What you carry at this position in your DNA and what research says about it.
Chemotherapy Heart Risk: 6/10 evidence, 16 publications.
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Sample genotype (not yours): G/G
Typical Risk of Chemotherapy-Induced Heart Damage
Standard baseline risks of heart toxicity during chemotherapy and typical susceptibility to fatty liver disease are expected. Normal cellular transport functions are fully preserved.
What this genotype means: Typical risk of doxorubicin-induced cardiotoxicity; Standard baseline risk of nonalcoholic fatty liver disease.
Sample genotype (not yours): A/A
Highest Risk of Chemotherapy-Induced Heart Damage
The highest risk of heart toxicity during specific chemotherapy regimens and a significantly increased susceptibility to fatty liver disease are present. A lower risk of chemotherapy-induced nerve damage acts as a partial trade-off.
What this genotype means: Highest risk of doxorubicin-induced cardiotoxicity; Significantly higher susceptibility to nonalcoholic fatty liver disease; Decreased risk of taxane-induced neuropathy.
Sample genotype (not yours): G/A
Increased Risk of Chemotherapy-Induced Heart Damage
Elevated risks of chemotherapy-induced heart damage and increased susceptibility to fatty liver disease are associated with this genetic profile. However, a reduced risk of nerve damage from certain other cancer drugs is also observed.
What this genotype means: Increased risk of doxorubicin-induced cardiotoxicity; Higher susceptibility to nonalcoholic fatty liver disease; Decreased risk of taxane-induced neuropathy.
Gene function and biological role
Gene Function: The ABCC2 gene encodes multidrug resistance-associated protein 2 (MRP2), an ATP-dependent efflux transporter primarily expressed in the liver, kidneys, and intestines [1]. This transporter plays a crucial role in the biliary excretion of organic anions, including conjugated bilirubin and various xenobiotics [1]. It also mediates the cellular export of numerous clinically important drugs, such as chemotherapeutics, statins, and antivirals [1]. Genetic variations in this gene can significantly alter the transport efficiency and clearance of these substances, leading to variations in drug efficacy and susceptibility to adverse drug reactions [1].
Variant Impact: A missense mutation in exon 32 of the ABCC2 gene results in a cysteine-to-tyrosine substitution at amino acid position 1515 (p.Cys1515Tyr). This amino acid change occurs in the last cytoplasmic domain of the transporter, a region critical for its function. In vitro studies have demonstrated that the tyrosine-encoding A allele significantly impairs the ATPase activity of the MRP2 transporter [1]. This functional defect leads to a reduced efflux capacity, causing a higher intracellular accumulation of its substrate drugs and endogenous compounds [1].
Key Insight: Although the variant A allele increases the risk of chemotherapy-induced heart damage, it simultaneously protects against chemotherapy-induced nerve damage.
Location: ABCC2. Chromosome 10 · 10q24.2 · 99.9 Mb
Estimated prevalence by population
Global 84.4%; European 88.9%; African 70.8%; East Asian 99.8%; South Asian 95.9%; Americas 86.4%; Ashkenazi 77.0%; Finnish 95.6%; Middle Eastern 67.2%; Amish 93.5%.
Estimated GG genotype frequency.
Global 14.7%; European 10.8%; African 26.7%; East Asian 0.2%; South Asian 4.1%; Americas 13.1%; Ashkenazi 21.5%; Finnish 4.4%; Middle Eastern 29.6%; Amish 6.4%.
Estimated GA genotype frequency.
Global 0.9%; European 0.3%; African 2.5%; East Asian < 0.1%; South Asian < 0.1%; Americas 0.5%; Ashkenazi 1.5%; Finnish 0.1%; Middle Eastern 3.3%; Amish 0.1%.
Estimated AA genotype frequency.
Showing effects for G/G genotype
Pharmacogenomics
Chemotherapy Response
Chemotherapy Heart Damage. Evidence: 6/10. Source: PMID 16330681. Typical Risk.
Chemotherapy Neuropathy. Evidence: 5/10. Source: PMID 24599932. Typical Risk.
Antimicrobial & Antiviral Response
HIV Drug Accumulation. Evidence: 3/10. Source: PMID 19842932. Typical Levels.
Organ Systems
Liver Function & Disease
Fatty Liver Disease. Evidence: 3/10. Source: PMID 18926681. Typical Risk.
Showing effects for A/A genotype
Chemotherapy Heart Damage. Evidence: 6/10. Source: PMID 16330681. Increased Risk.
Chemotherapy Neuropathy. Evidence: 5/10. Source: PMID 24599932. Decreased Risk.
HIV Drug Accumulation. Evidence: 3/10. Source: PMID 19842932. Higher Accumulation.
Fatty Liver Disease. Evidence: 3/10. Source: PMID 18926681. ~2.8x Increased Risk.
Showing effects for G/A genotype
What this genotype means for the people who carry it
Sample genotype: GG (Homozygous)
Normal, fully functional ATPase activity is maintained in the ABCC2 transporter when two copies of the common G allele are present [1]. During chemotherapy with anthracyclines like doxorubicin, this normal activity helps efficiently pump the drug out of cardiac cells, maintaining a typical baseline risk of cardiotoxicity [2]. Similarly, normal transport of organic anions in the liver helps protect against lipid accumulation, keeping the risk of nonalcoholic fatty liver disease at typical levels [3]. However, this genotype does not receive the protective effect against taxane-induced neuropathy seen in carriers of the variant allele [4].
Typical risk of doxorubicin-induced cardiotoxicity; Standard baseline risk of nonalcoholic fatty liver disease.
Sample genotype: AA (Homozygous)
Impaired ATPase activity occurs in all ABCC2 transporters when two copies of the A allele are present, leading to a pronounced defect in cellular efflux [1]. During treatment with anthracyclines like doxorubicin, this severe transport deficiency allows the drug to accumulate inside heart cells, significantly raising the risk of cardiotoxicity [2]. This genotype is also strongly linked to susceptibility to nonalcoholic fatty liver disease, with studies suggesting a nearly threefold increase in risk [3]. Conversely, this impaired transport appears to offer protection against taxane-induced peripheral neuropathy, lowering the risk of nerve damage during treatment [4].
Highest risk of doxorubicin-induced cardiotoxicity; Significantly higher susceptibility to nonalcoholic fatty liver disease; Decreased risk of taxane-induced neuropathy.
Sample genotype: GA (Heterozygous)
Reduced drug efflux capacity occurs because carrying one copy of the A allele results in a mixture of normal and partially dysfunctional ABCC2 transporters [1]. When treated with anthracycline chemotherapies such as doxorubicin, this reduced clearance can lead to drug accumulation in cardiac tissue, increasing the likelihood of heart damage [2]. This genotype is also associated with an estimated 2.8-fold increased risk of developing nonalcoholic fatty liver disease due to altered transport of hepatic lipids and organic anions [3]. On the positive side, carriers of this variant show a decreased likelihood of developing sensory neuropathy when treated with taxane-based chemotherapies [4].
Increased risk of doxorubicin-induced cardiotoxicity; Higher susceptibility to nonalcoholic fatty liver disease; Decreased risk of taxane-induced neuropathy.
Variants with shared genetic architecture
rs3740066 · ABCC2 Gene · Chr 10 · Pregnancy Liver Health
rs717620 · ABCC2 Gene · Chr 10 · Medication Response
rs2273697 · ABCC2 Gene · Chr 10 · Carbamazepine Side Effects
Content updated August 2026.
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