Journal ArticleDOI
Role of areca nut in betel quid-associated chemical carcinogenesis: current awareness and future perspectives
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TLDR
It would appear that AN toxicity is not completely due to its polyphenol, tannin and alkaloid content, and further studies are needed to delineate the metabolism of AN ingredient and their roles in the multi-step chemical carcinogenesis, to enhance the success of the future chemoprevention of oral cancer and oral submucous fibrosis.About:
This article is published in Oral Oncology.The article was published on 2001-09-01. It has received 382 citations till now. The article focuses on the topics: Oral submucous fibrosis & Areca.read more
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β-Phenethyl isothiocyanate induces death receptor 5 to induce apoptosis in human oral cancer cells via p38
TL;DR: Results suggest that DR5 is a potential molecular target for PEITC-induced apoptosis in oral cancer via p38 MAPK.
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Decline of oropharyngeal cancer in Chiangmai province, Thailand, between 1988 and 1999.
TL;DR: Examination of trends in the incidence of oropharyngeal cancer in the province of Chiangmai, Thailand found changes of traditional oral habits seem to have resulted in a marked decrease of oral cancer in both men and women in the recent past.
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Oral cancer and pre-cancer in Myanmar : a short review
P. A. Reichart,T. H. Way +1 more
TL;DR: A recent symposium on oral health stressed the necessity to introduce concepts of prevention, focusing on BQC habits and smoking as high-risk factors for oral cancer and pre-cancer in Myanmar.
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Risk of betel quid chewing on the development of liver cirrhosis: a community-based case-control study.
TL;DR: The results suggest that betel quid chewing may play an important role in the development of hepatic cirrhosis.
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Arecoline decreases interleukin-6 production and induces apoptosis and cell cycle arrest in human basal cell carcinoma cells.
TL;DR: Subcutaneous injection of arecoline led to decreased BCC-1/KMC tumor growth in BALB/c mice by inducing apoptosis, and demonstrates that are coline has potential for preventing BCC tumorigenesis by reducing levels of the tumor cell survival factor IL-6, increasing levels ofThe tumor suppressor factor p53, and eliciting cell cycle arrest, followed by apoptosis.
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Prooxidant states and tumor promotion.
TL;DR: Prooxidant states can be caused by different classes of agents, including hyperbaric oxygen, radiation, xenobiotic metabolites and Fenton-type reagents, modulators of the cytochrome P-450 electron-transport chain, peroxisome proliferators, inhibitors of the antioxidant defense, and membrane-active agents.
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Insertion of specific bases during DNA synthesis past the oxidation-damaged base 8-oxodG.
TL;DR: DCMP and dAMP are incorporated selectively opposite 8-oxodG with transient inhibition of chain extension occurring 3' to the modified base, and the potentially mutagenic insertion of dAMP is targeted exclusively to the site of the lesion.
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Oxyradicals and DNA damage
TL;DR: The levels of oxidative DNA damage reported in many human tissues or in animal models of carcinogenesis exceed the levels of lesions induced by exposure to exogenous carcinogenic compounds, and it seems likely that oxidativeDNA damage is important in the etiology of many human cancers.
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Apoptosis in cancer
Scott W. Lowe,Athena W. Lin +1 more
TL;DR: An intense research effort is uncovering the underlying mechanisms of apoptosis such that, in the next decade, one envisions that this information will produce new strategies to exploit apoptosis for therapeutic benefit.
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Free radicals as mediators of tissue injury and disease.
TL;DR: This review discusses cellular sources of various radical species and their reactions with vital cellular constituents to provide insights into the controversy over whether free radicals are important mediators of tissue injury.