Pankreatik adenokarsinom ve pankreatik intraepitelyal neoplazilerde immunohistokimyasal olarak p53 ve Ki 67 ekspresyonunun değerlendirilmesi

Pankreatik duktal adenokarsinomlar (PDA), pankreatik intraepitelyal neoplaziler (PanIN) olarak isimlendirilen noninvaziv displastik intraduktal lezyonlardan köken almaktadır. Morfolojik ve genetik çalışmalar, PanIN'lerin PDA'ların prekürsörü olabileceğinin güçlü bir kanıtını oluşturmuştur. Çalışmada PDA tandı 21 hasta değerlendirildi. PanIN ve PDA içeren histolojik kesitler gözden geçirildi. PanIN lezyon-ları sayıldı, derecelendirildi ve lokalizasyonları değerlendirildi. İmmunohistokimyasal (İHK) olarak Kİ67 ve P53 eks-presyonu araştırıldı. Olgularda, PanIN lezyonlarının interlobuler lokalizasyonu (%58.20) intralobuler lokalizasyonuna göre (%41.80) daha belirgin olup, interlobuler duktuslardaki PanIN 2 ve 3 lezyonları intralobuler duktuslara göre daha fazla olduğu göz­lendi (p=0.0026 ve p=0.006). PanIN'lerde Kİ67 ve P53 ekspresyonu istatistiksel olarak daha düşük bulundu (p=0.0045 ve p=0.0002). Tümör supresör gen olan p53 protein ve proliferasyon belirleyicisi olan Kİ67, PanIN lezyonlarının progresyon göstere­rek invazyon potansiyeli kazanabileceği hipotezine ek bir yarar sağlayacaktır.

Evaluation of p53 and Ki67 expression immunohistochemically in pancreatic ductal adenocarcinoma and pancreatic intraepithelial neoplasias

Pancreatic ductal adenocarcinoma (PDA) is thought to arise from noninvasive dysplastic intraductal lesions, named pancreatic intraepithelial neoplasias (PanIN). Morphologic and genetic observations have provided strong evidence that PanlNs can be the precursors of PDA. We evaluated 21 patients with diagnosis of PDA. The histologic sections, harboring both PanIN and PDA were identified. PanIN lesions were counted, graded and their localization was evaluated. We examined also the expression of Kİ67 and p53, immunohistochemically. Interlobular location of PanIN lesions (58.20%) were more intense than intralobular location (41.80%). PanIN 2 and 3 within interlobular ducts were significantly higher than intralobular ducts (p=0.0026 ve p=0.006,respectively). P53 and Kİ67 expression in PanIN were lower than PDA, statistically (p=0.0045 ve p=0.0002, respectively). P53 tumor suppressor gene and Kİ67, proliferation marker in PanlNs can provide additional support for the hypothesis that these lesions represent progression with the potential for invasion

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Ege Tıp Dergisi-Cover
  • ISSN: 1016-9113
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 1962
  • Yayıncı: Ersin HACIOĞLU
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