期刊
NATURE GENETICS
卷 41, 期 7, 页码 811-U65出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ng.393
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资金
- NCI NIH HHS [R01 CA085914-07, P30 CA006927-41, R01 CA085914-04, R01 CA085914-06, R01 CA085914, R01 CA085914-05, R01 CA085914-10, R01 CA085914-09, R01 CA085914-03, R01 CA085914-02S1, R01 CA114478-01A2, P30 CA006927, R01 CA085914-02, R01 CA085914-08, R01 CA114478, R01 CA085914-01] Funding Source: Medline
- NIEHS NIH HHS [P30 ES007033, P30 ES007033-15] Funding Source: Medline
Testicular germ cell tumors (TGCT) have been expected to have a strong underlying genetic component. We conducted a genome-wide scan among 277 TGCT cases and 919 controls and found that seven markers at 12p22 within KITLG (c-KIT ligand) reached genome-wide significance (P < 5.0 x 10 (-8) in discovery). In independent replication, TGCT risk was increased threefold per copy of the major allele at rs3782179 and rs4474514 (OR = 3.08, 95% CI = 2.29-4.13; OR = 3.07, 95% CI 2.29-4.13, respectively). We found associations with rs4324715 and rs6897876 at 5q31.3 near SPRY4 (sprouty 4; P < 5.0 x 10(-6) in discovery). In independent replication, risk of TGCT was increased nearly 40% per copy of the major allele (OR = 1.37, 95% CI = 1.14-1.64; OR = 1.39, 95% CI = 1.16-1.66, respectively). All of the genotypes were associated with both seminoma and nonseminoma TGCT subtypes. These results demonstrate that common genetic variants affect TGCT risk and implicate KITLG and SPRY4 as genes involved in TGCT susceptibility.
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