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  • 标题:Modulation of epithelial neoplasia and lymphoid hyperplasia in PTEN+/- mice by the p85 regulatory subunits of phosphoinositide 3-kinase
  • 本地全文:下载
  • 作者:Ji Luo ; Cassandra L. Sobkiw ; Nicole M. Logsdon
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2005
  • 卷号:102
  • 期号:29
  • 页码:10238-10243
  • DOI:10.1073/pnas.0504378102
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:Mice with heterozygous deletion of the PTEN tumor suppressor gene develop a range of epithelial neoplasia as well as lymphoid hyperplasia. Previous studies suggest that PTEN suppresses tumor formation by acting as a phosphoinositide phosphatase to limit signaling by phosphoinositide 3-kinase (PI3K). Here, we examined the effect of deleting various regulatory subunits of PI3K (p85{alpha} and p85{beta}) on epithelial neoplasia and lymphoid hyperplasia in PTEN+/- mice. Interestingly, we found the loss of one p85{alpha} allele with or without the loss of p85{beta} led to increased incidence of intestinal polyps. Signaling downstream of PI3K was enhanced in the PTEN+/-p85{alpha}+/-p85{beta}-/- polyps, as judged by an increased fraction of both cells with cytoplasmic staining of the transcription factor FKHR and cells with positive staining for the proliferation marker Ki-67. In contrast, the incidence of prostate intraepithelial neoplasia was not significantly altered in PTEN+/- mice heterozygous for p85{alpha} or null for p85{beta
  • 关键词:intestinal polyps ; prostate intraepithelial neoplasia ; AKT
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