Lin H-Y., Huang P-Y., Cheng C-H., Tung H-Y., Fang Z., Berglund AE., Chen A., French-Kwawu J., Harris D., Pow-Sang J., Yamoah K., Cleveland JL., Awasthi S., Rounbehler RJ., Gerke T., Dhillon J., Eeles R., Kote-Jarai Z., Muir K., UKGPCS collaborators None., Schleutker J., Pashayan N., APCB (Australian Prostate Cancer BioResource) None., Neal DE., Nielsen SF., Nordestgaard BG., Gronberg H., Wiklund F., Giles GG., Haiman CA., Travis RC., Stanford JL., Kibel AS., Cybulski C., Khaw K-T., Maier C., Thibodeau SN., Teixeira MR., Cannon-Albright L., Brenner H., Kaneva R., Pandha H., PRACTICAL consortium None., Srinivasan S., Clements J., Batra J., Park JY.

Risk classification for prostate cancer (PCa) aggressiveness and underlying mechanisms remain inadequate. Interactions between single nucleotide polymorphisms (SNPs) may provide a solution to fill these gaps. To identify SNP-SNP interactions in the four pathways (the angiogenesis-, mitochondria-, miRNA-, and androgen metabolism-related pathways) associated with PCa aggressiveness, we tested 8587 SNPs for 20,729 cases from the PCa consortium. We identified 3 KLK3 SNPs, and 1083 (P

KLK3 SNP-SNP interactions for prediction of prostate cancer aggressiveness.

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