Retinoic acid treatment

Griffiths CEM, Goldfarb MT, Finkel LJ, et al (1994) Topical tretinoin (retinoic acid) treatment of hyperpigmented lesions associated with photoaging in Chinese and Japanese patients a vehicle-con-trolled trial. J Am Acad Dermatol 30 76-84... 

Massaro, G. D., and Massaro, D. (1997). Retinoic acid treatment abrogates elastase-induced pulmonary emphysema in rats. Nat. Med. 3, 675-677. 

Impairment of the retinoid signal transduction pathways occurs as a result of prolonged UV exposure. Down regulation of nuclear receptors for Vitamin A occurs,269 resulting in a functional deficiency of Vitamin A. Application of Vitamin A derivatives would appear to be an obvious treatment modality. Topical application of Vitamin A does increase the HA in the epidermal layer, increasing the thickness of the HA meshwork after prolonged treatment.270 Vitamin A thus enhances repair, as can be demonstrated in photo-aged hairless mouse model.271 The decline in GAG, and in particular HA deposition that occurs with UVB irradiation, can be entirely prevented by retinoic acid treatment. 

Lundin, A., Berne, B., and Michaeelsson, G., Topical retinoic acid treatment of photoaged skin its effects on hyaluronan distribution in epidermis and on hyaluronan and retinoic acid in suction blister fluid, Acta Derm. Venere., 72, 423, 1992. 

Torromeo C, Latagliata R, Awisati G, Petti MC, Mandelli F. Intraventricular thrombosis during all-trans retinoic acid treatment in acute promyelocytic leukemia. Leukemia 2001 15(8) 1311-13. 

Suzumiya J, Asahara F, Katakami H, Kimuran N, Hisano S, Okumura M, Ohno R. Hypercalcaemia caused by all-trans retinoic acid treatment of acute promyelocytic leukaemia case report. Eur J Haematol 1994 53(2) 126-7. 

Ko BS, Tang JL, Chen YC, Yao M, Wang CH, Shen MC, Tien HF. Extramedullary relapse after all-trans retinoic acid treatment in acute promyelocytic leukemia—the occurrence of retinoic acid syndrome is a risk factor. Leukemia 1999 13(9) 1406-8. 

Bulengo-Ransby SM, Griffiths CE, Kimbrough-Green CK, et al. Retinoic acid treatment for hyperpigmented lesions caused by inflammation of the skin in black patients. N Engl J Med 1993 328 1486-7. 

Biochemical Studies The self-renewal of mES cells depends largely on LIF (leukemia inhibitory factor) and BMP (bone morphologic protein). However, SCI maintained an mES ability to self-renew for more than 10 passages in an undifferentiated/pluripotent state and showed relatively low cellular toxicity. The compound reversibly inhibited differentiation of mES cells induced by either FBS or retinoic acid treatment, and after washout SCI, mES cells were selectively induced to differentiate into neural/neuronal, cardiac muscle, and endodermal cells. 

Bally-Cuif, L., Gulisano, M., Broccoli, V., Boncinelli, E. 1995. C-otx2 is expressed in two different phases of gastrulation and is sensitive to retinoic acid treatment in chick embryo. Mech. Dev. 49, 49-63. 

Therefore, it appears that abnormal expressions of retinoic receptors may be involved in neoplastic progressions, and in some cases, these may completely hinder RA responsiveness. In other cases, as in remission of acute promyelocytic leukaemia, abnormal gene regulation by mutant RARs can be overcome by retinoic acid treatment. 

Rowe, A., Richman, J.M. Brickell, P.M. (1991). Retinoic acid treatment alters the distribution of retinoic acid receptor- transcripts in the embryonic chick face. Development, 111, 1007-16. 

Laminas (LMN-ACO) serve as scaffolds for the anchoring of nuclear chromatin. Neuroblastoma cells with lamina genes deleted and lacking nuclear lamina, fail to differentiate in response to retinoic acid treatment. Lamina-defective neuroblastoma xenografts released cells with accelerated locomotion lamina-free tumor cells formed large tumors rapidly, and exhibited resistance to chemotherapy (doxorubicin, etoposide, paclitaxel). Laminary structures in place were necessary for organ differentiation [1627]. 

De Bemardi, F., C. Sotgia, and G. Ortolani. 1994. Retinoic Acid Treatment of Ascidian Embryos Effects on Larvae and Metamorphosis. Anim Dev 3 75-81. 

Boylan, J. F., Lohnes, D., Taneja, R., Chambon, P., and Gudas, L. J. (1993) Loss of retinoic acid receptor gamma function in F9 cells by gene disruption results in aberrant Hoxa-1 expression and differentiation upon retinoic acid treatment. Proc. Natl Acad Sci. USA 90,9601-9605. 

Not all transformed cells respond to retinoic acid treatment with an inhibition of growth, nor are inhibitory effects on growth limited to neoplastic cells. 

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