Disease relevance of Leukoplakia

• In the DMBA-painted animals receiving 13-cis-retinoic acid, the leukoplakia and epidermoid carcinomas developed more slowly and were better differentiated microscopically [1].
• The patient had the classic triad of cutaneous findings: reticulated hyperpigmentation, nail dystrophy, and leukoplakia [2].
• Fenretinide was well tolerated and effective at preventing relapses and new leukoplakias during treatment and after [3].
• GSH or its precursor cysteine inhibits activation of the nuclear transcription factor kB(NFkB), and has been shown to be protective against chemically induced oral cancer and leukoplakia [4].
• Moreover, the urinary biomarkers NNAL-Gluc, NNAL, and cotinine were associated with the presence of leukoplakia, which provides biochemical support for the role of smokeless tobacco products as a cause of oral leukoplakia [5].

High impact information on Leukoplakia

• When preceded by high-dose induction therapy, low-dose isotretinoin therapy was significantly more active against leukoplakia than beta carotene and was easily tolerated [6].
• High-dose isotretinoin therapy has been determined to be an effective treatment for leukoplakia [6].
• METHODS: A single-arm phase II study using the nontoxic agent alpha-tocopherol to treat oral premalignant leukoplakia was performed at seven institutions affiliated with the CCOP through The University of Texas M [7].
• Clinical studies have demonstrated that retinoids, including retinol (Vitamin A) and its synthetic derivatives, can eradicate leukoplakia and suppress the formation of squamous cell carcinoma of the head and neck (SCCHN) [8].
• Retinoids, particularly 13-cis retinoic acid, can frequently reverse leukoplakia [9].

Chemical compound and disease context of Leukoplakia

• Randomized, double-blind, placebo-controlled phase IIb trial of the cyclooxygenase inhibitor ketorolac as an oral rinse in oropharyngeal leukoplakia [10].
• When the total levels of NNAL-Gluc, NNAL, or NNAL-Gluc + NNAL were divided into tertiles, there was a significant association between the presence of leukoplakia and increasing levels of these metabolites; a similar relationship was found between urinary cotinine and leukoplakia [5].
• In the leukoplakia lesions, CK8 CK13, CK19 and involucrin were detected in 13.8, 100, 74.2 and 100% of the specimens, respectively [11].
• In this group, initially alpha(v)beta6 integrin-positive leukoplakia specimens had high tendency for disease progression while alpha(v)beta6-negative specimens did not progress [12].
• Fifty-nine oral mucosa leukoplakia patients, diagnosed by established clinical and pathological criteria, were randomly divided into a treated group (3 g mixed tea oral administration and topical treatment) and a control group (placebo and glycerin treatment) [13].

Biological context of Leukoplakia

• In this study, the prevalence of GSTM1 and GSTT1 null genotypes (GSTM1*2 and GSTT1*2) in oral premalignant leukoplakia cases and controls was ascertained in genomic DNA by a multiplex PCR technique [14].
• But variant haplotypes, containing one variant allele, on XRCC1 increased the risk of leukoplakia (OR, 1.3; 95% CI, 1.0-1.7) [15].
• The expression of Ki67 and p53 in various forms of leukoplakia point to the increasing instability of the genome in parallel with the severity of leukoplakia [16].
• LOH at MCC gene was not detected either in tumor or in leukoplakia DNAs [17].
• CYP1A1 polymorphism and GSTM1 or GSTT1 gene deletion was analyzed in genomic DNA from lung parenchyma, WBCs, or oral biopsies (leukoplakia patients from India) and from oral exfoliated cells (healthy controls) [18].

Anatomical context of Leukoplakia

• Furthermore, we analyzed expression of hmw-MAP2 protein in 88 oral specimens consisting of clinicopathologically pre-malignant (leukoplakia) and malignant (OSCC) lesions, along with their adjacent normal mucosa [19].
• Cryosections from normal, premalignant or malignant oral mucosa were used for immunostaining and the observations were confirmed by immunoprecipitation. p53 protein was detected in 55% (15/27) premalignant oral lesions (leukoplakia) [20].
• The various endpoints differed in degree and time course to the administration of beta-carotene and vitamin A. Following termination of the beta-carotene or vitamin A administration, micronucleated cells and leukoplakia recurred in the oral cavity of chewers who continued this habit throughout the trial period [21].
• MDM2 and Bcl-2 expression in keratinocytes were quantitatively greater in leukoplakia than in OLP [22].
• CONCLUSIONS: Since HNP-1 is a non-specific defensive peptide present in neutrophils, it may play an important role in the protection against diseases such as oral lichen planus, leukoplakia, and glossitis associated with iron deficiency [23].

Gene context of Leukoplakia

• In this hospital-based case-control study, 310 cancer patients, 197 leukoplakia patients, and 348 controls were studied to determine risk of the disease due to polymorphisms at three sites on XRCC1 and one site on XRCC3 [15].
• Pretreatment expression of EGFR, TGF-alpha, and HER-2/neu in leukoplakia was increased when compared to normal-appearing mucosa [24].
• Immunohistochemical detection of p53 oncoprotein in human oral squamous cell carcinomas and leukoplakias: comparison with proliferating cell nuclear antigen staining and correlation with clinicopathological findings [25].
• CONCLUSIONS: The increased apoptotic and Ki67 indices may indicate an unfavorable prognosis for leukoplakia [16].
• The results indicate that the "rare" C allele at the DraI polymorphic site in CYP2E1 gene may enhance susceptibility to leukoplakia among tobacco users in this population [26].

Analytical, diagnostic and therapeutic context of Leukoplakia

• Serum homocysteine levels in patients with HNSCC were significantly higher compared with homocysteine levels both in the smoker and nonsmoker control groups and in patients with laryngeal leukoplakia [27].
• We investigated the localization of hBD-2 peptide in tissue sections of oral lichen planus, leukoplakia, candidal leukoplakia and radicular cysts using immunohistochemistry [28].
• Frozen sections of 20 specimens of leukoplakia were stained with DNA-binding bisbenzimide Hoechst 33258 [29].
• In sections of 373 formalin-fixed and paraffin-embedded samples taken from benign and precancerous leukoplakias and squamous cell carcinomas, HPV DNA could be identified in 56 specimens by in situ hybridization technique [30].
• This report deals with a male liver transplant recipient receiving FK506 (5 mg/day) and prednisone (20 mg/day) who was diagnosed with a homogeneous leukoplakia on the floor of the mouth 4 months after transplantation, and 4 months later with a squamous cell carcinoma growth at the site of this lesion [31].

References