isotretinoin and Pituitary-Neoplasms

Topics: Acne Vulgaris; Adolescent; Anti-Inflammatory Agents; Child, Preschool; Craniopharyngioma; Diagnosis, Differential; Duodenum; Female; Humans; Infant; Isotretinoin; Klinefelter Syndrome; Male; Pituitary Neoplasms; Prednisone; Prognosis; Reye Syndrome; Tomography, X-Ray Computed; Whooping Cough

Retinoic acid produced a time and dose-dependent depletion of thyroid hormone receptors in GH1 cells without modifying their affinity for triiodothyronine (T3). A maximal decrease (50-70%) was obtained after 24-48 h incubation with 5-10 microM retinoic acid. Treatment with 0.8 nM T3 for 24 h caused a similar reduction and did not potentiate the decrease produced by these concentrations of retinoic acid. However, the combination of sub-maximally effective doses of both ligands had an additive effect on receptor levels. The reduction of receptor caused by retinoic acid is accompanied by a decreased expression of c-erbA alpha 1 and alpha 2 mRNAs, but the retinoid did not reduce the abundance of c-erbA beta mRNA. In contrast, T3 decreased the levels of both alpha and beta transcripts.

Topics: Animals; Cell Line; Etretinate; Isotretinoin; Kinetics; Macromolecular Substances; Pituitary Neoplasms; Poly A; Proto-Oncogene Proteins; Rats; Receptors, Thyroid Hormone; RNA; RNA, Messenger; RNA, Neoplasm; Transcription, Genetic; Tretinoin; Triiodothyronine; Vitamin A