Indian Journal of Pathology and Microbiology
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ORIGINAL ARTICLE
Year : 2015  |  Volume : 58  |  Issue : 2  |  Page : 154-157

Analysis of epithelial-cadherin and human epidermal growth factor receptor 2/ expression in gastric carcinoma using immunohistochemistry


Department of Pathology, Army Hospital Research and Referral, Delhi Cantt, New Delhi, India

Correspondence Address:
Dr. Khushboo Dewan
Department of Pathology, Army Hospital Research and Referral, Delhi Cantt, New Delhi
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0377-4929.155303

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Context: Gastric adenocarcinoma (GAC) is a common malignancy with high mortality-rate. Analysis of molecular markers could form a foundation for the future use of targeted therapies to reduce morbidity and mortality. Aims: To find the prevalence and relation of epithelial cadherin (E-cadherin) and human epidermal growth factor receptor 2 (HER-2/neu) protein expression with histological type and grade of GAC using immunohistochemistry (IHC). Materials and Methods: A total of 100 cases of GAC diagnosed over a 2 year period were studied. Expression of E-cadherin and HER-2/neu was analyzed by IHC in relation to the histological type and grade. Results: Of the 100 cases of GAC studied, 11 revealed a loss of E-cadherin and over-expression of HER-2/neu was seen in 17 cases. Loss of E-cadherin was seen in 50% of signet ring-cell carcinomas but only in 8% of tubular and none of papillary and mucin-secreting GAC (P = 0.003). Of all the cases of tubular GAC with loss of E-cadherin expression, majority (71.4%) were Grade III (P = 0.04). Of all the tubular GAC cases with an over-expression of HER-2/neu, 20% and 67% were Grade I and II GAC respectively while only 13% were Grade III (P < 0.001). Conclusions: Although poorly-differentiated tumors show loss of E-cadherin, better-differentiated tumors over-express HER-2/neu protein. Signet ring-cell carcinoma is more likely to exhibit a loss of E-cadherin protein. Targeted therapy toward HER-2/neu in GAC should be considered. Novel therapy to block E-cadherin down-regulation is justified.


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