25nrwgu47
10.3205/25nrwgu47
urn:nbn:de:0183-25nrwgu475
Meeting Abstract
Integrated analysis of genetic polymorphism in the Cox-2 promoter and protein expression in urine samples from patients with cisplatin resistance
von Brandenstein
von Brandenstein
Melanie
M
Uniklinik Köln, Urologie, Köln, Deutschland
author
Storz
Storz
Enno
E
Uniklinik Köln, Urologie, Köln, Deutschland
author
Kessler
Kessler
Carolina
C
Uniklinik Köln, Urologie, Köln, Deutschland
author
Sperber
Sperber
Laurenz
L
Uniklinik Köln, Urologie, Köln, Deutschland
author
Gehle
Gehle
Paul
P
Uniklinik Köln, Urologie, Köln, Deutschland
author
Bouillon
Bouillon
Bianca
B
Uniklinik Köln, Urologie, Köln, Deutschland
author
Wirtz
Wirtz
Ralph
R
Stratifyer Molecular Pathology GmbH, Köln, Deutschland
author
Heidenreich
Heidenreich
Alex
A
Uniklinik Köln, Urologie, Köln, Deutschland
author
German Medical Science GMS Publishing House
Düsseldorf
610
20250402
engl
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung).
M0609
47
Nordrhein-Westfälische Gesellschaft für Urologie e.V.
70. Kongress der Nordrhein-Westfälischen Gesellschaft für Urologie
Posterbegehung II
Münster
20250403
20250404
P 2.4
TextIntroduction: A known target of the NFκB transcription factor complex is the promoter region of Cyclooxygenase 2 (Cox-2). Overexpression of Cox-2 is particularly associated with the development of cisplatin resistance. Mxi-2 forms a complex with the NFκB p65 subunit. It is now being investigated whether the overexpression of Cox-2 in cisplatin resistance is due to a base substitution in the NFκB binding region and whether Mxi-2 is involved in the overexpression of Cox-2.Materials and methods: DNA was isolated from urothelial carcinoma cell lines (RT4, HTB-9, T24(-R), TCCSUP(-R)) and analyzed for the T/G base exchange at the Cox-2 promoter using TaqMan SNP analysis. DNA was also isolated from urine samples from patients with cisplatin-sensitive (n=11) and -resistant bladder cancer (n=12) and analyzed using SNP analysis. The Mxi-2 ELISA was performed according to established standard protocols.Results: SNP analysis identified homozygous mutated type (G/G), heterozygous mutated type (T/G), or wild type (T/T) in the cell lines and urine samples used. The ELISA showed overexpression of Mxi-2 in patients with cisplatin-sensitive bladder cancer (OD Median 0.50 ± 0,029) vs cisplatin-resistant bladder cancer (OD Median 0.43 ± 0,078).Conclusion: The collected results suggest that predictive statements regarding the effectiveness of cisplatin-containing therapy may be possible by determining the polymorphism in the NFκB binding site of the Cox-2 promoter in combination with patient Mxi-2 level. Patients with low Mxi-2 levels and a heterozygous or homozygous mutated type should undergo close imaging controls during neoadjuvant chemotherapy.
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