[TP53 and RB tumor suppressor pathways collaborate in retinoblastoma genesis]

Med Sci (Paris). 2007 Apr;23(4):356-8. doi: 10.1051/medsci/2007234356.
[Article in French]
No abstract available

Publication types

  • News
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Cell Cycle Proteins
  • Cell Transformation, Neoplastic / genetics*
  • Cellular Senescence / genetics
  • Cyclin D
  • Cyclin-Dependent Kinases / physiology
  • Cyclins / physiology
  • DNA Damage
  • Eye Neoplasms / drug therapy
  • Eye Neoplasms / genetics*
  • Genes, Retinoblastoma*
  • Genes, p16
  • Genes, p53*
  • Humans
  • Imidazoles / administration & dosage
  • Imidazoles / pharmacology
  • Mice
  • Models, Biological
  • Nuclear Proteins / physiology
  • Piperazines / administration & dosage
  • Piperazines / pharmacology
  • Proto-Oncogene Proteins / physiology
  • Proto-Oncogene Proteins c-mdm2 / antagonists & inhibitors
  • Proto-Oncogene Proteins c-mdm2 / physiology
  • Retinoblastoma / drug therapy
  • Retinoblastoma / genetics*
  • Retinoblastoma Protein / physiology*
  • Topotecan / administration & dosage
  • Tumor Suppressor Protein p14ARF / physiology
  • Tumor Suppressor Protein p53 / physiology*
  • Xenograft Model Antitumor Assays

Substances

  • Cell Cycle Proteins
  • Cyclin D
  • Cyclins
  • Imidazoles
  • MDM4 protein, human
  • Nuclear Proteins
  • Piperazines
  • Proto-Oncogene Proteins
  • Retinoblastoma Protein
  • Tumor Suppressor Protein p14ARF
  • Tumor Suppressor Protein p53
  • nutlin 3
  • Topotecan
  • MDM2 protein, human
  • Mdm2 protein, mouse
  • Proto-Oncogene Proteins c-mdm2
  • Cyclin-Dependent Kinases