It was with great interest that we read the article concerning the impact of biomarkers in multivariate algorithms for the diagnosis of bladder cancer in patients with hematuria by Abogunrin et al.1 In this fascinating and well-done study, the authors concluded that biomarkers can significantly improve the receiver operating characteristic statistic based on demographics.1 Moreover, they highlighted that benign prostatic hyperplasia is a significant confounding pathology and that the identification of non–muscle-invasive urothelial cancer remains a challenge.1 In our previous studies, we investigated the role of loss of heterozygosity (LOH) on 10 sequences located on chromosomes 4, 9, 16, and 18 for the detection of urothelial cell carcinoma of the urinary bladder.2, 3 We enrolled patients diagnosed with urothelial bladder cell carcinoma and patients diagnosed with nononcological diseases as the control group.3 The majority of patients in the control group were affected by benign prostatic hyperplasia. Test sensitivity and specificity were 80.8% and 85.1%, respectively.3 In particular, 78.5% of those patients with benign prostatic hyperplasia were found to have no alteration on the LOH analysis, demonstrating that this test might be useful for screening populations and monitoring patients with associated urological or nonurological diseases.3 Several authors, moreover, have reported that LOH analysis could improve the standard diagnostic accuracy of urine cytology for the detection of bladder cancer.4 Furthermore, Seripa et al clearly found that none of the patients without evidence of bladder cancer demonstrated LOH and/or microsatellite instability in urine samples, indicating that microsatellite marker analysis is more sensitive than conventional urine cytology in detecting bladder cancer cells in urine and represents a potential clinical tool for monitoring patients with urothelial bladder cancer.5 From this background, we pose 2 questions: can the microsatellite analysis improve the diagnostic accuracy of the algorithm by decreasing the number of patients with false-positive results (benign prostatic hyperplasia)? Moreover, why were men with both non–muscle-invasive and muscle-invasive bladder cancer enrolled? It is well known that muscle-invasive bladder cancer often demonstrates different molecular pathways of development and progression from non–muscle-invasive forms.
CONFLICT OF INTEREST DISCLOSURES
The authors made no disclosures.