Effects of Polyoxyethylene Sorbitan Monostearate (Tween 60) upon Experimental Oral Carcinogenesis in the Hamster

Dachi, Stephen F.

doi:10.1177/00220345620410022201

Cited by 13 publications

(5 citation statements)

References 7 publications

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“…Dysplastic and neoplastic lesions developed more rapidly, grew to a larger size and were more deeply invasive and anaplastic than in the control group. Dachi (1962) showed that Tween 60 (polyoxyethylene sorbitan monostearate), a powerful promoter in the skin, aeted co-eareinogenically with DMBA in the eheek poueh. Tween 80 (polyoxyethylene sorbitan monooleate), however, appeared to have no influenee on DMBA-indueed eheek-poueh careinogenesis (Sabes et al 1959).…”

Section: ) Co-carcinogetiesismentioning

confidence: 99%

Animal models of infra‐oral chemical carcinogenesis: A review

Eveson

1981

J Oral Pathology Medicine

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Early attempts to induce malignant oral tumours were largely unsuccessful, us the oral mucosa is considerably more resistant to the actions of chemical carcinogens than skin. The first consistent success came when strong carcinogens were applied to the hamster cheek pouch. This model remains the most popular for studies of intra‐oral carcinogenesis and is discussed at length. The advantages and disadvantages are critically reviewed. The models of intra‐oral carcinogenesis in extra‐pouch sites in the hamster, mouse, rat and nonhuman primates arc considered. The possible reasons for the relative resistance of oral mucosa to chemical carcinogens are discussed, particularly in relation to portals of entry and saliva. Finally, the relative merits of the more popular models of intra‐oral carcinogenesis are briefly discussed.

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Section: ) Co-carcinogetiesismentioning

confidence: 99%

Animal models of infra‐oral chemical carcinogenesis: A review

Eveson

1981

J Oral Pathology Medicine

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“…The investigators further suggested a second role of alcohol in oral carcinogenesis, namely that it may act as a promoter or cocarcinogen on the exposed oral membranes. Since the work of Berenblum6 and the postulation of a two-stage phenomenon of carcinogenesis consisting of an initiation and promotion stage, agents such as irritation,7 polyoxyethylene sorbitan monosterate (Tween 60), 8 and croton oil9 have been successfully shown This study was supported by USPHS institutional grant S01 FR 5345-04.…”

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confidence: 99%

Local Effect of Alcohol in Combination with DMBA on Hamster Cheek Pouch

Elzay

1966

J Dent Res

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SYNOPSIS IN INTERLINGUA LE EFFECTO LOCAL EXERCITE SUPER LE CAVITATE VESTIBULAR DEL HAMSTER PER ALCOHOL IN COMBINATION CON DMBA (7,12-DIMETHYL-BENz-(a)-ANTHRACENo).-Le cavitates esseva pingite con solutiones de DMBA in oleo mineral, solutiones de DMBA in alcohol ethylic, oleo mineral, e alcohol ethylic durante 9 septimanas e tenite sub observation durante 18. Le periodos latente e le magnitude e numero del resultant tumores esseva registrate. Le constatationes microscopic esseva correlationate subsequentemente con le constatationes clinic. Le cavitates tractate con DMBA in alcohol exhibiva tumores plus precocemente e de magnitude e numero plus grande que cavitates tractate con DMBA in oleo mineral. Alcohol sol non produceva tumores. Per consequente il pare que alcohol age localmente como agente promotori in experimental carcinogenese oral.Numerous clinical statistical and epidemiological reports attest to the strong correlation existing between oral cancer and the drinking of alcohol and smoking of tobacco.'-3 Ketcham, Wexler, and Mantel4 have studied the effect of alcohol as source of fluid intake upon skin carcinogenesis in mice and found the alcohol regimen did not alter carcinogenesis or stimulate the metastatic spread of tumor transplant. Protzel, Giardina, and Albano5 studied one hypothesis regarding the relation of alcohol to oral cancer. Their study assumed that alcohol primarily affected the liver, producing cirrhosis and thus interfering with the metabolism of the carcinogen (benzpyrene) in the hepatobiliary system. Alcohol-drinking rats, the buccal mucosas of which were painted with a carcinogen, developed liver damage and decreased latency with increased frequency of oral tumor development. The investigators further suggested a second role of alcohol in oral carcinogenesis, namely that it may act as a promoter or cocarcinogen on the exposed oral membranes. Since the work of Berenblum6 and the postulation of a two-stage phenomenon of carcinogenesis consisting of an initiation and promotion stage, agents such as irritation,7 polyoxyethylene sorbitan monosterate (Tween 60),8 and croton oil9 have been successfully shown This study was supported by USPHS institutional grant S01 FR 5345-04.

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“…Studies of oral mucosal co-carcinogenesis, rather than two-stage eareinogenesis, have been reported previously. Tween 60 (polyoxyethylene .sorbitan monostearate), whieh has been shown to act as a promotor in skin, has co-careinogenie activity in the hamster eheek poueh model when applied together with DMBA (5). Similarly, it has been shown that eroton oil acts co-earcinogenieally with DMBA in eheek-poueh eareinogenesis in old hamsters, but not in young hamsters (6).…”

Section: Discussionmentioning

confidence: 99%

“…In the field of experimental oral mueosal eareinogenesis, several studies of eo-carcinogenesis, rather than strietly two-stage eareinogenesis, have been undertaken (. [5][6][7][8], some with eontradietory results. When hamsters treated with dimethylbenz-anthracene (DMBA) are given a 30"/o v/v aqueous solution of cthanol instead of water to drink no difference in latent period or numbers of neoplasms in the eheek pouches can be demonstrated (7).…”

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confidence: 99%

Initiation and promotion of experimental oral mucosal carcinogenesis in mice

Steidler

Reade

1986

J Oral Pathology Medicine

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While there is considerable evidence that skin carcinogenesis proceeds as a step‐wise series of changes, little evidence is available to indicate that a similar mechanism applies to oral mucosal carcinogenesis. In the current study, a mouse model of mucosal carcinogenesis was used to examine the effects of repeated applications of the phorbol ester phorbol‐12,13‐didecanoate (FDD) following various periods of treatment with the carcinogen 4‐nitroquinoline‐1‐oxide (4NQO). All animals were histologically examined at 50 weeks. Oral epithelial dysplasia was seen in animals treated with 4NQO for as little as 2 weeks, and oral squamous cell carcinomas developed in all animals treated with 4NQO for 12 weeks. In those mice treated with PDD as well, carcinomas developed in mice receiving as little as 2 weeks treatment with 4NQO, and 100% of mice treated with 4NQO for 12 weeks, followed by PDD treatment, developed carcinomas. The results indicate that irreversible changes in the oral mucosa of mice occur relatively early during treatment with 4NQO, and the development of carcinomas can be enhanced with subsequent PDD treatment, giving an indication of staged carcinogenesis in this model system.

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Effects of Polyoxyethylene Sorbitan Monostearate (Tween 60) upon Experimental Oral Carcinogenesis in the Hamster

Cited by 13 publications

References 7 publications

Animal models of infra‐oral chemical carcinogenesis: A review

Animal models of infra‐oral chemical carcinogenesis: A review

Local Effect of Alcohol in Combination with DMBA on Hamster Cheek Pouch

Initiation and promotion of experimental oral mucosal carcinogenesis in mice

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