Kasa invaze mesane kanserinde sigara kullanım miktarının kanser kök hücre özelliklerine etkisi
Küçük Resim Yok
Tarih
2023
Yazarlar
Dergi Başlığı
Dergi ISSN
Cilt Başlığı
Yayıncı
Trakya Üniversitesi
Erişim Hakkı
info:eu-repo/semantics/openAccess
Özet
Mesane kanseri dünyada en sık teşhis edilen onuncu kanser türüdür. Mesane kanseri tanısı alan hastaların yaklaşık %20'si tanı anında kasa invazedir. Kasa invaze mesane kanseri daha ileri evre ve uzak organ metastazı ile ilişkili olup radikal sistektomi, kemoterapi ve radyoterapi gibi daha agresif tedaviler uygulanmaktadır. Mesane kanserinde sigara kullanımı bilinen ispatlanmış en yaygın risk faktörüdür. Sigaranın mesane mukozasında DNA hasarı oluşturarak tamir mekanizmasında bozukluğa neden olduğu, ayrıca büyüme faktörlerinin de aşırı uyarılıp apoptozu baskılayarak mesanede kanser oluşumunu tetiklediği düşünülmektedir. Sigara kullanımının solid organ kanserlerinde kanser kök hücrelerini uyardığı ve epitelyal mezenkimal dönüşümü tetiklediği düşünülmektedir. Çalışmamızda uygun kriterlere sahip 40 hastayı 30 paket/yıldan az ve fazla sigara kullanımı öyküsüne göre 20 hastadan oluşan iki gruba ayırdık. Bu hastaların parafine gömülü kasa invaze mesane kanseri dokuları kullanılarak doku deparafinizasyonu ve total RNA izolasyonu yapıldı. Elde edilen total RNA'dan komplementer DNA sentezlendi ve gerçek zamanlı polimeraz zincir reaksiyonu ile kanser kök hücre belirteçleri olan CD44, CD133, ALDH1, NANOG, SOX2, OCT 3/4, vimentin, fibronektin, okludin, E-kaderin, N-kaderin, MMP2 ve MMP9'un mRNA düzeyinde gen ifade oranları karşılaştırdık. Sigara kullanım miktarının artmasının CD44, CD133, ALDH1, OCT 3/4, NANOG, N-kaderin, vimentin, fibronektin ve okludinin mRNA düzeyinde ifadesini arttırdığı tespit edildi. Sonuç olarak bu çalışma ile sigara kullanım miktarının kasa invaze mesane kanserinde kanser kök hücrelerininin köklülüğünü etkilediği, kanser kök hücre yüzey membran belirteçleri ve transkripsiyon faktörlerinin mRNA düzeyinde ifadesini arttırdığı ve EMT mekanizmasını etkileyerek mesane kanserinin daha agresif ve metastaza yatkın hale getirdiği görüldü. Anahtar kelimeler: Mesane Kanseri, Sigara, Kanser Kök Hücresi, Epitelyal Mezenkimal Geçiş
Bladder cancer is the tenth most commonly diagnosed cancer type in the world. Approximately 20% of the patients diagnosed are muscle invasive at the time of diagnosis. Muscle invasive bladder cancer is associated with more advanced and distant organ metastases and is treated with radical cystectomy, chemotherapy and more aggressive treatments such as radiotherapy. Smoking in bladder cancer is the most common known proven risk factor. DNA damage in the bladder mucosa from smoking causes a malfunction in the repair mechanism, and growth factors are thought to trigger cancer formation in the bladder by overstimulating and suppressing apoptosis. Cigarette smoking stimulates cancer stem cells in solid organ cancers and is thought to trigger epithelial-mesenchymal transformation. In our study, 40 patients investigated with the appropriate criteria were smoking less than 30 packs/year or more. We divided into two groups of 20 patients according to their history of use. These patients were embedded in paraffin. Tissue deparaffinization and the using muscle-invasive bladder cancer tissues total RNA isolation was done. Complementary DNA was synthesized from the total RNA with a real-time polymerase chain reaction. We compared the expression rates of cancer stem cell markers; CD44, CD133, ALDH1, NANOG, SOX2, OCT 3/4, vimentin, fibronectin, occludin, E-cadherin, N-cadherin, MMP2 and MMP9 at the mRNA level. It was determined that the amount of cigarette smoking increased the expression of CD44, CD133, ALDH1, OCT 3/4, NANOG, N-cadherin, vimentin, fibronectin, and occludin at the mRNA level. As a result, in this study, the amount of cigarette smoking in muscle-invasive bladder cancer increases the steamless and It was seen that the amount of cigarette smoking affecting bladder cancer to become more aggressive and prone to metastasis by increasing the expression of transcription factors and cancer stem cell surface membrane markers at the mRNA level and affecting the EMT mechanism. Keywords: Bladder Cancer, Smoking, Cancer Stem Cell, Epithelial Mesenchymal Transition
Bladder cancer is the tenth most commonly diagnosed cancer type in the world. Approximately 20% of the patients diagnosed are muscle invasive at the time of diagnosis. Muscle invasive bladder cancer is associated with more advanced and distant organ metastases and is treated with radical cystectomy, chemotherapy and more aggressive treatments such as radiotherapy. Smoking in bladder cancer is the most common known proven risk factor. DNA damage in the bladder mucosa from smoking causes a malfunction in the repair mechanism, and growth factors are thought to trigger cancer formation in the bladder by overstimulating and suppressing apoptosis. Cigarette smoking stimulates cancer stem cells in solid organ cancers and is thought to trigger epithelial-mesenchymal transformation. In our study, 40 patients investigated with the appropriate criteria were smoking less than 30 packs/year or more. We divided into two groups of 20 patients according to their history of use. These patients were embedded in paraffin. Tissue deparaffinization and the using muscle-invasive bladder cancer tissues total RNA isolation was done. Complementary DNA was synthesized from the total RNA with a real-time polymerase chain reaction. We compared the expression rates of cancer stem cell markers; CD44, CD133, ALDH1, NANOG, SOX2, OCT 3/4, vimentin, fibronectin, occludin, E-cadherin, N-cadherin, MMP2 and MMP9 at the mRNA level. It was determined that the amount of cigarette smoking increased the expression of CD44, CD133, ALDH1, OCT 3/4, NANOG, N-cadherin, vimentin, fibronectin, and occludin at the mRNA level. As a result, in this study, the amount of cigarette smoking in muscle-invasive bladder cancer increases the steamless and It was seen that the amount of cigarette smoking affecting bladder cancer to become more aggressive and prone to metastasis by increasing the expression of transcription factors and cancer stem cell surface membrane markers at the mRNA level and affecting the EMT mechanism. Keywords: Bladder Cancer, Smoking, Cancer Stem Cell, Epithelial Mesenchymal Transition
Açıklama
Tıpta Uzmanlık
Anahtar Kelimeler
Üroloji, Urology
