Genes, APC

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  Subject Areas on Research

  • A germline mutation at the extreme 3' end of the APC gene results in a severe desmoid phenotype and is associated with overexpression of beta-catenin in the desmoid tumor. 
  • APC I1307K and the risk of prostate cancer. 
  • Activity level, apoptosis, and development of cachexia in Apc(Min/+) mice. 
  • Adenomatous polyposis coli gene mutation alters proliferation through its beta-catenin-regulatory function in aggressive fibromatosis (desmoid tumor). 
  • Antihelminth compound niclosamide downregulates Wnt signaling and elicits antitumor responses in tumors with activating APC mutations. 
  • Detection and quantification of mutations in the plasma of patients with colorectal tumors. 
  • Detection of APC mutations in fecal DNA from patients with colorectal tumors. 
  • Development of a colon cancer GEMM-derived orthotopic transplant model for drug discovery and validation. 
  • Genetic deletion of receptor for hyaluronan-mediated motility (Rhamm) attenuates the formation of aggressive fibromatosis (desmoid tumor). 
  • High-fat diet enhances stemness and tumorigenicity of intestinal progenitors. 
  • IFN-{beta} signaling positively regulates tumorigenesis in aggressive fibromatosis, potentially by modulating mesenchymal progenitors. 
  • Increased beta-catenin protein and somatic APC mutations in sporadic aggressive fibromatoses (desmoid tumors). 
  • Interaction of Galpha 12 and Galpha 13 with the cytoplasmic domain of cadherin provides a mechanism for beta -catenin release. 
  • Intestinal tumorigenesis is suppressed in mice lacking the metalloproteinase matrilysin. 
  • Matrix metalloproteinase activity modulates tumor size, cell motility, and cell invasiveness in murine aggressive fibromatosis. 
  • Muscle oxidative capacity during IL-6-dependent cancer cachexia. 
  • Mutation in the mismatch repair gene Msh6 causes cancer susceptibility. 
  • Predominance of beta-catenin mutations and beta-catenin dysregulation in sporadic aggressive fibromatosis (desmoid tumor). 
  • Targeting stem cell behavior in desmoid tumors (aggressive fibromatosis) by inhibiting hedgehog signaling. 
  • Testosterone regulates cell proliferation in aggressive fibromatosis (desmoid tumour).