Disease relevance of Leukoplakia, Oral

• We conclude that 13-cis-retinoic acid, even in short-term use, appears to be an effective treatment for oral leukoplakia and has an acceptable level of toxicity [1].
• Telomerase activity was detectable in 14 of 16 human head and neck squamous cell carcinomas and 10 of 26 oral leukoplakia tissues [2].
• Randomized trial of fenretinide (4-HPR) to prevent recurrences, new localizations and carcinomas in patients operated on for oral leukoplakia: long-term results [3].
• Evaluation of TGF-alpha and EGFR expression in oral leukoplakia and oral submucous fibrosis by quantitative immunohistochemistry [4].
• Successful treatment of oral verrucous hyperplasia and oral leukoplakia with topical 5-aminolevulinic acid-mediated photodynamic therapy [5].

Psychiatry related information on Leukoplakia, Oral

• Besides oral leukoplakia and nail dystrophies, there was evidence of pancytopenia, growth retardation, alopecia, mental retardation and microcephaly [6].

High impact information on Leukoplakia, Oral

• 13-cis-retinoic acid in the treatment of oral leukoplakia [1].
• The purpose of this study is to investigate the presence of telomerase activity in oral leukoplakia and the relationship between the enzyme and multistep tumorigenesis [2].
• Cells cultured from four oral leukoplakia lesions were also examined and found to express RAR beta mRNA at relatively normal levels, but they expressed RAR gamma message at half the level of epithelial cells cultured from normal tissue [7].
• Response of oral leukoplakia to beta-carotene [8].
• Beta-carotene is a naturally occurring, nontoxic carotenoid with biologic properties that suggest that it might be efficacious against oral leukoplakia [8].

Chemical compound and disease context of Leukoplakia, Oral

• This trial evaluated if a topically delivered oral rinse containing ketorolac was as safe as and more effective than oral rinse alone in reducing the area of oral leukoplakia [9].
• Some recent findings suggest roles for beta-carotene and/or vitamin C in reversing or reducing the risk of cervical dysplasia and oral leukoplakia [10].
• Expression of alpha(v)beta6 integrin in oral leukoplakia [11].
• Metabolites of a tobacco-specific nitrosamine, 4-(methylnitrosamino)- 1-(3-pyridyl)-1-butanone (NNK), in the urine of smokeless tobacco users: relationship between urinary biomarkers and oral leukoplakia [12].
• Cytologic and DNA-cytometric follow-up of oral leukoplakia after CO2- and Er:YAG-laser assisted ablation: a pilot study [13].

Biological context of Leukoplakia, Oral

• In a controlled multicenter study, 170 patients operated on for oral leukoplakias with benign postoperative histology were randomized to 200 mg fenretinide daily for 1 year vs. no intervention [3].
• In a previous study on this population, it was shown that the GSTM3 (A/A) genotype increased the risk of oral leukoplakia and cancer among smokers, which has also been substantiated in this study with expanded sample sizes [14].
• Furthermore, of four oral leukoplakias with dysplasia, one showed LOH at 9q33 and two showed DBCCR1 hypermethylation [15].
• Expression of p27 and apoptosis in oral leukoplakia [16].
• From these results, we suggest that the abundance of p27 in oral leukoplakia may inhibit cell proliferation and lead premalignant tumor cells to apoptosis, and thus is concerned with prevention of tumor progression [16].

Anatomical context of Leukoplakia, Oral

• After withdrawal of vitamin A or beta-carotene treatment, oral leukoplakias reappeared, frequency of micronuclei in oral mucosa increased, and nuclear textures reverted to those present before the administration of chemo-preventive agents [17].
• The telomerase activity was detected in normal oral squamous epithelium and in 75% of the oral leukoplakias and oral carcinomas [18].
• RESULTS: The pretreatment expression of TGF-alpha and EGFr in dysplastic oral leukoplakia was increased when compared with their expression in adjacent normal-appearing mucosa (p = 0.001 and p = 0.01, respectively) [19].
• To evaluate the role of telomerase reactivation as a diagnostic and prognostic marker in oral carcinogenesis activity was investigated in mortal and immortal cell lines in eight oral leukoplakias (OL) and 46 oral squamous cell carcinomas (OSCC) [20].
• We report the first case of the combined manifestation of oral keratosis follicularis and oral squamous cell carcinoma and discuss the possible involvement of ATP2A2 (located in 12q23-24.1) which encodes the sarco/endoplasmic reticulum Ca(2+)-ATP isoform 2 (SERCA2), in the pathogenesis [21].

Gene context of Leukoplakia, Oral

• Immunolocalization of p53, glutathione S-tranferase pi and CD57 antigens in oral leukoplakia [22].
• The purpose of this study was to evaluate a potential association between the loss of syndecan-1 expression and the expression of p53 protein and Ki-67 antigen, and to identify reliable markers for predicting malignant changes in oral leukoplakia with epithelial dysplasia [23].
• GSTT1 polymorphism and oral leukoplakia [24].
• GSTM1 polymorphism and oral leukoplakia [25].
• Comparison of cytokeratin, filaggrin and involucrin profiles in oral leukoplakias and squamous carcinomas [26].

Analytical, diagnostic and therapeutic context of Leukoplakia, Oral

• Eight clinical trials have now shown that beta-carotene and vitamin E produce regression of oral leukoplakia, but chemoprevention studies in oral leukoplakia have limitations, which we review [27].
• Carbon dioxide laser surgery of oral leukoplakia [28].
• In a double-blind study 10 patients with oral leukoplakia were treated daily (three topical applications) with 0.1% isotretinoin gel or a placebo for 4 months [29].
• Total hemolytic complement (CH50) and its fractions (C3 and C4) were estimated in the sera of 50 patients with oral leukoplakia, 50 patients with oral submucous fibrosis and 50 oral cancer patients [30].

References