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Li Chuan Chen - One of the best experts on this subject based on the ideXlab platform.
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Effect of excess dietary retinoic acid on Skin Papilloma and carcinoma formation induced by a complete carcinogenesis protocol in female Sencar mice
Cancer letters, 1994Co-Authors: Li Chuan Chen, Susan Kirchhoff, Luigi M. De LucaAbstract:Previously, we have shown that dietary retinoic acid (RA) at pharmacological doses (30 μg/g of diet) inhibited the malignant conversion of Skin Papillomas to carcinomas induced by a two-stage carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene (DMBA) as initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as promoter (De Luca et al., Carcinogenesis, 14 (1993) 539–542). The purpose of this study was to determine the effect of dietary RA on Skin Papilloma and carcinoma formation induced by a complete carcinogenesis protocol with repeated DMBA treatment in female Sencar mice. Mice at 3 weeks of age were weaned onto a diet containing either 3 (control) or 30 (excess) μg of RA/g of diet and treated topically with DMBA (25.5 μg) once per week for 20 weeks. Mice fed excess dietary RA did not significantly differ from control mice in the following parameters: body weight, survival rate, Papilloma incidence, cumulative carcinoma incidence (19.4% versus 23.7%), carcinoma yield (0.19 versus 0.26 per mouse), carcinoma conversion efficiency (5.2% versus 3.9%), and average age of carcinoma development (22.7 ± 4.7 versus 23.3 ± 2.8 weeks). However, Papilloma yield was decreased by about 50% (i.e. 3.7 versus 7.0 at week 20, P < 0.01) between weeks 17 and 22 of age by excess dietary RA treatment. Contrary to other routes of administration (i.e. topical and systemic) of RA (Verma et al., Cancer Res., 42 (1982) 3519–3525), excess dietary RA did not enhance Skin tumor formation. In addition, excess dietary RA failed to inhibit malignant conversion of Papillomas to carcinomas in the complete carcinogenesis protocol. Thus, the modulation of RA on Skin Papilloma and carcinoma formation is dependent on carcinogenesis protocol and route of RA administration.
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Retinol and β‐carotene concentrations in Skin, Papillomas and carcinomas, liver, and serum of mice fed retinoic acid or β‐carotene to suppress Skin tumor formation
Nutrition and cancer, 1994Co-Authors: Carol S Jones, Li Chuan Chen, Linda Sly, Theresa Ben, M. Brugh-collins, Ulrike Lichti, L M De LucaAbstract:Abstract Using 7,12‐dimethylbenz[a] anthracene as the initiator and 12‐O‐tetradecanoyl‐13‐acetate as the tumor promoter on the dorsal Skin of Sencar mice, we previously showed that pharmacological dietary all‐trans‐retinoic acid and β‐carotene inhibit the conversion of Papillomas to carcinomas in a two‐stage system of chemical carcinogenesis. The purpose of this study was to determine the influence of dietary retinoic acid and β‐carotene on retinoidand β‐carotene concentrations in Skin and other tissues. We were unable to measure tissue retinoic acid because of the relatively limited amount of tissue available for analysis and the fast rate of metabolism. Different dietary levels of retinoic acid or β‐carotene did not influence total retinol of Skin, Papilloma, and carcinoma tissues, which all showed a concentration of approximately 1 ± 0.5 μg/g wet wt. Equally refractory to dietary retinoic acid or β‐carotene was serum retinol concentration. In contrast, dietary retinoic acid protected loss of liver reti...
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effects of dietary retinoic acid on Skin Papilloma and carcinoma formation in female sencar mice
Carcinogenesis, 1993Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Previously we have shown that dietary retinoids are essential for Papilloma formation induced by either an initiation-promotion or a complete Skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on Papilloma formation and the conversion of Papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar Papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest Papilloma yield (approximately 14 Papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These Papillomas later regressed such that mice from all three groups had about the same Papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of Papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of Papillomas to carcinomas without affecting Papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered Papilloma yield.
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dietary retinoids are essential for Skin Papilloma formation induced by either the two stage or the complete tumorigenesis model in female sencar mice
Cancer Letters, 1992Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Abstract Our previous work has shown that dietary retinoic acid (RA) is necessary for Skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334–2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 μg), followed by 20 applications of TPA (2 μg), or by 20 applications of DMBA (25 μg for 2 weeks and 51 μg thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 μg/g of diet) or retinyl palmitate (RP, 6 μg/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for Skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol.
Luigi M. De Luca - One of the best experts on this subject based on the ideXlab platform.
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topical retinoic acid reduces Skin Papilloma formation but resistant Papillomas are at high risk for malignant conversion
Cancer Research, 1998Co-Authors: Tamar Tennenbaum, Luigi M. De Luca, David T Lowry, Nadine Darwiche, David L Morgan, Marina Gartsbein, Laura A Hansen, Henry Hennings, Stuart H YuspaAbstract:Retinoic acid (RA) was topically applied to the Skin of Sencar mice during the promotion phase of specific tumor induction protocols that produce Papillomas at low (12-O-tetradecanoylphorbol-13-acetate promoted, TPA) or high (mezerein-promoted) risk for premalignant progression and malignant conversion. RA consistently reduced the yield of Papillomas and carcinomas in both protocols, but the frequency of malignant conversion in Papillomas that emerged during RA treatment was not reduced. When TPA was reapplied after cessation of RA treatment, the number of Papillomas increased 2-fold, suggesting that RA had not eliminated initiated cells. In vitro, RA prevented the emergence of transformed keratinocytes in an assay that mimics malignant conversion, suggesting that RA can suppress conversion if applied during the stage of premalignant progression. Examination of tumor markers at weeks 14 and 22 of the tumor-induction experiments in vivo indicated that Papillomas evolving during RA treatment exhibited a phenotype of high progression risk, even in the TPA-promoted groups. In the majority of these tumors, the alpha6beta4 integrin and retinoid X receptor alpha transcripts were detected suprabasally, indicating an advanced state of premalignant progression. RA-treated tumors also expressed higher levels of transcripts for transforming growth factor (TGF)-beta1 and localized TGF-beta1 peptide in the basal portions of the tumor fronds. Because up-regulated expression of TGF-beta1 suppresses Papilloma formation, these studies suggest a mechanism whereby RA can prevent Papilloma eruption via a TGF-beta intermediate, but Papillomas resistant to RA may have altered TGF-beta signaling and progress to carcinomas at an increased frequency.
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Effect of excess dietary retinoic acid on Skin Papilloma and carcinoma formation induced by a complete carcinogenesis protocol in female Sencar mice
Cancer letters, 1994Co-Authors: Li Chuan Chen, Susan Kirchhoff, Luigi M. De LucaAbstract:Previously, we have shown that dietary retinoic acid (RA) at pharmacological doses (30 μg/g of diet) inhibited the malignant conversion of Skin Papillomas to carcinomas induced by a two-stage carcinogenesis protocol with 7,12-dimethylbenz[a]anthracene (DMBA) as initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as promoter (De Luca et al., Carcinogenesis, 14 (1993) 539–542). The purpose of this study was to determine the effect of dietary RA on Skin Papilloma and carcinoma formation induced by a complete carcinogenesis protocol with repeated DMBA treatment in female Sencar mice. Mice at 3 weeks of age were weaned onto a diet containing either 3 (control) or 30 (excess) μg of RA/g of diet and treated topically with DMBA (25.5 μg) once per week for 20 weeks. Mice fed excess dietary RA did not significantly differ from control mice in the following parameters: body weight, survival rate, Papilloma incidence, cumulative carcinoma incidence (19.4% versus 23.7%), carcinoma yield (0.19 versus 0.26 per mouse), carcinoma conversion efficiency (5.2% versus 3.9%), and average age of carcinoma development (22.7 ± 4.7 versus 23.3 ± 2.8 weeks). However, Papilloma yield was decreased by about 50% (i.e. 3.7 versus 7.0 at week 20, P < 0.01) between weeks 17 and 22 of age by excess dietary RA treatment. Contrary to other routes of administration (i.e. topical and systemic) of RA (Verma et al., Cancer Res., 42 (1982) 3519–3525), excess dietary RA did not enhance Skin tumor formation. In addition, excess dietary RA failed to inhibit malignant conversion of Papillomas to carcinomas in the complete carcinogenesis protocol. Thus, the modulation of RA on Skin Papilloma and carcinoma formation is dependent on carcinogenesis protocol and route of RA administration.
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effects of dietary retinoic acid on Skin Papilloma and carcinoma formation in female sencar mice
Carcinogenesis, 1993Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Previously we have shown that dietary retinoids are essential for Papilloma formation induced by either an initiation-promotion or a complete Skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on Papilloma formation and the conversion of Papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar Papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest Papilloma yield (approximately 14 Papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These Papillomas later regressed such that mice from all three groups had about the same Papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of Papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of Papillomas to carcinomas without affecting Papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered Papilloma yield.
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dietary retinoids are essential for Skin Papilloma formation induced by either the two stage or the complete tumorigenesis model in female sencar mice
Cancer Letters, 1992Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Abstract Our previous work has shown that dietary retinoic acid (RA) is necessary for Skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334–2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 μg), followed by 20 applications of TPA (2 μg), or by 20 applications of DMBA (25 μg for 2 weeks and 51 μg thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 μg/g of diet) or retinyl palmitate (RP, 6 μg/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for Skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol.
Carol S Jones - One of the best experts on this subject based on the ideXlab platform.
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Retinol and β‐carotene concentrations in Skin, Papillomas and carcinomas, liver, and serum of mice fed retinoic acid or β‐carotene to suppress Skin tumor formation
Nutrition and cancer, 1994Co-Authors: Carol S Jones, Li Chuan Chen, Linda Sly, Theresa Ben, M. Brugh-collins, Ulrike Lichti, L M De LucaAbstract:Abstract Using 7,12‐dimethylbenz[a] anthracene as the initiator and 12‐O‐tetradecanoyl‐13‐acetate as the tumor promoter on the dorsal Skin of Sencar mice, we previously showed that pharmacological dietary all‐trans‐retinoic acid and β‐carotene inhibit the conversion of Papillomas to carcinomas in a two‐stage system of chemical carcinogenesis. The purpose of this study was to determine the influence of dietary retinoic acid and β‐carotene on retinoidand β‐carotene concentrations in Skin and other tissues. We were unable to measure tissue retinoic acid because of the relatively limited amount of tissue available for analysis and the fast rate of metabolism. Different dietary levels of retinoic acid or β‐carotene did not influence total retinol of Skin, Papilloma, and carcinoma tissues, which all showed a concentration of approximately 1 ± 0.5 μg/g wet wt. Equally refractory to dietary retinoic acid or β‐carotene was serum retinol concentration. In contrast, dietary retinoic acid protected loss of liver reti...
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effects of dietary retinoic acid on Skin Papilloma and carcinoma formation in female sencar mice
Carcinogenesis, 1993Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Previously we have shown that dietary retinoids are essential for Papilloma formation induced by either an initiation-promotion or a complete Skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on Papilloma formation and the conversion of Papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar Papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest Papilloma yield (approximately 14 Papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These Papillomas later regressed such that mice from all three groups had about the same Papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of Papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of Papillomas to carcinomas without affecting Papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered Papilloma yield.
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dietary retinoids are essential for Skin Papilloma formation induced by either the two stage or the complete tumorigenesis model in female sencar mice
Cancer Letters, 1992Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Abstract Our previous work has shown that dietary retinoic acid (RA) is necessary for Skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334–2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 μg), followed by 20 applications of TPA (2 μg), or by 20 applications of DMBA (25 μg for 2 weeks and 51 μg thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 μg/g of diet) or retinyl palmitate (RP, 6 μg/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for Skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol.
Hajime Iizuka - One of the best experts on this subject based on the ideXlab platform.
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Photodynamic therapy using a novel irradiation source, LED lamp, is similarly effective to photodynamic therapy using diode laser or metal‐halide lamp on DMBA‐ and TPA‐induced mouse Skin Papillomas
The Journal of dermatology, 2014Co-Authors: Hidetoshi Takahashi, Susumu Nakajima, Ryuji Asano, Yoshinori Nakae, Isao Sakata, Koji Ogasawara, Hajime IizukaAbstract:Photodynamic therapy (PDT) is useful for superficial Skin tumors such as actinic keratosis and Bowen disease. Although PDT is non-surgical and easily-performed treatment modality, irradiation apparatus is large and expensive. Using 7, 12-dimethylbenz[a]anthracene (DMBA) and 12-ο-tetradecanoylphorbol-13-acetate (TPA)-induced mouse Skin Papilloma model, we compared the efficacy of TONS501- and ALA-PDT with a LED lamp, a diode laser lamp or a metal-halide lamp on the Skin tumor regression. TONS501-PDT using 660 nm LED lamp showed anti-tumor effect at 1 day following the irradiation and the maximal anti-tumor effect was observed at 3 days following the irradiation. There was no significant difference in the anti-tumor effects among TONS501-PDT using LED, TONS501-PDT using diode laser, and 5-aminolevulinic acid hydrochloride (ALA)-PDT using metal-halide lamp. Potent anti-tumor effect on DMBA- and TPA-induced mouse Skin Papilloma was observed by TONS501-PDT using 660 nm LED, which might be more useful for clinical applications.
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Photodynamic therapy using a novel photosensitizer, TONS501, is similarly effective to ALA and EC036 photodynamic therapy on DMBA-and TPA-induced mouse Skin Papilloma
Journal of dermatological science, 2012Co-Authors: Hidetoshi Takahashi, Susumu Nakajima, Ryuji Asano, Yoshinori Nakae, Isao Sakata, Hajime IizukaAbstract:Abstract Background Although topical photodynamic therapy (PDT) using 5-aminolevulinic acid (ALA) is applied for Skin tumors including actinic keratosis, Bowen disease, and squamous cell carcinoma, there are no approved photosensitizers in dermatological field in Japan. TONS501 and TONS504 are novel hydrophobic photosensitizers with anionic and cationic chemical characteristics, respectively. Objective Using 7, 12-dimethylbenz[a]anthracene (DMBA) and 12-ο-tetradecanoylphorbol-13-acetate (TPA)-induced mouse Skin Papilloma model, we compared the efficacy of ALA-, TONS501-, and TONS504-PDT on the Skin tumor regression. Methods Following application of ALA, TONS501, TONS504 ointment or TONS501 lotion on DMBA- and TPA-induced mouse Papillomas, 670 nm laser irradiation by LD670-05 diode laser was performed. Then tumor regression rate was calculated at the indicated time. Results The anti-tumor effect of ALA, TONS501, and TONS504 ointment was detected at 24 h and the maximal response was observed at 3 day following the PDT treatment. The maximal response was observed at 150 J/cm2 irradiation in all 3 photosensitizers. Although both ALA, TONS501 (ointment)-PDT showed more potent anti-tumor effect compared with that of TONS504 ointment or TONS501 lotion, no significant difference was detected between ALA ointment and TONS501 ointment. Conclusion A novel TONS501ointment-PDT shows potent anti-tumor effect on DMBA- and TPA-induced mouse Skin Papilloma and might be more useful for the clinical applications.
Linda Sly - One of the best experts on this subject based on the ideXlab platform.
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Retinol and β‐carotene concentrations in Skin, Papillomas and carcinomas, liver, and serum of mice fed retinoic acid or β‐carotene to suppress Skin tumor formation
Nutrition and cancer, 1994Co-Authors: Carol S Jones, Li Chuan Chen, Linda Sly, Theresa Ben, M. Brugh-collins, Ulrike Lichti, L M De LucaAbstract:Abstract Using 7,12‐dimethylbenz[a] anthracene as the initiator and 12‐O‐tetradecanoyl‐13‐acetate as the tumor promoter on the dorsal Skin of Sencar mice, we previously showed that pharmacological dietary all‐trans‐retinoic acid and β‐carotene inhibit the conversion of Papillomas to carcinomas in a two‐stage system of chemical carcinogenesis. The purpose of this study was to determine the influence of dietary retinoic acid and β‐carotene on retinoidand β‐carotene concentrations in Skin and other tissues. We were unable to measure tissue retinoic acid because of the relatively limited amount of tissue available for analysis and the fast rate of metabolism. Different dietary levels of retinoic acid or β‐carotene did not influence total retinol of Skin, Papilloma, and carcinoma tissues, which all showed a concentration of approximately 1 ± 0.5 μg/g wet wt. Equally refractory to dietary retinoic acid or β‐carotene was serum retinol concentration. In contrast, dietary retinoic acid protected loss of liver reti...
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effects of dietary retinoic acid on Skin Papilloma and carcinoma formation in female sencar mice
Carcinogenesis, 1993Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Previously we have shown that dietary retinoids are essential for Papilloma formation induced by either an initiation-promotion or a complete Skin carcinogenesis protocol. The present study was conducted to further determine the effect of dietary retinoic acid (RA) on Papilloma formation and the conversion of Papillomas to carcinomas. Skin tumors were induced in 3 week old female SENCAR mice by an initiation-promotion protocol with one application of 20 micrograms of 7,12-dimethylbenz[a]anthracene (DMBA), followed by 20 weekly applications of 2 micrograms of 12-O-tetradecanoylphorbol-13-acetate (TPA). Mice were fed RA at one of the three doses: 0.3 (nutritionally marginal dose), 3 (near physiological) and 30 (pharmacological) micrograms/g of diet. Mice fed 30 micrograms of RA/g of diet had the same survival rate as the other two groups despite a lower body weight and all three groups had similar Papilloma incidence, which reached 100% at age 18 weeks. Mice fed 3 micrograms of RA/g of diet had the highest Papilloma yield (approximately 14 Papillomas/mouse) of all groups and it peaked between weeks 18 and 38 of age. These Papillomas later regressed such that mice from all three groups had about the same Papilloma yield at week 44 of age. Mice fed 30 micrograms of RA/g of diet failed to develop any visible carcinoma, while mice fed 0.3 or 3 micrograms/g showed 1.9% conversion of Papillomas to carcinomas. Therefore, dietary RA at 30 micrograms/g of diet inhibited the conversion of Papillomas to carcinomas without affecting Papilloma incidence. In addition, dietary RA at 30 and 0.3 micrograms/g of diet lowered Papilloma yield.
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dietary retinoids are essential for Skin Papilloma formation induced by either the two stage or the complete tumorigenesis model in female sencar mice
Cancer Letters, 1992Co-Authors: Luigi M. De Luca, Linda Sly, Carol S Jones, Li Chuan ChenAbstract:Abstract Our previous work has shown that dietary retinoic acid (RA) is necessary for Skin tumor formation induced by the two-stage protocol with the initiator 7,12-dimethylbenz[a]anthracene (DMBA) and the promoter 12-O-tetradecanoyl phorbol-13-acetate (TPA) (De Luca et al., Cancer Res., 36 (1976) 2334–2339). Here we report that retinoids are required for tumorigenesis by the two-stage as well as by the complete tumorigenesis protocol. Mice were treated with a single dose of DMBA (20 μg), followed by 20 applications of TPA (2 μg), or by 20 applications of DMBA (25 μg for 2 weeks and 51 μg thereafter). Regardless of the tumor induction protocol, tumor formation was inhibited by vitamin A-deficiency, while RA (3 μg/g of diet) or retinyl palmitate (RP, 6 μg/g) supplementation permitted the appearance of tumors. In addition, in comparison to the purified diets and regardless of their RA levels, the non-purified Purina chow diet enhanced tumor yield especially in the two-stage tumorigenesis protocol. This effect was less striking in mice with tumors induced by the complete tumorigenesis protocol. In summary, dietary retinoids are essential for Skin tumor formation induced either by the two-stage or the complete tumorigenesis protocol.