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Journal ArticleDOI

Role of areca nut in betel quid-associated chemical carcinogenesis: current awareness and future perspectives

Jiiang-Huei Jeng, +2 more
- 01 Sep 2001 - 
- Vol. 37, Iss: 6, pp 477-492
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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.
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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.

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Journal ArticleDOI

Functional Genetic Variant of Long Pentraxin 3 Gene Is Associated With Clinical Aspects of Oral Cancer in Male Patients

TL;DR: It is suggested that PTX3 rs3816527 plays a role in oral cancer development and was correlated with the development of late-stage cancer (odds ratio], 2.328; 95% confidence interval [CI], 1.078–5.027).
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Prevalence of Head and Neck Cancer in the State of Meghalaya: Hospital-based Study

TL;DR: A 5 years retrospective study of cancer patients from 2007 to 2011 who have been registered in Civil Hospital, Shillong to quantify the spectrum of head and neck cancer (HNC) in the region hoping that this paper will help the health professionals to understand the burden of HNC in the area so as to generate strategies for future planning.
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Arecoline N-oxide initiates oral carcinogenesis and arecoline N-oxide mercapturic acid attenuates the cancer risk.

TL;DR: In this article, the authors estimate the oral squamous cell carcinoma inductive activity between arecoline metabolites in human cancer specimens/OSCC cells using LC-MS/MS.
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Arecoline inhibits the growth of 3T3-L1 preadipocytes via AMP-activated protein kinase and reactive oxygen species pathways.

TL;DR: The results suggested that arecoline selectively affected a particular CDK subfamily, and the effects of are coline on preadipocyte growth may be related to the mechanism underlying the modulatory effect ofArecoline on body weight.
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Betel Nut Arecoline Induces Different Phases of Growth Arrest between Normal and Cancerous Prostate Cells through the Reactive Oxygen Species Pathway

TL;DR: Arecoline oxidant exerts differential effects on the cell cycle through modulations of regulatory proteins, and the antioxidant N-acetylcysteine blocked the arecoline-induced increase in reactive oxygen species production, decreased cell viability, altered thecell cycle, and changed the cell Cycle regulatory protein levels.
References
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Journal ArticleDOI

Prooxidant states and tumor promotion.

Peter A. Cerutti
- 25 Jan 1985 - 
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

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.
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