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Model Introduction
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Inflammatory associated colon cancer model
AOM/DSS model damages intestinal mucosa through inflammation and atypical hyperplasia of colon mucosa and promotes tumor generation. It is the most widely used chemical induction model for ulcerative colitis at present. Clinical symptomatology, morphology and pathology observation have proved that this model is very similar to the carcinogenesis process of human ulcerative colitis.
Dextran Sodium Sulfate (DSS) + Azomethane oxide (AOM)
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Gastric cancer model 01
N-methyl-n-nitrosyrea (MNU) is a potent direct alkylating agent and carcinogen that is often used in experimental studies to induce many types of tumors, including gastric, colorectal, and breast cancers.
N-methyl-n-nitrosyl urea（MNU）
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Gastric cancer model 02
N-methyl-n '-nitro-n-nitroguanidine (MNNG) can alkalize the bases on the DNA strand, resulting in mutations, and is often used in experimental studies to induce stomach cancer.
MNNG
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Hepatoma model 01
Diethylnitrosamine (DEN) is the most common chemical carcinogen, which has specific toxicity to the liver, causing large area necrosis of liver cells, and eventually inducing the occurrence of primary liver cancer.
Diethylnitrosamine（DEN）
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Hepatoma model 02
Aflatoxin, a toxin produced by certain molds and commonly found in damp grains, nuts and other foods, is classified by the International Agency for Research on Cancer as a Group 1 carcinogen, meaning a substance that is clearly carcinogenic to humans. Aflatoxin produces a highly active epoxy compound during metabolism in the body, which is able to bind to DNA to form admixtures, causing DNA damage and thus promoting tumor development.
Aflatoxin（AFB）
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Hepatoma model 03
After 4 to 6 months of continuous feeding with DAB feed, the model can be formed, and the induction speed is fast, but the cancer induction rate is about 60%.
P-dimethylaminoazobenzene (DAB)
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Hepatoma model 04
TAA entering the body can cause hepatocyte necrosis and liver fibrosis, and at the same time, it is easy to produce enterogenic endotoxemia, which further worsens liver function and eventually leads to liver cancer.
Thioacetamide（TAA）
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Highly differentiated liver cancer model
2-AFF can form near-carcinogens through the metabolic activation process, and these near-carcinogens can bind to DNA, cause gene mutations, and thus trigger tumors. Liver cancer induced by 2-AAF mostly belongs to highly differentiated liver cancer.
2-acetic acid amino acid（2-AAF）
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Bladder cancer model 01
The main risk factors for bladder cancer are environmental carcinogens, such as nitrosamines such as n-butyl-N -(4-hydroxybutyl) nitrosamines (BBN). BBN will undergo oxidation and glucuronic acid conjugation after entering the body. Its oxidized product N-butyl-N -(3-carboxypropyl) -nitrosamine (BCPN) forms adducts with the DNA of urothelium cells, thereby inducing tumorigenosis. Therefore, long-term exposure to BBN is a routine method for inducing bladder cancer in rodent models.
N-butyl -N-(4-hydroxybutyl) nitrosamine（BBN）
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Bladder cancer model 02
FANFT is an indirect carcinogenic compound of nitrofuran. The tumor formation rate of bladder cancer in experimental animals induced by feeding diets containing FANFT for more than 8 months was close to 100%.
Nitrofuranothiazole formamide (FANFT)
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