Human papillomavirus DNA sequences in esophagus squamous cell carcinoma

Togawa, Kazumi; Jaśkiewicz, K.; Takahashi, Hiroshi; Meltzer, Stephen J.; Rustgi, Anil K.

doi:10.1016/0016-5085(94)90070-1

Cited by 74 publications

(31 citation statements)

References 32 publications

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“…People exposed to bracken fern, whether as spores or in the diet, are at greater risk of developing oesophageal and gastric carcinoma (Hirayama, 1979;Galpin et al, 1990;Villalobos-Salazar et al, 1995;Alonso-Amelot et al, 1996Marliere et al, 2000). Moreover, HPV-16 has been found in up to approximately 50% of oesophageal cancers and precancers in developing countries (Chang et al, 1990;Togawa et al, 1994;Cooper et al, 1995;Suzuk et al, 1996;de Villiers et al, 1999;Syrjanen, 2002). There is a geographical overlap between consumption of bracken fern, infection of the alimentary canal mucosa by HPV and upper GI tract cancer, particularly in Asia and South America.…”

Section: Discussionmentioning

confidence: 99%

“…HPV16 has been associated with up to 50% of oesophageal precancers and cancers particularly in developing countries (Chang et al, 1990;Togawa et al, 1994;Cooper et al, 1995;Suzuk et al, 1996;de Villiers et al, 1999;Syrjanen, 2002). The highly variable geographical incidence of oesophageal cancer and of HPV detection in the cancer suggest a multifactorial aetiology and the involvement of environmental dietary cofactors (Syrjanen, 2002).…”

Section: Kip1mentioning

confidence: 99%

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Quercetin elevates p27Kip1 and arrests both primary and HPV16 E6/E7 transformed human keratinocytes in G1

Beniston

Campo

2003

Oncogene

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Section: Discussionmentioning

confidence: 99%

Section: Kip1mentioning

confidence: 99%

Quercetin elevates p27Kip1 and arrests both primary and HPV16 E6/E7 transformed human keratinocytes in G1

Beniston

Campo

2003

Oncogene

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“…Finally, human papilloma virus (HPV) may play a role in the etiology of esophageal SCC. A low frequency of HPV-16 or HPV-18 positivity has been reported in esophageal tumor samples (23).…”

mentioning

confidence: 99%

Protection Against Esophageal Cancer in Rodents With Lyophilized Berries: Potential Mechanisms

Stoner¹,

Chen²,

Kresty³

et al. 2006

Nutrition and Cancer

107

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For several years, our laboratory has been evaluating the ability of lyophilized (freeze-dried) black raspberries (Rubus occidentalis, BRBs), blackberries (R. fructicosus, BBs), and strawberries (Fragaria ananasia, STRWs) to inhibit carcinogen-induced cancer in the rodent esophagus. To assure "standardized" berry preparations for study, each berry type is of the same cultivar, picked at about the same degree of ripeness, washed and frozen within 2-4 h of the time of picking, and freeze-dried under conditions that preserve the components in the berries. Some of the known chemopreventive agents in berries include vitamins A, C, and E and folic acid; calcium and selenium; β-carotene, α-carotene, and lutein; polyphenols such as ellagic acid, ferulic acid, pcoumaric acid, quercetin, and several anthocyanins; and phytosterols such as β-sitosterol, stigmasterol, and kaempferol. In initial bioassays, freeze-dried STRW, BRB, and BB powders were mixed into AIN-76A synthetic diet at concentrations of 5% and 10% and fed to Fischer 344 rats before, during, and after treatment with the esophageal carcinogen Nnitrosomethylbenzylamine (NMBA). At 25 wk of the bioassay, all three berry types were found to inhibit the number of esophageal tumors (papillomas) in NMBA-treated animals by 24-56% relative to NMBA controls. This inhibition correlated with reductions in the formation of the NMBA-induced O 6 -methylguanine adduct in esophageal DNA, suggesting that the berries influenced the metabolism of NMBA leading to reduced DNA damage. Studies are ongoing to determine the mechanisms by which berries influence NMBA metabolism and DNA adduct formation. BRBs and STRWs were also tested in a postinitiation scheme and were found to inhibit NMBA-induced esophageal tumorigenesis by 31-64% when administered in the diet following treatment of the animals with NMBA. Berries, therefore, inhibit tumor promotion and progression events as well as tumor initiation. In vivo mechanistic studies with BRBs indicate that they reduce the growth rate of premalignant esophageal cells, in part, through down-regulation of cyclooxygenase-2 leading to reduced prostaglandin production and of inducible nitric oxide synthase leading to reduced nitrate/nitrite levels in the esophagus. Based upon the preclinical data on rodents, we have initiated prevention trials in humans to determine if berries might exhibit chemopreventive effects in the esophagus.

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“…Furthermore, diseases affecting the esophagus and nearby structures such as achalasia, previous head and neck cancer, and Plummer-Vision syndrome are associated with an increased risk for esophageal SCC (Layke and Lopez, 2006). Finally, a role for human papilloma virus (HPV) has also been suggested in the etiology of SCC of the esophagus (Togawa et al, 1994). To date, however, the exact role of HPV infections in the development of the disease has not been elucidated.…”

Section: Etiology Of Esophageal Sccmentioning

confidence: 99%

Chemoprevention of esophageal squamous cell carcinoma

Stoner

Wang

Chen

2007

Toxicology and Applied Pharmacology

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Esophageal squamous cell carcinoma (SCC) is responsible for approximately one-sixth of all cancerrelated mortality worldwide. This malignancy has a multifactorial etiology involving several environmental, dietary and genetic factors. Since esophageal cancer has often metastasized at the time of diagnosis, current treatment modalities offer poor survival and cure rates. Chemoprevention offers a viable alternative that could well be effective against the disease. Clinical investigations have shown that primary chemoprevention of this disease is feasible if potent inhibitory agents are identified. The Fischer 344 (F-344) rat model of esophageal SCC has been used extensively to investigate the biology of the disease, and to identify chemopreventive agents that could be useful in human trials. Multiple compounds that inhibit tumor initiation by esophageal carcinogens have been identified using this model. These include several isothiocyanates, diallyl sulfide and polyphenolic compounds. These compounds influence the metabolic activation of esophageal carcinogens resulting in reduced genetic (DNA) damage. Recently, a few agents have been shown to inhibit the progression of preneoplastic lesions in the rat esophagus into tumors. These agents include inhibitors of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF) and c-Jun [a component of activator protein-1 (AP-1)]. Using a food based approach to cancer prevention, we have shown that freeze-dried berry preparations inhibit both the initiation and promotion/progression stages of esophageal SCC in F-344 rats. These observations have led to a clinical trial in China to evaluate the ability of freeze-dried strawberries to influence the progression of esophageal dysplasia to SCC.

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Human papillomavirus DNA sequences in esophagus squamous cell carcinoma

Cited by 74 publications

References 32 publications

Quercetin elevates p27Kip1 and arrests both primary and HPV16 E6/E7 transformed human keratinocytes in G1

Quercetin elevates p27Kip1 and arrests both primary and HPV16 E6/E7 transformed human keratinocytes in G1

Protection Against Esophageal Cancer in Rodents With Lyophilized Berries: Potential Mechanisms

Chemoprevention of esophageal squamous cell carcinoma

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