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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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Using the “target constituent removal combined with bioactivity assay” strategy to investigate the optimum arecoline content in charred areca nut

TL;DR: It is suggested that the strategy of “target constituent removal combined with bioactivity assay” is a promising method to identify the optimum arecoline content in CAN, which is approximately 0.12%.
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Low dietary n-6/n-3 polyunsaturated fatty acid ratio prevents induced oral carcinoma in a hamster pouch model.

TL;DR: The lower dietary n-6/n-3 fatty acid ratio exerted chemopreventive effects in the DMBA- and BQE-induced hamster oral cancer model, showing a significantly lower tumor number, volume, and burden than those of the other groups.
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Carcinoma arising in the background of oral submucous fibrosis

TL;DR: Oral squamous cell carcinoma arising from a background of oral submucous fibrosis follows a distinct clinical presentation andMalignant transformation occurs in younger age group and with better histological grading.
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Helioxanthin suppresses the cross talk of COX‐2/PGE2 and EGFR/ERK pathway to inhibit Arecoline‐induced Oral Cancer Cell (T28) proliferation and blocks tumor growth in xenografted nude mice

TL;DR: It is demonstrated that Helioxanthin exerts its anticancer activity against oral cancer cells by downregulating EGFR/ERK/c‐fos signaling pathway to inhibit COX‐2 level and by activating cyclin‐dependent kinase inhibitor (p27) to further induce G2/M cell cycle arrest.
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Effect on micronucleus frequency and DNA damage in buccal epithelial cells of various factors among pan masala and gutkha chewers

TL;DR: The results of the present study reveal that the micronucleus frequency and comet tail length in buccal epithelial cells are higher in gutkha users as compared to pan masala users and also to controls.
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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