Retardation of experimental oral cancer development by retinyl acetate

Abstract

Sixty young adult Syrian hamsters were divided into five groups. Group 1 and Group 2 animals were treated with 0.25% dimethylbenz(a)anthracene (DMBA), painted on their left buccal pouches thrice weekly for 20 weeks. Starting at 12 weeks, at which time there was clinical evidence of leukoplakia and initial tumor formation, Group 2 animals received 10 mg retinyl acetate 3 times/week in a 5% solution in peanut oil, while Group 1 animals received only peanut oil. Two animals in Group 1 and two animals in Group 2 were sacrificed weekly from week 12 to week 20. Left buccal pouches were examined, tumors were counted, and tumor size was measured. Group 3 animals were untreated controls, Group 4 animals were retinyl acetate controls, and Group 5 animals received only peanut oil. It was found that DMBA-treated animals receiving retinyl acetate from week 12 to week 20 developed fewer tumors, and their average tumor size was less than that in DMBA-treated animals not receiving retinyl acetate. It appears that retinyl acetate, administered systemically, can retard tumor development even after leukoplakia has been established and tumors have begun to develop.

Differential effects of chromosome 3p deletion on the expression of the putative tumor suppressor RARβ and on retinoid resistance in human squamous carcinoma cells

“…Retinoids have demonstrated some ecacy in animal models (Burge-Bottenbley and Shklar (1983); Schwartz et al (1985) and in clinical trials with patients with oral premalignant lesions (Hong et al (1986). 13-cisRetinoic acid was also found to prevent the development of second primary tumors arising in patients who had been treated curatively for the ®rst primary HNSCC (Hong et al, 1990).…”

Modulatory effects of snuff, retinoic acid, andß‐carotene on DMBA‐induced hamster cheek pouch carcinogenesis in relation to keratin expression

“…Vitamin A in the form of either 13-m-retinoic acid or retinyl acetate or as /3-carotene has been shown to inhibit DMBA-induced HCP carcinogenesis (21)(22)(23). Our observations showed a total inhibitory effect of DMBA-induced carcinogenesis by carotenoids.…”

Treatment of advanced squamous cell carcinoma of the head and neck with isotretinoin: a phase II randomized trial

“…Recent laboratory trials have demonstrated that retinoic acid can significantly increase the number of EGF receptors, which also correlated with growth inhibition in certain cell lines [8,10]. In vivo animal models for testing drugs in SCCA of the head and neck further support the use of retinoids in this disease [13,14].…”

“…Retinoids, the synthetic and natural analogs of vitamin A, are active in certain premalignant and malignant epithelial disorders [6,9,11] and have in vitro [12] and in vivo activity in animals [13,14] against SCCA. Several nonrandomized studies have demonstrated that retinoids -including isotretinoin, or 13-cis retinoic acid -are active in oral leukoplakia [15][16][17][18][19] and laryngeal papillomatosis [20,21], precursors of head and neck SCCA, and in certain advanced human malignancies, such as mycosis fungoides [11,22,23] and refractory SCCA of the skin [11,24].…”