Research Article Deregulation of Annexin-A1 and Galectin-1 Expression in Precancerous Gastric Lesions: Intestinal Metaplasia and Gastric Ulcer Ana Flávia Teixeira Rossi, 1 Márcia Cristina Duarte, 1 Ayla Blanco Poltronieri, 1 Marina Curado Valsechi, 1 Yvana Cristina Jorge, 1 Dalísio de-Santi Neto, 2 Paula Rahal, 1 Sonia Maria Oliani, 1 and Ana Elizabete Silva 1 1 Department of Biology, S˜ ao Paulo State University (UNESP), Cˆ ampus S˜ ao Jos´ e do Rio Preto, Rua Crist´ ov˜ ao Colombo 2265, 15054-000 S˜ ao Jos´ e do Rio Preto, SP, Brazil 2 Legal Medicine Department and Pathology Service, Hospital de Base, Avenida Brigadeiro Faria Lima 5544, 15090-000 S˜ ao Jos´ e do Rio Preto, SP, Brazil Correspondence should be addressed to Ana Elizabete Silva; anabete@ibilce.unesp.br Received 14 October 2013; Revised 15 January 2014; Accepted 15 January 2014; Published 25 February 2014 Academic Editor: Fulvio D’Acquisto Copyright © 2014 Ana Fl´ avia Teixeira Rossi et al. his is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Annexin-A1 (ANXA1/AnxA1) and galectin-1 (LGALS1/Gal-1) are mediators that play an important role in the inlammatory response and are also associated with carcinogenesis. We investigated mRNA and protein expression in precancerous gastric lesions that participate in the progression cascade to gastric cancer, such as intestinal metaplasia (IM) and gastric ulcer (GU). Methods. Quantitative real-time PCR (qPCR) and immunohistochemical techniques were used to analyze the relative quantiication levels (RQ) of ANXA1 and LGALS1 mRNA and protein expression, respectively. Results. Increased relative expression levels of ANXA1 were found in 100% of cases, both in IM (mean RQ = 6.22 ± 0.06) and in GU (mean RQ = 6.69 ± 0.10). However, the LGALS1 presented basal expression in both groups (IM: mean RQ = 0.35 ± 0.07; GU: mean RQ = 0.69 ± 0.09). Immunohistochemistry revealed signiicant positive staining for both the AnxA1 and Gal-1 proteins in the epithelial nucleus and cytoplasm as well as in the stroma of the IM and GU groups ( < 0.05) but absence or low immunorectivity in normal mucosa. Conclusion. Our results bring an important contribution by evidencing that both the AnxA1 and Gal-1 anti-inlammatory proteins are deregulated in precancerous gastric lesions, suggesting their involvement in the early stages of gastric carcinogenesis, possibly due to an inlammatory process in the gastric mucosa. 1. Introduction Precancerous lesions are related to the development of tumors in several organs, such as intestinal-type gastric cancer that develops through the progression of various sequential lesions that frequently start with a Helicobacter pylori infection. his infection causes supericial gastritis that can progress to chronic atrophic gastritis, intestinal metaplasia, dysplasia, and, inally, carcinoma [1]. Intestinal metaplasia, characterized by the diferentiation of gastric stem cells into intestinal-phenotype cells [2], is associated with more than 80% of intestinal-type adenocarcinoma [3]. Besides this metaplasia-dysplasia-carcinoma pathway, gastric carcinogenesis can originate from gastric ulcer [4], a lesion in the mucosa that develops in low acid concentration sites and severe inlammation [5, 6]. Eighty-ive percent of gastric ulcer cases occur in the presence of H. pylori infection [5, 7]. he progression of the lesions cascade depends on many genetic factors in both the host and the bacterium, besides environmental factors [8]. H. pylori may persist for many years in the host, causing a chronic inlammation. his results in a great amount of inlammatory mediators and the reactive oxygen and nitrogen species that induce genetic and epigenetic changes in protooncogene and tumor suppressor Hindawi Publishing Corporation Mediators of Inflammation Volume 2014, Article ID 478138, 11 pages http://dx.doi.org/10.1155/2014/478138