Cyclin D1 is not an essential target of beta-catenin signaling during intestinal tumorigenesis, but it may act as a modifier of disease severity in multiple intestinal neoplasia (Min) mice.
作者： Walter Bodmer , Mohammad Ilyas , Jenny Wilding , Clive Dickson , Julie Bee
DOI:
关键词: Beta-catenin 、 Cell cycle 、 Cyclin D 、 Biology 、 Cyclin D1 、 Cyclin B 、 Intestinal Neoplasm 、 Carcinogenesis 、 Cancer research 、 Familial adenomatous polyposis
摘要: Deregulation of beta-catenin activity is an important step in the development colorectal cancers. One consequence this transcriptional activation cyclin D1, oncogene known to be overexpressed We tested hypothesis that D1 gene for intestinal tumorigenesis. Multiple neoplasia mice (a model human familial adenomatous polyposis) were crossed with knockout (Ccnd1(-/-)) mice. Despite absence tumors still developed. However, Ccnd1(-/-) multiple developed significantly fewer than Ccnd1(+/-) or Ccnd1(+/+) (P = 0.003). conclude not essential tumorigenesis, but it may act as a modifier gene.
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