Abstract
INTRODUCTION: Gastric cancer develops in a multistep progression and is determined by genetic and environmental factors. Over-expression of Alpha Methylacyl CoA Racemase (AMACR) is useful in diagnosis of prostate cancer. There is plenty of genetic alteration that occurs in gastric adenocarcinoma. The present study was planned to determine if AMACR can be used as a diagnostic marker in gastric adenocarcinoma similar to prostate cancer. AIM: To study the expression of AMACR in gastric adenocarcinoma and correlate its expression with density of Helicobacter pylori. MATERIALS AND METHODS: This cross-sectional, prospective study was conducted from August 2013-2015. Fifty gastric cancer biopsies were taken. Adjacent biopsy from normal/reactive mucosa was also taken from 21 cases. Samples were stained with H&E for morphological details, Loeffler's methylene blue for Helicobacter pylori and immunohistochemistry (IHC) was done to check for the expression of AMACR proteins. Statistical analysis was done using chi square test, Spearman's correlation coefficient and Fisher's exact test. The p-value ≤ 0.05 was taken as critical level of significance. RESULTS: Overexpression of AMACR was observed in 88.89% of intestinal type and 78.05% of diffuse type adenocarcinoma. AMACR expression was significantly less in adjacent reactive/dysplastic mucosa. Helicobacter pylori were seen in 8/9 (88.89%) and 35/41(85.36%) cases of intestinal adenocarcinoma and diffuse adenocarcinoma respectively. When grades of Helicobacter pylori were compared with the positivity of AMACR, no significant association and correlation was found. CONCLUSION: The expression of AMACR in neoplastic tissue was significantly higher as compared to adjacent dysplastic, reactive or normal tissue. Thus, IHC for AMACR can be used for differentiating the cases of reactive atypia from early neoplastic lesions similar to its role in prostatic tissue. Helicobacter pylori does not affect the expression of AMACR in neoplastic gastric lesions.