What you carry at this position in your DNA and what research says about it.
Prostate Cancer Survival: 5/10 evidence, 16 publications.
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Sample genotype (not yours): T/T
Shorter Prostate Cancer Survival
This genetic profile is associated with faster testosterone uptake, which may shorten survival times in prostate cancer patients. It also increases the risk of organ rejection when taking certain transplant medications, though it offers some protection against chemotherapy-induced platelet drops.
What this genotype means: Shorter survival in prostate cancer; Increased risk of lung transplant rejection; Lower risk of low platelet counts during chemotherapy.
Sample genotype (not yours): G/G
Longer Prostate Cancer Survival
Two copies of the major guanine allele are associated with slower hormone uptake and improved survival in prostate cancer. However, this profile increases the risk of anemia during chemotherapy and raises the likelihood of gastrointestinal side effects from transplant drugs.
What this genotype means: Longer survival in prostate cancer; Increased risk of chemotherapy-induced anemia; Higher risk of gastrointestinal toxicity from transplant drugs.
Sample genotype (not yours): T/G
Carrying one copy of the thymine allele is linked to faster hormone uptake and poorer prostate cancer outcomes. It also increases the risk of transplant rejection and can lead to a poorer response to certain leukemia treatments.
What this genotype means: Shorter survival in prostate cancer; Increased risk of lung transplant rejection; Poorer response to imatinib therapy.
Gene function and biological role
Gene Function: The SLCO1B3 gene encodes the organic anion transporting polypeptide 1B3 (OATP1B3), a crucial influx transporter primarily expressed in the liver [1]. This protein is responsible for transporting various endogenous compounds, such as bile acids and hormones, from the blood into hepatocytes [1]. It also plays a pivotal role in the hepatic uptake and clearance of numerous clinical drugs, including statins, immunosuppressants, and chemotherapy agents [2]. Variations in this gene can significantly alter drug pharmacokinetics, leading to differences in treatment efficacy and side effect risks [2].
Variant Impact: The rs4149117 variant is a missense mutation in the SLCO1B3 gene that results in a serine-to-alanine amino acid substitution at position 112 of the OATP1B3 transporter [1]. This structural alteration modifies the transporter's affinity and clearance rate for specific substrates, including hormones like testosterone and various prescription medications [1]. Because the variant alters how efficiently these compounds are taken up by liver cells, it directly impacts systemic drug levels and tissue exposure [2]. Consequently, it is a key genetic determinant of chemotherapy toxicity, transplant drug response, and cancer progression [2].
Key Insight: This single genetic change acts as a double-edged sword, where the allele that protects against chemotherapy side effects simultaneously increases the risk of transplant rejection.
Location: SLCO1B3. Chromosome 12 · 12p12.2 · 20.9 Mb
Estimated prevalence by population
Global 10.9%; European 2.2%; African 31.9%; East Asian 7.8%; South Asian 1.0%; Americas 3.5%; Ashkenazi 1.2%; Finnish 6.5%; Middle Eastern 1.4%; Amish 2.1%.
Estimated TT genotype frequency.
Global 33.3%; European 25.1%; African 49.2%; East Asian 40.3%; South Asian 18.0%; Americas 30.5%; Ashkenazi 19.6%; Finnish 37.9%; Middle Eastern 21.1%; Amish 24.7%.
Estimated TG genotype frequency.
Global 55.8%; European 72.8%; African 19.0%; East Asian 51.8%; South Asian 81.1%; Americas 66.0%; Ashkenazi 79.2%; Finnish 55.6%; Middle Eastern 77.5%; Amish 73.3%.
Estimated GG genotype frequency.
Showing effects for T/T genotype
Cancer & Oncology
Cancer Prognosis & Treatment Outcome
Prostate Cancer Prognosis. Evidence: 3/10. Source: PMID 21266523. Shorter Survival.
Pharmacogenomics
Chemotherapy Response
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 26267044. Lower Platelet Risk.
Leukemia Drug Response. Evidence: 5/10. Source: PMID 25056761. Typical Response.
Immunosuppressant & Biologic Response
Transplant Drug Response. Evidence: 5/10. Source: PMID 30992538. Higher Rejection Risk.
Immunity & Inflammation
Autoimmune Diseases
Rheumatoid Arthritis. Evidence: 5/10. Source: PMID 40732356. Typical Risk.
Showing effects for G/G genotype
Prostate Cancer Prognosis. Evidence: 3/10. Source: PMID 21266523. Longer Survival.
Chemotherapy Toxicity. Evidence: 5/10. Source: PMID 26267044. Higher Anemia Risk.
Leukemia Drug Response. Evidence: 5/10. Source: PMID 25056761. Poorer Response.
Transplant Drug Response. Evidence: 5/10. Source: PMID 30992538. Higher GI Toxicity.
Rheumatoid Arthritis. Evidence: 5/10. Source: PMID 40732356. Higher Anemia Risk.
Showing effects for T/G genotype
What this genotype means for the people who carry it
Sample genotype: TT (Homozygous)
Active transport of hormones and medications is significantly altered by the presence of two thymine alleles [1]. In prostate cancer, this variant is linked to rapid cellular uptake of testosterone, which can fuel tumor growth and lead to shorter recurrence-free survival [1]. When undergoing lung or kidney transplantation, patients with this genotype face an elevated risk of organ rejection and reduced survival when treated with mycophenolic acid [2]. However, during chemotherapy with carboplatin and paclitaxel, this profile is associated with a decreased likelihood of experiencing dangerously low platelet counts [3]. It also allows for faster metabolism of the antifungal drug voriconazole, so the drug reaches lower levels [4].
Shorter survival in prostate cancer; Increased risk of lung transplant rejection; Lower risk of low platelet counts during chemotherapy.
Sample genotype: GG (Homozygous)
Slower transport of certain hormones and medications characterizes this common genetic profile [1]. In prostate cancer patients, slower testosterone uptake by tumor cells is linked to significantly longer recurrence-free survival and better clinical outcomes [1]. However, this slower clearance rate can lead to drug accumulation and toxicity for several medications. During chemotherapy with carboplatin, paclitaxel, or methotrexate, this genotype is associated with a significantly higher risk of developing anemia [2] [3]. It also increases the risk of severe gastrointestinal toxicity when taking the immunosuppressant mycophenolate mofetil [4]. Additionally, patients taking the blood thinner warfarin may be more sensitive to it because of altered drug disposition [5].
Longer survival in prostate cancer; Increased risk of chemotherapy-induced anemia; Higher risk of gastrointestinal toxicity from transplant drugs.
Sample genotype: TG (Heterozygous)
Hormone and drug transport rates are moderately altered in individuals carrying one copy of each allele [1]. This intermediate transport profile is associated with shorter recurrence-free survival in prostate cancer patients due to enhanced cellular uptake of androgens [1]. In transplant recipients, this genotype is linked to an increased risk of lung transplant rejection and lower overall survival when taking mycophenolic acid [2]. Patients being treated for chronic myeloid leukemia with imatinib may also experience a poorer therapeutic response [3]. On the other hand, this genotype provides a protective effect against severe platelet drops during carboplatin and paclitaxel chemotherapy [4].
Shorter survival in prostate cancer; Increased risk of lung transplant rejection; Poorer response to imatinib therapy.
Variants with shared genetic architecture
rs11045585 · SLCO1B3 Gene · Chr 12 · Chemotherapy Side Effect Risk
rs7311358 · SLCO1B3 Gene · Chr 12 · Medication Response
rs1801158 · DPYD Gene · Chr 1 · Chemotherapy Toxicity Risk
Pharmacogenetic of voriconazole antifungal agent in pediatric patients.
Content updated August 2026.
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