Abstract
The high occurrence of bladder cancer and its tendency to recur in combination with a lifelong surveillance make the treatment of superficial bladder cancer one of the most expensive and time-consuming. Moreover, carcinoma in situ often leads to muscle invasion with an unfavorable prognosis. Currently, invasive methods including cystoscopy and cytology remain a gold standard. The aim of this study was to explore urine-based biomarkers to find the one with the best specificity and sensitivity, which would allow optimizing the treatment plan. In this review, we sum up the current knowledge about Cytokeratin fragments (CYFRA 21.1), Excision Repair Cross-Complementation 1 (ERCC1), Tumour Protein p53 (Tp53), Fibroblast Growth Factor Receptor 3 (FGFR3), Tumor-Associated Trypsin Inhibitor (TATI) and their potential applications in clinical practice.
Highlights
Bladder Cancer Issues and BiomarkersBladder cancer is the most common urinary site of malignancy and the second most common reason of cancer deaths from the genitourinary tract after prostate cancer in the United States, with 81,400 new cases and 17,980 deaths in the year 2020 [1]
Similar conclusions were made in Hemdan's report. They evaluated a group of 244 patients who underwent radical cystectomy or neoadjuvant chemotherapy and radical cystectomy
Negative Excision Repair Cross-Complementation 1 (ERCC1) correlated with a worse overall survival in the group with only surgical treatment
Summary
Bladder cancer is the most common urinary site of malignancy and the second most common reason of cancer deaths from the genitourinary tract after prostate cancer in the United States, with 81,400 new cases and 17,980 deaths in the year 2020 [1]. There are about 430,000 new cases diagnosed each year [2]. Non-invasive lesions constitute approximately 75–80% of newly diagnosed urothelial bladder cancers (UBC). More than 50% of UBCs are caused by smoking. Other important factors include occupational exposure to aromatic amines and polycyclic hydrocarbons. Less evident is the impact of diet and environmental pollution. Increasing data indicate that genetic predisposition plays a role in UBC pathogenesis [2,3,4]
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