Allelic Loss of Chromosome 6q in Gastric Carcinoma
| Autor: | S.C.Sydney Chung, Chit Chow, Enders K.W. Ng, Brenda C. Y. Li, Wing Y. Chan, Christine Y. S. Li |
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| Rok vydání: | 2003 |
| Předmět: |
Adult
Male Gastric carcinoma Adenocarcinoma Biology Long arm Polymerase Chain Reaction Pathology and Forensic Medicine Stomach Neoplasms medicine Humans Molecular Biology In Situ Hybridization Fluorescence Aged DNA Primers Neoplasm Staging Aged 80 and over Metaplasia Stomach digestive oral and skin physiology Cancer Intestinal metaplasia Chromosome DNA Neoplasm Cell Biology Middle Aged medicine.disease digestive system diseases medicine.anatomical_structure Cancer research Chromosomes Human Pair 6 Female Chromosome Deletion Allelic loss Microsatellite Repeats |
| Zdroj: | Diagnostic Molecular Pathology. 12:193-200 |
| ISSN: | 1052-9551 |
| DOI: | 10.1097/00019606-200312000-00003 |
| Popis: | Loss of the long arm of chromosome 6 (6q) has frequently been reported in gastric carcinoma, and most gastric cancer patients have evidence of intestinal metaplasia in the stomach. However, the relationship between loss of chromosome 6q and intestinal metaplasia has not been studied. In the first part of the study, we define the critical deletion region of chromosome 6q using loss of heterozygosity technique (LOH). Seventeen microsatellite markers were used to detect loss of heterozygosity (LOH) in 37 microdissected gastric tumors. We also examined intestinal metaplasia (IM) foci of the stomach in the same cancer patient (17 cases). Losses on chromosome 6q were detected in high frequency (51%) by LOH. Two distinct regions of common allelic loss were identified: one centered on the marker D6S300 (at 6q16.1) and the second on D6S446 (at 6q27), with LOH frequency of 36% and 31.3%, respectively. The deletions fall into 2 discrete regions, suggesting the existence of at least 2 tumor suppressor genes in 6q. The losses at 6q27 were confirmed by fluorescence in situ hybridization study (FISH). In the cases with LOH in the tumor, no LOH were detected in the autologous IM areas, but losses were detected by FISH. In some cases, these genetic changes may be acquired in the transition from normal gastric mucosa to intestinal metaplasia. |
| Databáze: | OpenAIRE |
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