Phenotype of mice lacking functional Deleted in colorectal cancer (Dcc) gene

Nature. 1997 Apr 24;386(6627):796-804. doi: 10.1038/386796a0.


The DCC (Deleted in colorectal cancer) gene was first identified as a candidate for a tumour-suppressor gene on human chromosome 18q. More recently, in vitro studies in rodents have provided evidence that DCC might function as a receptor for the axonal chemoattractant netrin-1. Inactivation of the murine Dcc gene caused defects in axonal projections that are similar to those observed in netrin-1-deficient mice but did not affect growth, differentiation, morphogenesis or tumorigenesis in mouse intestine. These observations fail to support a tumour-suppressor function for Dcc, but are consistent with the hypothesis that DCC is a component of a receptor for netrin-1.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Axons / pathology
  • Brain / abnormalities
  • Brain / embryology
  • Brain Neoplasms / genetics
  • Cell Adhesion Molecules / genetics
  • Cell Adhesion Molecules / physiology*
  • Cell Division
  • Chimera
  • Chromosome Mapping
  • Colorectal Neoplasms / genetics
  • DCC Receptor
  • Gene Targeting
  • Genes, DCC*
  • Humans
  • Intestinal Mucosa / pathology
  • Intestinal Neoplasms / genetics*
  • Intestinal Polyps / genetics
  • Mice
  • Mice, Inbred C57BL
  • Mutagenesis*
  • Nerve Growth Factors / physiology
  • Netrin-1
  • Phenotype
  • Receptors, Cell Surface / metabolism
  • Spinal Cord / abnormalities
  • Spinal Cord / embryology
  • Tumor Suppressor Proteins*


  • Cell Adhesion Molecules
  • DCC Receptor
  • DCC protein, human
  • Dcc protein, mouse
  • NTN1 protein, human
  • Nerve Growth Factors
  • Ntn1 protein, mouse
  • Receptors, Cell Surface
  • Tumor Suppressor Proteins
  • Netrin-1