[Retinoic acid nuclear receptors: a common molecular basis for liver cancer and acute promyelocytic leukemia].
Our team was at the origin of the discovery of the relationship between rearrangements in genes encoding the retinoic acid receptors and tumorigenesis in human. Studying the molecular basis for hepatitis B virus (HBV)-associated liver cancer, we demonstrated that the viral DNA can behave as an insertional mutagen. This work also led to the identification of the first gene (RAR beta) encoding a receptor for the active derivative of vitamin A, retinoid acid. In collaboration with L. Degos, we then demonstrated the existence a systematic alteration of another retinoic acid receptor, RAR alpha, in acute promyelocytic leukemia (APL). Most recent work allowed us to involve a novel subnuclear organelle, the so-called PML Nuclear Bodies, in APL pathogenesis, underlying the major role played by the functional organization of the nucleus both in the normal and the pathological cell.
Dejean
Anne
A
L'Académie des Sciences, Unité de Recombinaison et Expression Génétique, INSERM U163, Institut Pasteur, 28 rue du Dr Roux-75015 Paris.
D002467:Cell Nucleus / Q000473:pathology; D006509:Hepatitis B / Q000150:complications*; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000235:genetics* / Q000503:physiopathology; D008113:Liver Neoplasms / Q000503:physiopathology* / Q000821:virology*; D018168:Receptors, Retinoic Acid / Q000235:genetics* / Q000502:physiology; D000072482:Retinoic Acid Receptor alpha
C000607071:RARA protein, human; D018168:Receptors, Retinoic Acid; D000072482:Retinoic Acid Receptor alpha; C082925:retinoic acid receptor beta