Papillomas and carcinomas were induced on the skin of mice by initiation with dimethylbenzanthracene, followed by promotion with 12-O-tetradecanoylphorbol-13-acetate. Retinoic acid was applied topically, either chronically, throughout the promotion period, or acutely, to the papillomas or carcinomas. All tumor types were verified histologically. Tumor tissue was incubated with labeled glucosamine and labeled glycoproteins released into media were fractionated on DEAE-Sephadex. For papillomas, one peak (eluted with 0.17 m NaCl) appeared and another (0.40 m) all but disappeared as a result of retinoic acid treatment. Carcinomas also showed the 0.40 m peak released by papillomas, which was also suppressed by retinoic acid. Carcinomas released a 0.26 m peak instead of the 0.17 m peak in response to the retinoid. All three peaks yielded single, symmetrical peaks on gel filtration columns. They were all resistant to mild alkaline hydrolysis. Labeling experiments revealed the presence also of mannose, galactose, and traces of fucose in all three glycoproteins. The 0.17 and 0.26 m peaks were bound by concanavalin A-Sepharose columns, the 0.40 m peak was not. Molecular weights, as determined by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, were approximately 80,000 and 105,000 (0.17 m peak), 67,000 (0.26 m peak), 70,000 and 80,000 (0.4 m peak).


This study was supported in part by NIH Grant CA13792.

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