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Aims: Bladder cancer-specific nuclear matrix protein-4 (BLCA-4) is a protein expressed mainly in bladder cancer tissues. Therefore, the aim of this study was to investigate its assisting diagnostic potential in non-muscle-invasive bladder cancer (NMIBC).
Methods: Twenty patients with NMIBC, 20 with benign prostatic hyperplasia (BPH), and 20 normal controls were included in this study. Blood and urine samples were collected from all patients. Moreover, cancer foci and adjacent tissue samples were collected from NMIBC patients, and normal bladder tissue samples were collected from patients with BPH. A competitive enzyme-linked immunosorbent assay was used to determine the BLCA-4 level in serum and urine, and immunohistochemistry was used to examine BLCA-4 expression in bladder cancer, adjacent, and normal tissues.
Results: Median urinary BLCA-4 levels in the NMIBC, BPH, and normal control groups were 0.759 ng/mL, 0.309 ng/mL, and 0.171 ng/mL, respectively. Urinary BLCA-4 level was significantly higher in the NMIBC group than in the other 2 groups ( < 0.01); meanwhile, the BPH group was higher than the normal control group ( < 0.05). Median serum BLCA-4 levels in the NMIBC, BPH, and normal control groups were 5.680 ng/mL, 5.928 ng/mL, and 5.473 ng/mL, respectively, showing no significant difference among groups ( > 0.05).
Conclusion: As a new marker of bladder cancer, urinary BLCA-4 level detection might apply for clinical diagnosis or postoperative monitoring for NMIBC.
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http://dx.doi.org/10.1155/2018/5609395 | DOI Listing |
Future Oncol
September 2025
Department of General Surgery, Institute of General Surgery, Northern Jiangsu People's Hospital Affiliated to Yangzhou University, Yangzhou University, Yangzhou, China.
Immune checkpoint therapy has demonstrated significant potential in the treatment of various solid tumors. Among these, tumor-induced immunosuppression mediated by programmed cell death protein 1 (PD-1) represents a critical checkpoint. PD-1/programmed death-ligand 1 (PD-L1) inhibitors have been proven to exhibit substantial efficacy in solid tumors such as melanoma and bladder cancer.
View Article and Find Full Text PDFFuture Cardiol
September 2025
Department of Internal Medicine, Valley Health System Graduate Medical Education, Las Vegas, NV, USA.
A 71-year-old black male with a history of hypertension, dyslipidemia, type 2 diabetes, history of bladder cancer status-post resection now in remission, history of multiple transient ischemic attacks, and coronary artery disease (CAD) presented with non-exertional substernal chest pain radiating to the left arm, accompanied by shortness of breath and nausea. Initial evaluation revealed elevated troponins and nonspecific electrocardiogram changes, consistent with non-ST elevation myocardial infarction. Coronary angiography demonstrated severe multivessel disease, including critical left main stenosis.
View Article and Find Full Text PDFNat Rev Urol
September 2025
Department of Genitourinary Oncology, H. Lee Moffitt Cancer Center and Research Institute, Tampa, FL, USA.
Low-grade non-muscle invasive bladder cancer is a specific category of bladder cancer with a favourable prognosis; however, its management presents several challenges. The risk of stage progression is very low, but approximately half of patients will experience recurrence within the first 5 years after diagnosis. This high propensity for recurrence, coupled with the threat of progression, mandates ongoing surveillance.
View Article and Find Full Text PDFNat Commun
September 2025
Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, USA.
With the approval of the antibody-drug conjugate enfortumab vedotin (EV), NECTIN4 has emerged as a bona fide therapeutic target in urothelial carcinoma (UC). Here, we report the development of a NECTIN4-directed chimeric antigen receptor (CAR) T cell, which exhibits reactivity across cells expressing a range of endogenous NECTIN4, with enhanced activity in high expressors. We demonstrate that the PPARγ pathway, critical for luminal differentiation, transcriptionally controls NECTIN4, and that the PPARγ agonist rosiglitazone primes and augments NECTIN4 expression, thereby increasing sensitivity to NECTIN4-CAR T cell-mediated killing.
View Article and Find Full Text PDFUrol Oncol
September 2025
Nutritional, Genes and Human Disease Laboratory, Department of Biochemistry and Molecular Biology, University of Dhaka, Dhaka, Bangladesh. Electronic address:
Background: Understanding the mutational landscape is critical for elucidating the molecular mechanisms driving cancer progression. This study aimed to profile somatic mutations in bladder cancer patients (N=7) from Bangladesh to provide insights into the genetic alterations underlying this malignancy.
Methods: We performed targeted sequencing of 50 oncogenes and tumor suppressor genes using the Ion AmpliSeq Cancer Hotspot Panel v2 on tumor and matched blood samples from seven bladder cancer patients.