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Anti-Retinoic Acid (RA) Antibody Binding to Human Premalignant Oral Lesions, Which Occurs Less Frequently Than Binding to Normal Tissue, Increases after 13-cis-RA Treatment in Vivo and Is Related to RA Receptor ß Expression¹

Departments of Tumor Biology and Epidemiology [X-C. X., R. L.], Thoracic/Head and Neck Medical Oncology [S. M. L., J. S. L., W. K. H.], and Biomathematics [J. J. L.], University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030, and Department of Food Science and Human Nutrition, Michigan State University, East Lansing, Michigan 48824 [M. H. Z.]

Nuclear retinoic acid receptor ß (RAR-ß) expression decreases in human premalignant oral lesions (POLs). RAR-ß suppression could result from a decrease in the cellular level of retinoids because RAR-ß gene transcription is enhanced by retinoids. To explore this hypothesis, we compared the binding of a monoclonal antibody (mAb) against all-trans-retinoic acid (RA; anti-RA mAbs) to normal oral tissue and POLs. All 7 normal specimens stained positive with the antibody compared to only 20 of 43 POLs; similarly, 7 of 7 normal specimens contained RAR-ß mRNA compared to only 14 of 43 POLs. Twenty-four specimens were available before and after a 3-month treatment with 13-cis-RA in vivo. Anti-RA mAb binding to these specimens increased from 10 of 24 before to 22 of 24 after treatment, and the expression of RAR-ß mRNA increased from 7 of 24 before to 21 of 24 after treatment, respectively. There was a strong agreement between the binding of anti-RA mAbs and the expression of RAR-ß. Thus, we propose that the binding of anti-RA mAbs reflects the level of retinoids in the tissues and that this level is related strongly to RAR-ß expression.

¹ This study was supported in part by USPHS Grant PO1 CA52051 from the National Cancer Institute, the Abell-Hanger Foundation Professorship (R. L.), a fellowship from the Houston Endowment (X-C. X.), United States Department of Agriculture Grant 93-37200-6285 (M. H. Z.), and the Michigan Agricultural Experiment Station (M. H. Z.).

² To whom requests for reprints should be addressed, at Department of Tumor Biology-108, University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030.

Received 9/11/95. Accepted 10/19/95.

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