Evaluation of carcinogenic/co-carcinogenic activity of a common chewing product, pan masala, in mouse skin, stomach and esophagus

Ramchandani, Asha G.; D'Souza, A. V.; Borges, Anita M.; Bhisey, Rajani A.

doi:10.1002/(sici)1097-0215(19980119)75:2<225::aid-ijc10>3.0.co;2-c

Cited by 25 publications

(18 citation statements)

References 31 publications

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“…24 The genotoxic and cytotoxic effects on various types of cells have also been detected. 25 Ramchandani et al 26 further indicated that habitual use of pan masala, a common chewing product used with areca nut in India, may exert a carcinogenic and co-carcinogenic influence in the stomach and esophagus.…”

Section: Discussionmentioning

confidence: 99%

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Lee

et al. 2004

Intl Journal of Cancer

211

175

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A multicenter case-control study was conducted in northern and southern Taiwan to clarify the independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer. A total of 513 patients with newly diagnosed and histopathologically confirmed squamous cell carcinoma of the esophagus and 818 gender, age and study hospitalmatched controls were included. We found a significant doseresponse relationship between the duration and intensity of consumption of the 3 substances and the development of this neoplasm in this site. Although the amount of alcohol consumed had a stronger effect on the risk of esophageal cancer than the number of years it was consumed, however, the number of years one smoked had a stronger effect on the risk than the amount of cigarettes consumed. The strongest risk factor of esophageal cancer was alcohol intake, with highest risk (OR ‫؍‬ 13.9) being for those who consumed more than 900 g/day-year. Combined exposure to any 2 of 3 substances brought the risks up to 8.8 -19.7 fold and, to all 3 substances, to 41.2-fold. A multiplicative interaction effect for alcohol drinkers who smoked on cancer risk was detected, whereas an additive interaction effect was found among drinkers who chewed. The combined effect of all 3 substances accounted for 83.7% of the attributable fraction of contracting esophageal cancer in this population. In conclusion, these results suggest that the intensity and the length of time alcohol and tobacco are used play different roles in the etiology of esophageal cancer. Alcohol separately interacts with tobacco and betel quid in a differently synergistic way in determining the development of this site of cancer.

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Section: Discussionmentioning

confidence: 99%

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Lee

et al. 2004

Intl Journal of Cancer

211

175

View full text Add to dashboard Cite

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“…24 Both chromosome regions harbor genes related to the prostaglandin system, 32,33 which may play a role in the pathogenesis of EC-SCC. 32,34 Conversely, the betel nut, a common carcinogen found in both Taiwan and South Africa, has been identified recently as a possible factor in esophageal carcinogenesis, 35 and the carcinogenic effect of betel nuts has been related to the prostaglandin system. 36 Thus, the possible association between betel nuts and aberrations of chromosomal regions related to the prostaglandin system deserves further studies.…”

Section: Discussionmentioning

confidence: 99%

Comparative genomic hybridization of esophageal squamous cell carcinoma

Yen

M.D.²,

Chen

et al. 2001

Cancer

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“…As a positive control for detection of mutations in human Ha-ras codons 12 and 61, DNA from T24 cells (GGC to GTC in codon 12) 33) (JCRB0711, obtained from Health Science Research Resources Bank, Japan Health Sciences Foundation, Tokyo) and a pSK2 plasmid (CTG to CAG in codon 61) 31) (CO001, obtained from Health Science Research Resources Bank, Japan Health Sciences Foundation) was used.…”

Section: Methodsmentioning

confidence: 99%

“…7,8) Therefore the Hras128 rats generated in our laboratory have great potential for studies of neoplasia. 9,10) For esophageal tumors, rats are preferable to mice 11,12) due to the availability of the organotropic carcinogens and the larger size of the organ.Human esophageal squamous cell carcinomas are presumed to be caused by exposure to nitrate and nitrite, precursors of nitrosamines.13) The promutagenic adduct, O 6 -methylguanine, formed due to nitrosamine attack has been detected in DNA from esophageal cancer patients in China 14,15) and N-nitrosomethylbenzylamine (NMBA) is known to be a potent esophageal carcinogen in rats. [16][17][18][19] Its mechanism of action is through microsomal activation to the methyldiazonium ion, an electrophilic metabolite which methylates DNA, producing O 6 -and O 7 -methylguanine adducts.…”

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confidence: 99%

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Transgenic Rats Carrying Human c‐Ha‐ras Proto‐oncogene Are Highly Susceptible to N‐Nitrosomethylbenzylamine Induction of Esophageal Tumorigenesis

Asamoto

Toriyama‐Baba

Ohnishi

et al. 2002

Japanese Journal of Cancer Research

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A transgenic rat line carrying three copies of the human c-Ha-ras proto-oncogene, including its own promoter region, has been established in our laboratory (Hras128 rats), and shown to be highly susceptible to induction of mammary and urinary bladder tumors. Mutation analysis of induced lesions indicated the majority to contain some but not all cells with transgene mutation. In the present study, the susceptibility of Hras128 rats to N-nitrosomethylbenzylamine (NMBA) induction of esophageal tumors was examined with a similar mutation analysis of the transgenes. Male 6-week-old Hras128 and wild littermate rats were treated with NMBA, 0.5 mg/kg subcutaneously, 3 times a week for 5 weeks and then maintained for 5 weeks without any further treatment. Multiple esophageal tumors, squamous cell papillomas and carcinomas, rapidly developed within this 10-week experimental period in Hras128 rats (11.05 ± ± ± ±7.83/rat). In contrast, wild-type littermates had only small numbers of mostly benign tumors (1.67 ± ± ± ±2.06/rat). The Hras128 rats had no other tumors or abnormalities. In their esophageal lesions, codon 12 GGC to GAC mutations of the transgene were frequently detected by restriction fragment length polymorphisms (RFLP) and subsequent direct sequencing analysis (19/25, 76%). In the endogenous rat c-Ha-ras gene they were less frequent (2/25, 8%), than in wild-type rats (8/14, 57.1%). The densities of mutated bands in the RFLP analysis indicated that mutated cells were major populations in tumors, in contrast to the case with mammary and urinary bladder lesions. Furthermore, activated ras protein, detected by binding to raf protein, was clearly increased in tumors as compared to surrounding epithelium or the normal esophagus of untreated rats. The results show that Hras128 rats are highly susceptible to NMBA esophageal carcinogenesis, as well as induction of mammary and urinary bladder tumors, but that tissue-specific characteristics exist for the roles of transgene ras mutations.Key words: Transgenic rats -c-Ha-ras -Esophageal tumors -N-Nitrosomethylbenzylamine Transgenic mice are widely used for analysis of gene function and as animal models for various diseases. In the field of chemical carcinogenesis, transgenic mice harboring a human c-Ha-ras proto-oncogene, 1, 2) v-Ha-ras transgenic mice (Tg.AC mice),3) pim-1 transgenic mice 4) and p53 knockout mice 5) have been shown to be highly susceptible to tumor induction by certain carcinogens, with indication that the transgene is actively involved. However, for studies of chemical carcinogenesis, 6) rats have been more frequently used, so that abundant information has accumulated regarding various biological characteristics of preneoplasias. 7,8) Therefore the Hras128 rats generated in our laboratory have great potential for studies of neoplasia. 9,10) For esophageal tumors, rats are preferable to mice 11,12) due to the availability of the organotropic carcinogens and the larger size of the organ.Human esophageal squamous cell carcinomas are presumed to be caused by ...

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Evaluation of carcinogenic/co-carcinogenic activity of a common chewing product, pan masala, in mouse skin, stomach and esophagus

Cited by 25 publications

References 31 publications

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan

Comparative genomic hybridization of esophageal squamous cell carcinoma

Transgenic Rats Carrying Human c‐Ha‐ras Proto‐oncogene Are Highly Susceptible to N‐Nitrosomethylbenzylamine Induction of Esophageal Tumorigenesis

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