The insulin-like growth factor II receptor gene is mutated in genetically unstable cancers of the endometrium, stomach, and colorectum

Hong Ouyang, Hiromi O. Shiwaku, Hisashi Hagiwara, Ko Miura, Tadayoshi Abe, Yo Kato, Haruo Ohtani, Kenichi Shiiba, Rhonda F. Souza, Stephen J. Meltzer, Akira Horii

研究成果: Article査読

168 被引用数 (Scopus)

抄録

Disruption of the DNA mismatch repair system, characterized by microsatellite instability (MI), plays an important role in the course of human carcinogenesis. Repetitive sequences constitute targets for mutation in MI+ cells, and frequent mutations have indeed been reported in such regions within the transforming growth factor β receptor II (RII) gene in genetically unstable colorectal and gastric cancers. However, other genes that are targets for mutations in MI+ cells during the course of carcinogenesis have proven elusive. Because the insulin-like growth factor II receptor (IGFIIR) gene contains several repetitive sequences within its coding region, we examined mutations of this gene in MI+ cancers occurring at various primary sites. We found frameshift mutations in the poly(G)8 tract of IGFIIR in eight tumors, all of which were MI+: 4 of 26 (15%) MI + endometrial cancers, 3 of 12 (25%) MI + gastric cancers, and 1 of 18 (6%) MI+ colorectal cancers. In contrast, no mutation was found in 51 pancreatic cancers, 7 of which (14%) were MI+. These results implicate abnormal IGFIIR- mediated growth control in carcinogenesis involving the endometrium, stomach, and colorectum but not the pancreas.

本文言語English
ページ(範囲)1851-1854
ページ数4
ジャーナルCancer Research
57
10
出版ステータスPublished - 1997 5 15

ASJC Scopus subject areas

  • 腫瘍学
  • 癌研究

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