Anticancer research · 2001
Involvement of cancer-activating genes on chromosomes 7 and 8 in esophageal (Barrett's) and gastric cardia adenocarcinoma.
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Vissers K J, Riegman P H, Alers J C, Tilanus H W, van Dekken H
Аннотация
UNLABELLED: The incidence of adenocarcinomas of the distal esophagus (Barrett's esophagus) and proximal stomach (gastric cardia) has increased rapidly over the past decades. In contrast to this dramatic increase, genetic knowledge is sparse.
MATERIALS AND METHODS: We investigated genomic amplification on chromosomes 7 and 8 by comparative genomic hybridization (CGH) and protein expression of relevant oncogenes (EGFR, HGF, MET, CTSB, MYC) by immunohistochemistry (IHC) in 22 esophageal and 22 gastric cardia carcinomas.
RESULTS: The CGH and IHC patterns were very similar for the two cancer locations. IHC showed positive immunostaining in 93% of the adenocarcinomas for at least one of the investigated genes, whereas CGH disclosed genomic gains on chromosome 7 and/or 8 in 80%.
CONCLUSION: Cancer-activating genes on chromosomes 7 and 8 are frequently involved in gastro-esophageal junction adenocarcinomas. Moreover, the similarities in chromosomal changes and protein expression patterns strongly suggest that esophageal and gastric cardia adenocarcinomas have a shared etiology. This is in agreement with studies addressing gastroesophageal reflux disease and intestinal metaplasia at these locations.
MATERIALS AND METHODS: We investigated genomic amplification on chromosomes 7 and 8 by comparative genomic hybridization (CGH) and protein expression of relevant oncogenes (EGFR, HGF, MET, CTSB, MYC) by immunohistochemistry (IHC) in 22 esophageal and 22 gastric cardia carcinomas.
RESULTS: The CGH and IHC patterns were very similar for the two cancer locations. IHC showed positive immunostaining in 93% of the adenocarcinomas for at least one of the investigated genes, whereas CGH disclosed genomic gains on chromosome 7 and/or 8 in 80%.
CONCLUSION: Cancer-activating genes on chromosomes 7 and 8 are frequently involved in gastro-esophageal junction adenocarcinomas. Moreover, the similarities in chromosomal changes and protein expression patterns strongly suggest that esophageal and gastric cardia adenocarcinomas have a shared etiology. This is in agreement with studies addressing gastroesophageal reflux disease and intestinal metaplasia at these locations.