What you carry at this position in your DNA and what research says about it.
Detoxification and Cancer Risk: 5/10 evidence, 29 publications.
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Sample genotype (not yours): C/C
Typical Detoxification and Baseline Cancer Risk
Standard enzyme activity supports the typical clearance of environmental toxins and common pollutants. Baseline susceptibility to prostate and esophageal cancers is maintained.
What this genotype means: Standard phase II detoxification capacity; Baseline risk for prostate and esophageal cancers.
Sample genotype (not yours): C/T
Slightly Reduced Detoxification and Elevated Cancer Risk
Slightly lower enzyme activity may lead to a slower clearance of environmental toxins. Susceptibility to certain cancers and sensitivity to chemotherapy side effects are modestly increased.
What this genotype means: Slightly reduced phase II detoxification capacity; Modestly increased risk for prostate and esophageal cancers.
Sample genotype (not yours): T/T
Reduced Detoxification and Higher Cancer Risk
Significantly lower enzyme activity reduces the body's ability to clear environmental toxins. Susceptibility to prostate and esophageal cancers is elevated, and chemotherapy response may be altered.
What this genotype means: Reduced phase II detoxification capacity; Increased risk for prostate and esophageal cancers; Altered response to platinum-based chemotherapy.
Gene function and biological role
Gene Function: The GSTP1 gene encodes glutathione S-transferase pi 1, a critical phase II detoxification enzyme [1]. This enzyme is highly active in tissues directly exposed to the environment, such as the lungs, esophagus, and skin [1]. It functions by attaching glutathione to harmful foreign compounds, making them water-soluble and easier for the body to excrete [1]. Through this mechanism, the enzyme helps neutralize environmental pollutants, heavy metals, and chemotherapy drugs [1]. Variations in this gene can alter enzyme stability and substrate binding, directly impacting how efficiently cells clear toxic substances [1].
Variant Impact: The rs1138272 variant represents a single nucleotide change from cytosine to thymine in the GSTP1 gene. This genetic transition alters the encoded protein at position 114, substituting the amino acid alanine with valine. This structural alteration reduces the overall stability and catalytic efficiency of the resulting enzyme [1]. Consequently, the variant form is less effective at conjugating glutathione to toxic compounds [1]. This functional decline can lead to a slower clearance of environmental carcinogens and certain medications [1].
Key Insight: The variant form of this enzyme has a reduced ability to clear heavy metals and common air pollutants, making carriers more sensitive to environmental toxins.
Location: GSTP1. Chromosome 11 · 11q13.2 · 67.6 Mb
Estimated prevalence by population
Global 89.4%; European 83.8%; African 97.0%; East Asian 99.8%; South Asian 87.9%; Americas 93.8%; Ashkenazi 92.2%; Finnish 84.5%; Middle Eastern 91.3%; Amish 82.4%.
Estimated CC genotype frequency.
Global 10.2%; European 15.5%; African 3.0%; East Asian 0.2%; South Asian 11.7%; Americas 6.1%; Ashkenazi 7.6%; Finnish 14.8%; Middle Eastern 8.5%; Amish 16.8%.
Estimated CT genotype frequency.
Global 0.4%; European 0.7%; African < 0.1%; East Asian < 0.1%; South Asian 0.4%; Americas 0.1%; Ashkenazi 0.2%; Finnish 0.6%; Middle Eastern 0.2%; Amish 0.9%.
Estimated TT genotype frequency.
Showing effects for C/C genotype
Pharmacogenomics
Drug Metabolism Enzyme Activity
Detoxification Capacity. Evidence: 3/10. Source: PMID 18559526. Typical.
Chemotherapy Response
Cisplatin Response. Evidence: 5/10. Source: PMID 25592234. Typical Survival.
Cancer & Oncology
Prostate Cancer
Prostate Cancer. Evidence: 3/10. Source: PMID 32183092. Typical Risk.
Gastrointestinal Cancers
Esophageal Cancer. Evidence: 3/10. Source: PMID 20540773. Typical Risk.
Organ Systems
Respiratory Health
Air Pollution Sensitivity. Evidence: 3/10. Source: PMID 24465030. Typical Sensitivity.
Showing effects for C/T genotype
Detoxification Capacity. Evidence: 3/10. Source: PMID 18559526. Slightly Reduced.
Cisplatin Response. Evidence: 5/10. Source: PMID 25592234. Decreased Survival.
Prostate Cancer. Evidence: 3/10. Source: PMID 32183092. Slightly Increased.
Esophageal Cancer. Evidence: 3/10. Source: PMID 20540773. Slightly Increased.
Air Pollution Sensitivity. Evidence: 3/10. Source: PMID 24465030. Slightly Increased.
Showing effects for T/T genotype
Detoxification Capacity. Evidence: 3/10. Source: PMID 18559526. Reduced.
Prostate Cancer. Evidence: 3/10. Source: PMID 32183092. Increased Risk.
Esophageal Cancer. Evidence: 3/10. Source: PMID 20540773. Increased Risk.
Air Pollution Sensitivity. Evidence: 3/10. Source: PMID 24465030. Increased.
What this genotype means for the people who carry it
Sample genotype: CC (Homozygous)
Having two copies of the C allele ensures the production of the fully functional, standard glutathione S-transferase pi 1 enzyme [1]. This typical enzyme activity allows the body to efficiently neutralize and excrete environmental carcinogens, heavy metals, and reactive oxygen species [1]. Consequently, cellular damage from everyday exposures is kept to a minimum, maintaining a baseline risk profile for several cancers [2]. Studies indicate that this standard function is associated with typical survival outcomes during platinum-based chemotherapy treatments [3]. Maintaining a diet rich in cruciferous vegetables further supports this natural detoxification pathway.
Standard phase II detoxification capacity; Baseline risk for prostate and esophageal cancers.
Sample genotype: CT (Heterozygous)
Carrying one copy of the T allele results in a mixture of standard and lower-activity detoxification enzymes [1]. This partial reduction in enzyme efficiency can slow down the neutralization of environmental pollutants and heavy metals [1]. Over time, the slower clearance of these compounds may lead to higher cellular oxidative stress [2]. Research has linked this intermediate enzyme activity to a modestly increased risk of developing prostate and esophageal cancers [3]. Additionally, clinical studies have observed altered treatment outcomes and survival rates in patients undergoing cisplatin-based chemotherapy [4]. Minimizing exposure to secondhand smoke and air pollution is highly beneficial for supporting cellular health.
Slightly reduced phase II detoxification capacity; Modestly increased risk for prostate and esophageal cancers.
Sample genotype: TT (Homozygous)
Carrying two copies of the T allele leads to the exclusive production of the lower-activity valine variant of the enzyme [1]. This structural change significantly impairs the conjugation of glutathione to harmful substances, resulting in slower toxin clearance [1]. The accumulation of uncleared environmental carcinogens can increase cellular damage and oxidative stress over time [2]. Multiple genetic studies have associated this genotype with a significantly higher risk of prostate and esophageal cancers [3] [4]. Furthermore, clinical data indicates that this reduced clearance rate is linked to decreased survival outcomes during cisplatin chemotherapy [5]. Maximizing dietary antioxidants and avoiding known environmental toxins can help mitigate these cellular detoxification challenges.
Reduced phase II detoxification capacity; Increased risk for prostate and esophageal cancers; Altered response to platinum-based chemotherapy.
Variants with shared genetic architecture
rs1695 · GSTP1 Gene · Chr 11 · Detoxification and Lung Health
rs1800566 · NQO1 Gene · Chr 16 · Toxin Detoxification
rs3957357 · GSTA1 Gene · Chr 6 · Detoxification Capacity
Glutathione s-transferase p1: gene sequence variation and functional genomic studies.
GSTP1 rs1138272 Polymorphism Affects Prostate Cancer Risk.
The 341C/T polymorphism in the GSTP1 gene is associated with increased risk of oesophageal cancer.
Content updated August 2026.
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