Receptor Tyrosine Kinase Pathway and Infiltrating Urothelial Carcinoma

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dc.contributor.authorBüyücek, Şeyma
dc.contributor.authorCoşkun, Sinem Kantarcıoğlu
dc.contributor.authorÖnal, Binnur
dc.contributor.authorGamsızkan, Mehmet
dc.contributor.authorCangür, Şengül
dc.contributor.authorEsbah, Onur
dc.date.accessioned2023-07-26T11:51:17Z
dc.date.available2023-07-26T11:51:17Z
dc.date.issued2023
dc.departmentDÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümü, Tıbbi Patoloji Ana Bilim Dalıen_US
dc.description.abstractReceptor tyrosine kinase pathway is frequently searched for cancer causing mutations in tumors. Emerg-ing targeted therapies are gleam of hope for them. Infiltrating urothelial carcinoma can have many morphological aspects according to their differentiation/variants. To evaluate KRAS, BRAF, and PIK3CA mutations and HER2, EGFR, and p16 expression, we divided urothelial carcinomas into two groups: differentiated/variants (n = 12) and conventional (n = 12). We compared results with clinical, demographic, histopathologic features and survival rates. No statistically sig-nificant results could be obtained in the comparison of histopathologic properties/survival rates with mutation analysis and EGFR, HER2, and p16 status. Differentiated/variants urothelial carcinoma showed higher EGFR expression (P < 0.001). Glandular differentiation was the most frequent type, followed by squamous and sarcomatoid differentiation. We observed the most common mutation at KRAS with a propensity for urothelial carcinoma with glandular differentiation. More than one mutation/high protein expression was seen in some tumors. Targeted therapies for KRAS mutation can be effective at urothelial carcinoma with glandular differentiation. Heterologous expression of relevant proteins and genes can be a cause for targeted treatment obstacle. The determination of the molecular characters of tumors is a guide in creating targeted treatment algorithms and in choosing the patient.en_US
dc.identifier.endpage77en_US
dc.identifier.issn0731-8898
dc.identifier.issn2162-6537
dc.identifier.issue1en_US
dc.identifier.pmid36734953en_US
dc.identifier.scopus2-s2.0-85142304623en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage65en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12684/12532
dc.identifier.volume42en_US
dc.identifier.wosWOS:000915067100005en_US
dc.identifier.wosqualityQ3en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorBüyücek, Şeyma
dc.institutionauthorCoşkun, Sinem Kantarcıoğlu
dc.institutionauthorÖnal, Binnur
dc.institutionauthorGamsızkan, Mehmet
dc.institutionauthorCangür, Şengül
dc.institutionauthorEşbah, Onur
dc.language.isoenen_US
dc.publisherBegell House Incen_US
dc.relation.ispartofJournal of Environmental Pathology Toxicology and Oncologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz$2023V1Guncelleme$en_US
dc.subjectInfiltrating Urothelial Carcinoma; Receptor Tyrosine Kinase Pathway; Signal Transduction; Molecular Pathologyen_US
dc.subjectBladder-Cancer; 3-Kinase Pathway; Expression; Gene; Activation; Mutations; Variants; Pik3ca; Fgfr3; Krasen_US
dc.titleReceptor Tyrosine Kinase Pathway and Infiltrating Urothelial Carcinomaen_US
dc.typeArticleen_US

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