Abstract
ERCC1 is a key regulator of nucleotide excision repair (NER) pathway that repairs bulky DNA adducts, including intrastrand DNA adducts and interstrand crosslinks (ICLs). Overexpression of ERCC1 has been linked to increased DNA repair capacity and platinum resistance in solid tumors. Multiple single nucleotide polymorphisms (SNPs) have been detected in ERCC1 gene that may affect ERCC1 protein expression. Platinum-based treatment remains the cornerstone of urothelial cancer treatment. Given the expanding application of neoadjuvant and adjuvant chemotherapy in locally advanced bladder cancer, there is an emerging need for biomarkers that could distinguish potential responders to cisplatin treatment. Extensive research has been done regarding the prognostic and predictive role of ERCC1 gene expression and polymorphisms in bladder cancer. Moreover, novel compounds have been recently developed to target ERCC1 protein function in order to maximize sensitivity to cisplatin. We aim to review all the existing literature regarding the role of the ERCC1 gene in bladder cancer and address future perspectives for its clinical application.
Highlights
Worldwide, urothelial cancer is the 10th most common malignancy in both sexes accounting for 3% of all new cancer cases [1]
We aim to review all the existing literature regarding the role of the Excision repair cross-complementing 1 (ERCC1) gene in bladder cancer and address future perspectives for its clinical application
We review all existing data regarding the clinical application of ERCC1 and other repair genes in urothelial cancer
Summary
Urothelial cancer is the 10th most common malignancy in both sexes accounting for 3% of all new cancer cases [1]. 5-year survival rate does not exceed 70% for muscle-invasive bladder cancer (MIBC) and 5% for metastatic disease in the US [2]. Invasion of the detrusor muscle of the bladder constitutes a major contributor to disease prognosis, as 5-year survival rates reach 96% in the non-invasive population [2]. 20% of patients will present with MIBC, while 15–20% of non-muscle-invasive bladder cancer (NMIBC) will eventually expand to the muscle layer [3]. In case of muscle invasion, radical cystectomy (RC) and pelvic lymph node dissection remain the cornerstone of treatment. Cisplatin-based adjuvant chemotherapy remains a controversial issue that should be personalised in high-risk MIBC patients with extravesical or node-positive disease or positive margins [3,4,5]. As for locally advanced or metastatic disease, platinum-based treatment regimens remain the gold-standard of treatment
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