Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene.

@article{Oshima1995LossOA,
  title={Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene.},
  author={M. Oshima and H. Oshima and K. Kitagawa and M. Kobayashi and C. Itakura and M. Taketo},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1995},
  volume={92 10},
  pages={
          4482-6
        }
}
  • M. Oshima, H. Oshima, +3 authors M. Taketo
  • Published 1995
  • Biology, Medicine
  • Proceedings of the National Academy of Sciences of the United States of America
Mutations in the APC (adenomatous polyposis coli) gene appear to be responsible for not only familial adenomatous polyposis but also many sporadic cases of gastrointestinal cancers. Using homologous recombination in mouse embryonic stem cells, we constructed mice that contained a mutant gene encoding a product truncated at a 716 (Apc delta 716). Mendelian transmission of the gene caused most homozygous mice to die in utero before day 8 of gestation. The heterozygotes developed multiple polyps… Expand
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The threshold level of adenomatous polyposis coli protein for mouse intestinal tumorigenesis.
Intestinal adenomas can develop with a stable karyotype and stable microsatellites
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