The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo
Article Abstract:
Mutations in the SMAD4/DPC4 tumor suppressor gene are a factor in 50% of pancreatic cancers. The gene is an important signal transducer in most TGF beta-related pathways. The tumor suppressor gene Smad4/Dpc4 is necessary for gastrulation and for later anterior development in mouse embryos. It seems Smad4 is at the start necessary for the differentiation of the visceral endoderm. The gastrulation defect in the epiblast seems to be secondary and non-cell autonomous.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 1998
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Collaboration of Brca1 and Chk2 in tumor genesis
Article Abstract:
A study demonstrating that deficiency in Chk2 partially mimics the loss of p53 and rescues the defective development, growth, and cellular demise of Brca 1-deficient T cells at the expense of genomic instability and increased tumorigenicity is presented. Findings indicate that the loss of p53-dependent responses mediated by Chk2 may be critical for survival, development, and tumor progression triggered by loss of Brca1 function.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2004
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RhoC is dispensable for embroyogenesis and tumor initiation but essential for metastasis
Article Abstract:
A study is conducted on Rhoc deficient mice to show that RhoC is dispensable for embryonic and post-natal development. It is demonstrated that loss of RhoC does not affect tumor development but decreases tumor cell motility and metastatic cell survival leading to a drastic inhibition of metastasis.
Publication Name: Genes & Development
Subject: Biological sciences
ISSN: 0890-9369
Year: 2005
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