Carcinogenic effects stomach cancer

In a bioassay conducted by the National Cancer Institute (NCI), EDB was found to be carcinogenic to rats and mice when fed by gavage. The compound induced squamous cell carcinomas of the forestomach in rats (of both sexes), hepatocellular carcinomas in female rats, and hemangiosarcomas in male rats. In mice of both sexes, the compound induced squamous cell carcinomas of the forestomach as well as alveolar and broncheolar adenomas. The nature of adverse effects included abnormalities in offspring, mutations, and stomach cancer.417 The available data suggest that additional information is needed. 

In 10 552 Swedish patients (mean age 57 years) who received I for hyperthyroidism (mean follow-up 15 years) there were increases in overall cancer mortality and deaths due to carcinoma of the stomach, lung, and kidney. While the findings for stomach cancer may be of significance, for tumors at other sites, because of an association with time after I treatment (58 cases at 10 years or more of follow-up against the expected 44 cases), the lack of a relation between cancer mortality and either the time from radioiodine treatment or the dose administered argues against a carcinogenic effect of radioiodine (SEDA-17, 475) (25). 

DATS which are potent inhibitors of BP-induced fore-stomach cancer in mice, resulted in a significant increase, as compared with control, in bodi hepatic (3.0-, 3.2-and 4.4-fold, respectively) and fore-stomach (1.5-, 2.7-and 2.7-fold, respectively) glutathione transferase (GST) activity toward anti-7P,8a-dihy oxy-9a, 1 Oa-oxy-7,8,9,10-tetrahydrobenzo(a)pyrene (anti-BPDE), which is the ultimate carcinogen of BP [102, 107]. On the contrary, this activity was not increased in either organ by dipropyl sulfide (DPS), which is ineffective against BP-induced fore-stomach cancer. The pulmonary GST activity was not increased by any of the tested OSCs. Even though epoxide hydrolase (EH) activity was differentially altered by these OSCs, a correlation between chemopreventive efficacy of OSCs and their effects on EH activity was not apparent [102]. The chemopreventive efficacy of these OSCs correlated with their ability to increase the expression of GST n. For example, DAS treatment resulted in approximate increases of 1.7- and 2.2-fold in hepatic and fore-stomach GST n expression, respectively, over the control. Treatment of mice with DATS, which is a relatively more potent inhibitor of BP-induced fore-stomach cancer than DAS, resulted in about 3.8- and 3,2-fold increases, respectively, in hepatic and fore-stomach GST n expression over the control. On the contrary, the expression of hepatic and fore-stomach GST n was increased only marginally (10-20%) upon DPS administration [107],... 

Tumorigenicity Although butylated hydroxytoluene can induce tumors in rats, others have suggested that it may protect tissues against the carcinogenic effects of many different substances. In a study of the association between dietary intake of the synthetic antioxidants butylated hydroxyanisole and butylated hydroxytoluene and the risk of stomach cancer in 120852 men and women aged 55-69 years there was no significant association [25 ]. 

Radiation is carcinogenic. The frequency of death from cancer of the thyroid, breast, lung, esophagus, stomach, and bladder was higher in Japanese survivors of the atomic bomb than in nonexposed individuals, and carcinogenesis seems to be the primary latent effect of ionizing radiation. The minimal latent period of most cancers was <15 years and depended on an individual s age at exposure and site of cancer. The relation of radiation-induced cancers to low doses and the shape of the dose-response curve (linear or nonlinear), the existence of a threshold, and the influence of dose rate and exposure period have to be determined (Hobbs and McClellan 1986). 

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