Author/Authors :
Najjar Sadeghi, Rouhallah shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Azimzadeh, Pedram shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Vahedi, Mohsen shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Molaei, Mahsa shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Mohebbi, Reza shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Zojaji, Homayon shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Fatemi, Reza shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران , Zali, Mohammad Reza shahid beheshti university of medical sciences - Research Institute for Gastroenterology and Liver Disease, تهران, ايران
Abstract :
Aim: The purpose of this study was to assess the incidence of 16bp insertion of intron 3 p53 in gastritis lesion and its correlation with clinicopathological aspects. Background: p53 alterations have been implicated in the development of gastric malignancies. Patients and methods: 97 gastritis and normal adjacent tissues were investigated for p53 gene analysis using PCR—sequencing of intron3 and immunohisthochemistry technique. Results: All of samples express p53 protein. In addition 64.9% of patients had no insertion and 7.2% had homozygous insertion while the others were heterozygous. This alteration has no association with clinicopathological findings. Conclusion: Most of our patients had no insertion but an insertion frequency obtained here was found to be higher than those reports in a previous work on colorectal and esophageal cancer. It is possible that the polymorphism has correlation with gastritis and maybe with gastric cancer development. If so, this alteration associates with as yet unknown molecular and /or clinical factors which are involved in the (dys) regulation of p53 expression and function, and exerts its effects during gastritis development through them.
