Disease relevance of Mouth Neoplasms

• Tolonium (toluidine blue) rinse--a screening method for recognition of squamous carcinoma. Continuing study of oral cancer IV [1].
• Retinoids are useful in the treatment of premalignant oral lesions and in preventing the occurrence of second primary cancers after resection of the initial primary oral cancer, but long-term prognosis is still poor, presumably due to malignant cells escaping retinoid control [2].
• Inactivation of the Fanconi anemia/BRCA pathway in lung and oral cancers: implications for treatment and survival [3].
• NSAIDs for the chemoprevention of oral cancer: promise or pessimism?: Commentary re J. L. Mulshine et al., randomized, double-blind, placebo-controlled, phase IIB trial of the cyclooxygenase inhibitor ketorolac as an oral rinse in oropharyngeal leukoplakia. Clin. Cancer Res., 10: 1565-1573, 2004 [4].
• A lentiviral vector capable of expressing the HIV-1 vpr gene (Vpr lentiviral vector) was constructed, and its in vivo anticancer effect was determined against cutaneous tumors derived from the AT-84 oral cancer cells in immunocompetent mice [5].

Psychiatry related information on Mouth Neoplasms

• Fewer teach their clients how to perform oral cancer self-examinations (20%); or educate them regarding use of athletic mouth protectors (15%), the effects of xerostomia (19%), and the benefits of fluoride (38%) [6].

High impact information on Mouth Neoplasms

• CONCLUSIONS: The ADH3(1-1) genotype appears to substantially increase the risk of ethanol-related oral cancer, thus providing further evidence for the carcinogenicity of acetaldehyde [7].
• BACKGROUND: Fenretinide, a synthetic derivative of retinoic acid, is under study in clinical trials for the prevention of breast, skin basal cell, bladder, and oral cancer in patients at risk [8].
• Regression by vitamin E of experimental oral cancer [9].
• This suggests the possibility that in this population an increase in the dietary intake of retinol and/or carotene may reduce the incidence of oral cancer, which is an important neoplasm in many parts of Asia [10].
• Betel nuts, arecaidine, and oral cancer [11].

Chemical compound and disease context of Mouth Neoplasms

• Bombesin antagonist prevents CO2 laser-induced promotion of oral cancer [12].
• High serum levels of alpha-tocopherol also were related to a low oral cancer risk in later years, but the risks were elevated significantly with increasing serum levels of gamma-tocopherol and selenium [13].
• Our data suggest that in oral cancer cells the Ca(2+)- and cell cycle-dependent p53-S100A2 interaction might modulate proliferation [14].
• Potential role of beta-carotene in prevention of oral cancer [15].
• Cisplatin tumor concentrations after intra-arterial cisplatin infusion or embolization in patients with oral cancer [16].

Biological context of Mouth Neoplasms

• We propose that doc-1 is a novel tumor suppressor gene in oral cancer development [17].
• Because hCG2 has been implicated as a negative regulator in cell cycle progression, our results support that hCG2 dysregulation may play an important role in epithelial transformation and the early stages of human oral cancer development [18].
• Our results suggest that genetic variation of IGF2R may influence significantly the risk of oral cancer [19].
• While it has been shown that p53 gene mutations in the conserved midregion (exons 5-9) are a common feature of oral cancers in the developed world, there is no information on this type of genetic lesion in betel quid-associated oral cancers [20].
• Our purpose was to evaluate inherited short tandem repeat polymorphisms of the insulin-like growth factor II receptor gene (IGF2R) in oral cancer risk [19].

Anatomical context of Mouth Neoplasms

• Using the cheek pouch of the Syrian hamster as an experimental model for oral carcinogenesis, it has recently been shown that eosinophils at sites of developing oral cancer express the multifunctional cytokine, transforming growth factor alpha (TGF-alpha) [21].
• We found that high expression level of c-erbB-2 was frequently detected in oral cancer cell lines but not in the other head and neck SCC cell lines [22].
• Beta-carotene was estimated in exfoliated oral mucosa cells in groups of individuals at various risks for oral cancer [23].
• An elevated and statistically significant odds ratio (OR) was found for COPD deaths (OR = 2.53; 95% CI = 1.06-6.02), while nonsignificant increased ORs were present for oral cancers, cancers of the pharynx and larynx and leukemia [24].
• Such changes were observed in clinically normal epithelium from oral cancer patients, involving primarily substantial expression of keratins K8/K7 (using CAM 5.2) in the basal cells of 12 out of 34 biopsies, and also a trend towards a reduction in the complexity of keratin differentiation [25].

Gene context of Mouth Neoplasms

• Overexpression of 5-lipoxygenase and cyclooxygenase 2 in hamster and human oral cancer and chemopreventive effects of zileuton and celecoxib [26].
• This study was designed to test the hypothesis that concomitant expression of stromelysin 3, Ets-1, and/or VEGF affects the development, progression, and prognosis of oral cancer [27].
• Association between polymorphism in p21(Waf1/Cip1) cyclin-dependent kinase inhibitor gene and human oral cancer [28].
• Furthermore, increased lifetime exposure to chewing tobacco appeared to be associated with a 2-fold increase in oral cancer risk in GSTM1 null individuals [29].
• We now present evidence that in human oral cancer (in vivo and in vitro), TGF-alpha and EGFR mRNAs can also be consistently detected [30].
• Patients whose lesions showed positive DeltaNp63, podoplanin, and EIC had the highest oral cancer risk with a hazard ratio of 4.372 (95% confidence interval, 1.912-9.992; P = 0.0005) and 61% oral cancer development rate at 5 years compared with 15% of other OPL patients (P < 0.0001) [31].

Analytical, diagnostic and therapeutic context of Mouth Neoplasms

• The purpose of this study is to correlate in vivo the expression of p12DOC-1 in oral cancer tissues by immunohistochemistry with clinical and pathological parameters [32].
• Thus, gene therapy of human oral cancer by increasing the expression of MnSOD activity in target cells might be used to prevent or reduce human oral tumor malignancy [33].
• We examined the relationships between folate and methionine intake, serum homocysteine levels (as a biomarker for folate metabolism), and methylenetetrahydrofolate reductase (MTHFR) C677T polymorphism genotype and risk of oral cancer in a population-based, case-control study in Puerto Rico [34].
• Expression of p53, PCNA, Ki-67 and bcl-2 in relation to risk factors in oral cancer - a molecular epidemiological study [35].
• For tooth restoration and oral surgery, CO2 and neodymium:YAG lasers are used and lasers are used in photodynamic therapy for oral cancer [36].

References