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. Author manuscript; available in PMC: 2023 Jun 1.
Published in final edited form as: J Mol Cell Cardiol. 2022 Mar 28;167:85–91. doi: 10.1016/j.yjmcc.2022.03.010

Table 1.

Common genetic variants that are associated with risk of cancer therapy-induced cardiotoxicity

Proposed mechanism Gene Reference SNP ID Odds ratio p-value
Drug transport ABCB1 rs1045642 [34] 0.48 0.049
ABCB4 rs1149222 [33] 1.87 0.005
ABCC1 rs246221 [30] 1.59 0.02
rs4148350 [33] 3.44 0.001
ABCC2 rs8187694 [31] 2.3 0.049
rs8187710 [32] 4.33 < 0.01
SLC10A2 rs9514091 [33] 0.43 0.003
SLC28A3 rs4877847 [33] 0.60 0.009
rs7853758 [33] 0.31 1.0 x 10e-4
SLC22A7 rs4149178 [36] 0.45 0.001
SLC22A17 rs4982753 [36] 0.50 4.4 x 10e-4
Drug metabolism CBR3 rs1056892 [39] 3.3 (G/G genotype) 0.006 (G/G genotype)
Oxidative stress response HAS3 rs2232228 [42] 5.2 (G/A genotype)
9.9 (A/A genotype)
0.007 (G/A genotype)
0.002 (A/A genotype)
GSTM1 N/A (Homozygous deletion) [44] 2.7 0.007
Iron metabolism HFE rs1799945 [51] 3.44 0.005
Topoisomerase-mediated DNA damage RARG rs2229774 [57] 4.7 5.9 x 10e-8
Splicing of a sarcomere gene CELF4 rs1786814 [60] 2.3 0.006