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Cyclin D1 provides a link between development and oncogenesis in the retina and breast.

Mice lacking cyclin D1 have been generated by gene targeting in embryonic stem cells. Cyclin D1-deficient animals develop to term but show reduced body size, reduced viability, and symptoms of neurological impairment. Their retinas display a striking reduction in cell number due to proliferative failure during embryonic development. In situ hybridization studies of normal mouse embryos revealed an extremely high level of cyclin D1 in the retina, suggesting a special dependence of this tissue on cyclin D1. In adult mutant females, the breast epithelial compartment fails to undergo the massive proliferative changes associated with pregnancy despite normal levels of ovarian steroid hormones. Thus, steroid-induced proliferation of mammary epithelium during pregnancy may be driven through cyclin D1.

Pubmed ID: 7664341


  • Sicinski P
  • Donaher JL
  • Parker SB
  • Li T
  • Fazeli A
  • Gardner H
  • Haslam SZ
  • Bronson RT
  • Elledge SJ
  • Weinberg RA



Publication Data

August 25, 1995

Associated Grants

  • Agency: NIA NIH HHS, Id: AG11085
  • Agency: NCI NIH HHS, Id: R35CA39826

Mesh Terms

  • Animals
  • Cell Differentiation
  • Cell Division
  • Cyclin D1
  • Cyclins
  • Female
  • Gene Expression Regulation, Developmental
  • Gene Targeting
  • Male
  • Mammary Glands, Animal
  • Mice
  • Mice, Mutant Strains
  • Neoplasms, Experimental
  • Oncogene Proteins
  • Phenotype
  • Pregnancy
  • Receptors, Estrogen
  • Retina
  • Stem Cells
  • Steroids