerous drop in white blood cells, as well as severe diarrhea and hand-foot syndrome [3]. Because the clearance of these chemotherapy drugs is slower, the active compounds can build up to toxic levels in the bloodstream [2]. Knowing this genetic status can be highly valuable if fluoropyrimidine-based chemotherapy is ever prescribed [2].
Slower metabolism of fluorouracil and capecitabine; Increased risk of severe neutropenia and diarrhea during treatment.
Sample genotype: TT (Homozygous)
Having the T/T genotype means both copies of the DPYD gene carry the variant allele, leading to a more pronounced reduction in dihydropyrimidine dehydrogenase activity [1]. This genetic profile significantly impairs the body's ability to clear fluoropyrimidine chemotherapy drugs like fluorouracil and capecitabine [2]. As a result, standard doses of these medications can lead to rapid accumulation and severe, potentially life-threatening toxicities [3]. These toxicities often manifest as profound bone marrow suppression, severe gastrointestinal distress, and extreme skin reactions [2]. Clinical literature suggests that alternative treatments or highly customized dosing strategies are often considered for individuals with compromised DPD function [3]. Discussing these genetic findings with an oncologist prior to starting any fluoropyrimidine-based therapy is critical for safety [2].
Significantly impaired clearance of fluoropyrimidine chemotherapy; High risk of severe, life-threatening drug toxicity.
Variants with shared genetic architecture
rs56038477 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
rs75017182 · DPYD Gene · Chr 1 · Chemotherapy Drug Toxicity
rs17376848 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
Content updated August 2026.
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