Recent studies reported that rs2252004 at 10q26 was significantly associated with prostate cancer (PCa) risk in a Japanese population and was subsequently confirmed in a Chinese population. We aimed to assess the relationship between this locus and risk/aggressiveness of benign prostatic hyperplasia (BPH). The current study included 426 BPH cases and 1,008 controls from Xinhua Hospital in Shanghai, China. All BPH patients were treated with α-adrenergic blockers and 5α-reductase inhibitors for at least 9 months. Associations between rs2252004 and BPH risk/aggressiveness were tested using logistic regression. Associations between rs2252004 and clinical parameters including International Prostate Symptom Score (IPSS), total prostate volume (TPV), total PSA (tPSA), and free PSA (fPSA) were evaluated by linear regression. Allele “A” in rs2252004 was significantly associated with increased risk for aggressiveness of BPH in a Chinese population (OR？=？1.42, 95% CI: 1.04–1.96, ). Patients with the genotype “A/A” (homozygous minor allele) had an increase of IPSS and TPV after treatment ( and 0.024, resp.). No association was observed between rs2252004, BPH risk, and baseline clinicopathological traits (All ). Our study is the first to show that rs2252004 at 10q26 was associated with BPH aggressiveness and efficacy of BPH treatment. 1. Introduction Benign prostate hyperplasia (BPH) is an independent disease with clinical symptoms similar to those of carcinoma of the prostrate (PCa), and the prevalence of histologically identifiable BPH is >50% for 60-year-old men and ~90% by age 85 years [1]. While symptomatic BPH is not life threatening, it has a severe impact on the quality of life and requires immediate therapeutic interventions. While studies have shown that BPH causes significant morbidity, the etiology and determinants of severity of this condition remain poorly understood. According to epidemiological studies, 83.3% of PCa are associated with BPH, and 3–20% of patients who have undergone transurethral prostatectomy (TURP) or open prostatectomy for BPH subsequently develop PCa [2]. Although BPH is not considered to be a premalignant lesion or a precursor of PCa, studies have observed anatomic, pathologic, and epidemiological associations and genetic links between PCa and BPH [3]. Over 40 SNPs have been reported to contribute to PCa risk in different ethnicities [4–6]. Fifteen of these SNPs were associated with PCa risk in a Chinese population [7, 8]. The relationship between these SNPs and BPH was recently studied [9, 10]. Three SNPs: rs103294 at LILRA3,
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