ArticleAdvances in urology2026
Metabolic Profiling Reveals Insights Into Bladder Cancer Pathogenesis and Recurrence.
Article in Advances in urology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Metabolic Profiling Reveals Insights Into Bladder Cancer Pathogenesis and Recurrence.Advances in urology · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bladder cancer is characterized by abnormal cell proliferation within the bladder lining, yet the molecular mechanisms underlying its pathogenesis remain incompletely understood. This study aimed to identify metabolic differences between bladder cancer patients and healthy controls, as well as between patients with and without cancer recurrence, to elucidate the molecular mechanisms underlying disease progression and recurrence. A total of 102 participants were enrolled, comprising 82 individuals diagnosed with bladder cancer and 20 healthy controls. Based on cystoscopy and pathology findings, bladder cancer patients were further categorized into two groups: 29 with tumor recurrence and 41 without recurrence. Urinary metabolic profiling was conducted using ultra-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC/Q-TOF/MS). Data acquisition, classification, and metabolite identification were performed using Mass Profiler Professional and the XCMS online platform (https://xcmsonline.scripps.edu). Compared to healthy controls, patients exhibited downregulation of 11-hydroxyandrosterone and prostaglandin E2 (PGE2), while (±)12-hydroxyeicosatetraenoic acid ([±]12-HETE), 5α-dihydrodeoxycorticosterone, and 21-hydroxypregnenolone were upregulated. Notably, 11-hydroxyandrosterone was further downregulated in patients with recurrent disease compared to those without recurrence. The highest area under the curve (AUC) values for distinguishing bladder cancer and recurrence were observed for (±)12-HETE and PGE2. Elucidating the roles of steroid hormones and arachidonic acid metabolism in bladder cancer may provide critical insights into its molecular mechanisms and facilitate the development of novel therapeutic and diagnostic strategies to improve outcomes for patients.
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