Histogenesis of hepatoid adenocarcinoma of the stomach: molecular evidence of identical origin with coexistent tubular adenocarcinoma.
Hepatoid adenocarcinoma of the stomach is a highly malignant neoplasm. Most gastric hepatoid adenocarcinomas coexist with tubular adenocarcinoma. However, the relationship between hepatoid adenocarcinoma and tubular adenocarcinoma is still unclear. In the present study, the characteristics of the coexistent tubular adenocarcinomas were determined by examining their profiles of mucin production. Subsequently, molecular pathological techniques were applied to determine the clonality of 15 mixed hepatoid and tubular adenocarcinomas of the stomach. Mucin analysis suggested that the coexistent tubular adenocarcinomas with hepatoid adenocarcinoma were of the intestinal type. The patterns of chromosome X inactivation were identical between the hepatoid adenocarcinoma component and tubular adenocarcinoma component in all of 3 informative female cases. Mutations in the p53 gene were found in 5 cases. The sequences were identical within both tumor components in all 5 cases. Microsatellite analysis indicated more than 3 common patterns of loss of heterozygosity in 8 cases. These observations strongly suggested that hepatoid adenocarcinomas were of identical origin to coexistent tubular adenocarcinomas.
Akiyama
Sunao
S
Department of Pathology, Yamagata University School of Medicine, Yamagata, Japan.|Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan.
Tamura
Gen
G
Department of Pathology, Yamagata University School of Medicine, Yamagata, Japan.
Endoh
Yasushi
Y
Department of Pathology, Yamagata University School of Medicine, Yamagata, Japan.
Fukushima
Norimasa
N
Department of Surgery, Prefectural Central Hospital, Yamagata, Japan.
Ichihara
Yukihiro
Y
Department of Surgery, Prefectural Central Hospital, Yamagata, Japan.
Aizawa
Kikuo
K
Department of Surgery, Tsubame Rosai Hospital, Tsubame, Japan.
Kawata
Sumio
S
Department of Internal Medicine, Yamagata University School of Medicine, Yamagata, Japan.
Motoyama
Teiichi
T
Department of Pathology, Yamagata University School of Medicine, Yamagata, Japan.
D000230:Adenocarcinoma / Q000378:metabolism / Q000473:pathology*; D000368:Aged; D000369:Aged, 80 and over; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000473:pathology*; D041321:Chromosomes, Human, X / Q000235:genetics*; D004252:DNA Mutational Analysis; D004273:DNA, Neoplasm; D005260:Female; D005753:Gastric Mucosa / Q000378:metabolism; D016158:Genes, p53 / Q000235:genetics*; D011905:Genes, ras / Q000235:genetics; D006801:Humans; D008113:Liver Neoplasms / Q000378:metabolism / Q000473:pathology*; D019656:Loss of Heterozygosity; D008297:Male; D018895:Microsatellite Repeats; D008875:Middle Aged; D009077:Mucins / Q000378:metabolism*; D009154:Mutation / Q000235:genetics; D009367:Neoplasm Staging; D013270:Stomach / Q000473:pathology*; D013274:Stomach Neoplasms / Q000378:metabolism / Q000473:pathology*; D000509:alpha-Fetoproteins / Q000378:metabolism
D004273:DNA, Neoplasm; D009077:Mucins; D000509:alpha-Fetoproteins