Chromosomal imbalances are uncommon in chagasic megaesophagus

<p>Abstract</p> <p>Background</p> <p>Chagas' disease is a human tropical parasitic illness and a subset of the chronic patients develop megaesophagus or megacolon. The esophagus dilation is known as chagasic megaesophagus (CM) and one of the severe late consequences of CM is the increased risk for esophageal carcinoma (ESCC). Based on the association between CM and ESCC, we investigated whether genes frequently showing unbalanced copy numbers in ESCC were altered in CM by fluorescence in situ (FISH) technology.</p> <p>Methods</p> <p>A total of 50 formalin-fixed, paraffin-embedded esophageal mucosa specimens (40 from Chagas megaesophagus-CM, and 10 normal esophageal mucosa-NM) were analyzed. DNA FISH probes were tested for <it>FHIT</it>, <it>TP63</it>, <it>PIK3CA</it>, <it>EGFR, FGFR1</it>, <it>MYC</it>, <it>CDKN2A, YES1 </it>and <it>NCOA3 </it>genes, and centromeric sequences from chromosomes 3, 7 and 9.</p> <p>Results</p> <p>No differences between superficial and basal layers of the epithelial mucosa were found, except for loss of copy number of <it>EGFR </it>in the esophageal basal layer of CM group. Mean copy number of <it>CDKN2A and </it>CEP9 and frequency of nuclei with loss of <it>PIK3CA </it>were significantly different in the CM group compared with normal mucosa and marginal levels of deletions in <it>TP63</it>, <it>FHIT, PIK3CA, EGFR, CDKN2A, YES </it>and gains at <it>PIK3CA, TP63, FGFR1, MYC, CDNK2A </it>and <it>NCOA3 </it>were detected in few CM cases, mainly with dilation grades III and IV. All changes occurred at very low levels.</p> <p>Conclusions</p> <p>Genomic imbalances common in esophageal carcinomas are not present in chagasic megaesophagus suggesting that these features will not be effective markers for risk assessment of ESCC in patients with chagasic megaesophagus.</p

Genomic imbalances in esophageal squamous cell carcinoma identified by molecular cytogenetic techniques

This review summarizes the chromosomal changes detected by molecular cytogenetic approaches in esophageal squamous cell carcinoma (ESCC), the ninth most common malignancy in the world. Whole genome analyses of ESCC cell lines and tumors indicated that the most frequent genomic gains occurred at 1, 2q, 3q, 5p, 6p, 7, 8q, 9q, 11q, 12p, 14q, 15q, 16, 17, 18p, 19q, 20q, 22q and X, with focal amplifications at 1q32, 2p16-22, 3q25-28, 5p13-15.3, 7p12-22, 7q21-22, 8q23-24.2, 9q34, 10q21, 11p11.2, 11q13, 13q32, 14q13-14, 14q21, 14q31-32, 15q22-26, 17p11.2, 18p11.2-11.3 and 20p11.2. Recurrent losses involved 3p, 4, 5q, 6q, 7q, 8p, 9, 10p, 12p, 13, 14p, 15p, 18, 19p, 20, 22, Xp and Y. Gains at 5p and 7q, and deletions at 4p, 9p, and 11q were significant prognostic factors for patients with ESCC. Gains at 6p and 20p, and losses at 10p and 10q were the most significant imbalances, both in primary carcinoma and in metastases, which suggested that these regions may harbor oncogenes and tumor suppressor genes. Gains at 12p and losses at 3p may be associated with poor relapse-free survival. The clinical applicability of these changes as markers for the diagnosis and prognosis of ESCC, or as molecular targets for personalized therapy should be evaluated

beta-glucans in promoting health: Prevention against mutation and cancer

The polysaccharides beta-glucans occur as a principal component of the cellular walls. Some microorganisms, such as yeast and mushrooms, and also cereals such as oats and barley, are of economic interest because they contain large amounts of beta-glucans. These substances stimulate the immune system, modulating humoral and cellular immunity, and thereby have beneficial effect in fighting infections (bacterial, viral, fungal and parasitic). beta-Glucans also exhibit hypocholesterolemic and anticoagulant properties. Recently, they have been demonstrated to be anti-cytotoxic, antimutagenic and anti-tumorogenic, making them promising candidate as pharmacological promoters of health. (C) 2008 Elsevier B.V. All rights reserved