Role of matrix metalloproteinase-7 in colorectal adenomas.


Kirimlioglu H., Kirimlioglu V., Yilmaz S., Sagir V., Coban S., Turkmen E., ...Daha Fazla

Digestive diseases and sciences, cilt.51, sa.11, ss.2068-72, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 51 Sayı: 11
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1007/s10620-005-9070-4
  • Dergi Adı: Digestive diseases and sciences
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.2068-72
  • Anahtar Kelimeler: colon, adenoma, matrix metalloproteinase-7, immunohistochemistry, BETA-CATENIN, COLON-CANCER, EXPRESSION, MATRILYSIN, CARCINOMA, TUMORIGENESIS, PROGRESSION, ACTIVATION
  • İnönü Üniversitesi Adresli: Evet

Özet

Matrix metalloproteinases (MMPs) degregade and remodel the extracellular matrix. They are known to be overexpressed as normal mucosa progresses to adenomas and carcinomas. In our prospective study we measured the overexpression of MMP-7 immunohistochemically in various types of colonic adenomas. Although MMP-7 has already been shown to be overexpressed in various types of colonic adenomas, tubular versus villous adenomas had not been further seperated to date. Seventy-six patients had either normal mucosa (n=15) or tubular (n=32), tubulovillous (n=16), or villous (n=13) colonic adenoma. MMP-7 expression was classified into three categories, as negative, weakly stained, or strongly stained, depending on the percentage of cells stained. Each adenoma was graded according to the percentage of strongly stained areas in the adenoma as G0, G1, G2, or G3. Sixty-nine percent of villous adenomas showed grade 3 staining of MMP-7, versus none of the tubular adenomas. G0 and G1 staining was not detected in the villous adenomas. The results of the study show that the degrees of overexpression of the three subtypes of colonic adenomas were statistically significantly different. In conclusion, MMP-7 overexpression is thought to be an early event in the adenoma-carcinoma pathway.