Fig. 1. Schematic representation of experimental protocol

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Fig. 1. Schematic representation of experimental protocol Fig. 1. Schematic representation of experimental protocol. The downward arrows indicate injection of NMBA 1 mg/kg body wt; upward arrows indicate injection of resveratrol at 1 (groups 4, 6, 8 and 10), or 2 mg/kg body wt (groups 5, 7 and 9). The hatched box indicates injection of saline 1 ml/kg body wt or DMSO 5 ml/kg body wt. From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 2. Micrographs showing H&E stained histopathological representation of NMBA-induced tumorigenesis in the rat esophagus. ( A ) Photomicrograph of a normal rat esophagus (100× magnification). ( B ) Papilloma with a well-developed, peripherally branched stalk covered by acanthotic squamous epithelium (100× magnification). ( C ) Papilloma with atypia (pre-cancerous lesion with multiple keratic pearls) (100× magnification). ( D ) Early endophytic squamous cell carcinoma of the esophagus (100× magnification). From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 2. Micrographs showing H&E stained histopathological representation of NMBA-induced tumorigenesis in the rat esophagus. ( A ) Photomicrograph of a normal rat esophagus (100× magnification). ( B ) Papilloma with a well-developed, peripherally branched stalk covered by acanthotic squamous epithelium (100× magnification). ( C ) Papilloma with atypia (pre-cancerous lesion with multiple keratic pearls) (100× magnification). ( D ) Early endophytic squamous cell carcinoma of the esophagus (100× magnification). From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 2. Micrographs showing H&E stained histopathological representation of NMBA-induced tumorigenesis in the rat esophagus. ( A ) Photomicrograph of a normal rat esophagus (100× magnification). ( B ) Papilloma with a well-developed, peripherally branched stalk covered by acanthotic squamous epithelium (100× magnification). ( C ) Papilloma with atypia (pre-cancerous lesion with multiple keratic pearls) (100× magnification). ( D ) Early endophytic squamous cell carcinoma of the esophagus (100× magnification). From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 2. Micrographs showing H&E stained histopathological representation of NMBA-induced tumorigenesis in the rat esophagus. ( A ) Photomicrograph of a normal rat esophagus (100× magnification). ( B ) Papilloma with a well-developed, peripherally branched stalk covered by acanthotic squamous epithelium (100× magnification). ( C ) Papilloma with atypia (pre-cancerous lesion with multiple keratic pearls) (100× magnification). ( D ) Early endophytic squamous cell carcinoma of the esophagus (100× magnification). From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 5. Effect of resveratrol on NMBA-induced PGE <sub>2</sub> production. Group 1 is the normal esophageal mucosa; group 3 received NMBA alone; groups 8 and 9 were given resveratrol at different doses (1 and 2 mg/kg); group 10 also received resveratrol 1 mg/kg, while administration was continued for 20 weeks. N, non-tumor tissue; T, tumor tissue. Data are the means ± SD of pg/mg protein accumulation. Significance, determined by using Tukey–Kramer test, is expressed as follows: * P < 0.05, group 3 (tumor tissue) versus group 1 (normal mucosa); ** P < 0.01 groups 9 and 10 (tumor tissue) versus group 3 (tumor tissue). From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 3. Multiplex RT–PCR assay for COX-1 mRNA in relation to resveratrol treatment. Results for groups 1 (normal mucosa), 3 (NMBA alone), 8 (NMBA plus resveratrol 1 mg/kg), 9 (NMBA plus resveratrol 2 mg/kg) and 10 (NMBA plus resveratrol 1 mg/kg, continuous administration) are shown. N, non-tumor tissue; T, tumor tissue. GAPDH was used as the internal standard. PCR product sizes: COX-2, 702 bp; GAPDH, 230 bp. M, 100 bp molecular marker. From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press

Fig. 4. Multiplex RT–PCR assay for COX-2 mRNA in relation to resveratrol treatment. Results for groups 1 (normal mucosa), 3 (NMBA alone), 8 (NMBA plus resveratrol 1 mg/kg), 9 (NMBA plus resveratrol 2 mg/kg) and 10 (NMBA plus resveratrol 1 mg/kg, continuous administration) are shown. N, non-tumor tissue; T, tumor tissue. GAPDH was used as the internal standard. PCR product sizes: COX-2, 702 bp; GAPDH, 230 bp. M, 100 bp molecular marker. From: Suppression of N -nitrosomethylbenzylamine (NMBA)-induced esophageal tumorigenesis in F344 rats by resveratrol Carcinogenesis. 2002;23(9):1531-1536. doi:10.1093/carcin/23.9.1531 Carcinogenesis | © Oxford University Press