Induction of retinoid resistance by all-trans retinoic acid in acute promyelocytic leukemia after remission.
Acute promyelocytic leukemia (APL) results from a malignant process that leads to the accumulation in the blood and the bone marrow of myeloid precursor cells characterized by an abnormal behavior and a differentiation arrest. It aroused considerable interest well beyond the hematologic field during the last five years since APL has two unique features i) the remission of the disease obtained with all-trans retinoic acid (ATRA) treatment ii) the presence in APL blasts of an abnormal protein, the promyelocytic myeloid leukemia/retinoic acid receptor (PML/RAR alpha) protein. APL is characterized cytogenetically by a t(15;17) translocation which involves both the PML gene on chromosome 15 and the RAR alpha gene on chromosome 17 and gives rise to the PML/RAR alpha fusion protein.
Laboratoire de Biologie Cellulaire Hématopoïétique, Hôpital Saint-Louis, Paris, France.
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D002869:Chromosome Aberrations; D025063:Chromosome Disorders; D002986:Clinical Trials as Topic; D004351:Drug Resistance; D006801:Humans; D015473:Leukemia, Promyelocytic, Acute / Q000188:drug therapy* / Q000235:genetics; D018160:Receptors, Cytoplasmic and Nuclear / Q000502:physiology; D012074:Remission Induction; D012176:Retinoids / Q000494:pharmacology*; D014212:Tretinoin / Q000009:adverse effects* / Q000494:pharmacology
D018160:Receptors, Cytoplasmic and Nuclear; D012176:Retinoids; D014212:Tretinoin