rs11932853: what the research says
This variant demonstrates an effect in the same direction as previously identified GWAS hits for trastuzumab-induced cardiotoxicity.
What each genotype means
Baseline risk profile
This genotype represents the common state for this variant in many populations. Research has identified this variant as a potential marker for trastuzumab-induced cardiotoxicity, but it is not a diagnostic test. Please discuss your cardiac health and any planned cancer treatments with your oncologist or cardiologist to determine the best monitoring strategy for you.
This genotype is the most common form observed in the Japanese population studied in initial research.
Potential increased risk marker
This genotype has been associated with an increased statistical risk of developing cardiotoxicity during trastuzumab therapy in specific study populations. This finding is based on moderate evidence and does not guarantee that you will experience side effects. You should consult with your healthcare provider to review your personal risk factors and discuss appropriate cardiac surveillance during treatment.
This genotype is observed at a lower frequency than the homozygous baseline genotype in the populations where it has been studied.
Potential increased risk marker
This genotype has been associated with an increased statistical risk of developing cardiotoxicity during trastuzumab therapy in specific study populations. This finding is based on moderate evidence and does not guarantee that you will experience side effects. You should consult with your healthcare provider to review your personal risk factors and discuss appropriate cardiac surveillance during treatment.
This genotype is the least common of the three in the Japanese population cohorts where this variant was initially identified.
Unknown
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This variant is linked to decreased dihydropyrimidine dehydrogenase activity, increasing the risk of severe toxicity during fluoropyrimidine chemotherapy.
This SNP influences the expression levels of the CYP3A5 enzyme, impacting the clearance rates of tacrolimus.
This SNP is recognized as a modifier of inflammatory response, potentially affecting responses to anti-TNF therapies.
This variant is significantly correlated with patient outcomes and hematologic toxicity in cancer patients treated with gemcitabine-based chemotherapy.
This variant is associated with altered metabolism of various medications, including antidepressants and antipsychotics.
This variant is linked to the loss of function in the CYP2C19 enzyme, affecting clopidogrel efficacy.

