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  1. Awang MN
    Singapore Med J, 1986 Aug;27(4):317-20.
    PMID: 3798144
    Areca catechu (betel) nut is widely used as a chewing agent. The nut alkaloids have been implicated in the pathogenesis of oral precancerous lesions. Quantitative analysis of the chloroform extracts by gas-liquid chromatography of ten commercial nut samples from Bombay have shown a wide variations In their arecoline contents (0% - 1.4%; mean: 0.7%). Nut samples of Identical processing method also vary in their arecoline levels. These variations were suggested to be due to the difference In the raw materials and processing methods. Comparisons were made between the arecoline contents and the Incidence of oral precancerous lesions from the present studies and also from those of Kerala and Mysore. It was concluded that the difference in nut arecoline contents not only reflect their appeal, potency but also influence upon the incidence of these diseases.
    Matched MeSH terms: Mouth Neoplasms/chemically induced*
  2. Arjungi KN
    Arzneimittelforschung, 1976;26(5):951-6.
    PMID: 786304
    Areca cattechu Linn is commonly known as areca nut or betel nut. It is a very widely cultivated plant in eastern countries like India, Bangladesh, Ceylon, Malaya, the Philippines and Japan. The importance of this nut is due to its use for chewing purposes. It had an important place as a pharmaceutical in Ayurveda--the ancient Indian system of medicine--also in the Chinese medicinal practices. The pharmaceutical importance of areca nut is due to the presence of an alkaloid, arecoline. Synthetic arecoline hydrobromide is also shown to possess numerous pharmacological properties. Chewing of "betel quid" or areca nut is a typical oriental habit. Betel quid comprises betel leaf, areca nut, catechu, lime and sometimes also tobacco. It is shown that there exists a correlationship between betel quid or areca nut chewing habit and oral cancer. A number of investigators have been able to produce cellular changes such as leukoplakia by application of betel quid or areca nut extract to the buccal mucosa of different animal.
    Matched MeSH terms: Mouth Neoplasms/chemically induced
  3. Al-Afifi N, Alabsi A, Kaid F, Bakri M, Ramanathan A
    Clin Oral Investig, 2019 May;23(5):2287-2301.
    PMID: 30291495 DOI: 10.1007/s00784-018-2685-6
    OBJECTIVES: In vivo study was performed to determine the chemopreventive efficacy of the DC resin methanol extract on a 4-nitroquinoline-1-oxide (4NQO) oral cancer animal model.

    MATERIALS AND METHODS: This study involves administration of 4NQO solution for 8 weeks alone (cancer induction) or with Dracaena cinnabari (DC) extract at 100, 500, and 1000 mg/kg. DC extract administration started 1 week before exposure until 1 week after the carcinogen exposure was stopped. All rats were sacrificed after 22 weeks, and histological analysis was performed to assess any incidence of pathological changes. Immunohistochemical expressions of selected tumor marker antibodies were analyzed using an image analyzer computer system, and the expression of selected genes involved in apoptosis and proliferative mechanism related to oral cancer were evaluated using RT2-PCR.

    RESULTS: The incidence of OSCC decreased with the administration of DC extract at 100, 500, and 1000 mg/kg compared to the induced cancer group. The developed tumor was also observed to be smaller when compared to the induced cancer group. The DC 1000 mg/kg group inhibits the expression of Cyclin D1, Ki-67, Bcl-2, and p53 proteins. It was observed that DC 1000 mg/kg induced apoptosis by upregulation of Bax and Casp3 genes and downregulation of Tp53, Bcl-2, Cox-2, Cyclin D1, and EGFR genes when compared to the induced cancer group.

    CONCLUSIONS: The data indicated that systemic administration of the DC resin methanol extract has anticarcinogenic potency on oral carcinogenesis.

    CLINICAL RELEVANCE: Chemoprevention with DC resin methanol extract may significantly reduce morbidity and possibly mortality from OSCC.

    Matched MeSH terms: Mouth Neoplasms/chemically induced
  4. Lee CH, Ko AM, Yen CF, Chu KS, Gao YJ, Warnakulasuriya S, et al.
    Br J Psychiatry, 2012 Nov;201(5):383-91.
    PMID: 22995631 DOI: 10.1192/bjp.bp.111.107961
    Despite gradual understanding of the multidimensional health consequences of betel-quid chewing, information on the effects of dependent use is scant.
    Matched MeSH terms: Mouth Neoplasms/chemically induced
  5. Cheong SC, Chandramouli GV, Saleh A, Zain RB, Lau SH, Sivakumaren S, et al.
    Oral Oncol, 2009 Aug;45(8):712-9.
    PMID: 19147396 DOI: 10.1016/j.oraloncology.2008.11.002
    Oral squamous cell carcinoma (OSCC) is a world health problem and is associated with exposure to different risk factors. In the west, smoking and alcohol consumption are considered to be the main risk factors whilst in India and southeast Asia, betel quid (BQ) chewing is predominant. In this study, we compared the gene expression patterns of oral cancers associated with BQ chewing to those caused by smoking using Affymetrix microarrays. We found that 281 genes were differentially expressed between OSCC and normal oral mucosa regardless of aetiological factors including MMP1, PLAU, MAGE-D4, GNA12, IFITM3 and NMU. Further, we identified 168 genes that were differentially expressed between the BQ and smoking groups including CXCL-9, TMPRSS2, CA12 and RNF24. The expression of these genes was validated using qPCR using independent tissue samples. The results demonstrate that whilst common genes/pathways contribute to the development of oral cancer, there are also other gene expression changes that are specific to certain risk factors. The findings suggest that different carcinogens activate or inhibit specific pathways during cancer development and progression. These unique gene expression profiles should be taken into consideration when developing biomarkers for future use in prognostic or therapeutic applications.
    Matched MeSH terms: Mouth Neoplasms/chemically induced
  6. Muir CS, Evans MD, Roche PJ
    Br. J. Cancer, 1968 Dec;22(4):637-45.
    PMID: 5705133 DOI: 10.1038/bjc.1968.75
    Matched MeSH terms: Mouth Neoplasms/chemically induced
  7. Ramu A, Kathiresan S, Ali Ahmed B
    Phytomedicine, 2017 Sep 15;33:69-76.
    PMID: 28887922 DOI: 10.1016/j.phymed.2017.05.008
    BACKGROUND: Transforming growth factor-β (TGF-β) and its receptors are considered as a novel target in cancer chemotherapy. Gramine, an indole alkaloid, possesses various pharmacological properties including antiproliferative and anticancer. However, the anti-angiogenic property remains unexplored.

    PURPOSE: The present study was designed to evaluate the anti-angiogenic and apoptosis induction properties of gramine through inhibiting TGF-β on DMBA induced oral squamous cell carcinoma (OSCC) in the hamster buccal pouch (HBP).

    METHODS: The effects of gramine on TGF-β signalling in DMBA induced carcinogenic events such as angiogenesis and apoptosis were analysed by studying the mRNA expression using RT-PCR, protein expression by western blot and histopathological analysis using haematoxylin and eosin (H & E) staining.

    RESULTS: Gramine significantly inhibited phosphorylation and nuclear translocation of Smad2 and Smad4 by blocking activity of the TGFβ-RII, RI and activation of inhibitory Smad7. Gramine inhibited angiogenic markers such as MMP-2, MMP-9, HIF-1α, VEGF, and VEGF-R2 as well as increased TIMP-2 expression. Furthermore, gramine induced apoptosis in DMBA induced tumour bearing animals by up regulating the pro apoptotic proteins Bax, cytochrome C, apaf-1, caspase-9 caspase-3 and PARP.

    CONCLUSION: In this study, we clearly demonstrated that gramine treatment diminishes angiogenesis and induces apoptosis in hamster buccal pouch (HBP) carcinogenesis by modulating TGF-β signals.

    Matched MeSH terms: Mouth Neoplasms/chemically induced
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