Large scale gene expression pro®ling was carried out on laser capture microdissected (LCM) tumor and normal oral epithelial cells and analysed on high-density oligonucleotide microarrays. About 600 genes were found to be oral cancer associated. These oral cancer associated genes include oncogenes, tumor suppressors, transcription factors, xenobiotic enzymes, metastatic proteins, di erentiation markers, and genes that have not been implicated in oral cancer. The database created provides a veri®able global pro®le of gene expression during oral carcinogenesis, revealing the potential role of known genes as well as genes that have not been previously implicated in oral cancer. Oncogene (2001) 20, 6196 ± 6204.

Objective-Risks associated with smoking and drinking are not necessarily constant over the multistage pathway to oral cancer. We investigated whether smoking and drinking patterns differ for persons with oral cancer (OC) relative to those with oral epithelial dysplasia (OED), a precancerous condition.Methods-Incident cases of OC and OED were interviewed using a questionnaire containing questions on smoking and drinking. Odds ratios (ORs) compared the odds of smoking and drinking among persons with OC relative to OED.Results-No adjusted ORs for smoking achieved statistical significance; however, most were <1.0. The odds of OC relative to OED increased with drinking level; the adjusted OR for 19+ drinks/week was 3.03 (1.56-5.87). Age drinking began and years of drinking were not notably different for OC and OED cases; a higher proportion of OC cases reported discontinuing alcohol for 9+ years before diagnosis. Conclusions-The relationship between smoking and OED was at least as strong as that for smoking and OC, suggesting that smoking may have its greatest impact on oral carcinogenesis prior

Ulcerated lesions of the oral cavity have many underlying etiologic factors, most commonly infection, immune related, traumatic, or neoplastic. A detailed patient history is critical in assessing ulcerative oral lesions and should include a complete medical and medication history; whether an inciting or triggering trauma, condition, or medication can be identified; the length of time the lesion has been present; the frequency of episodes in recurrent cases; the presence or absence of pain; and the growth of the lesion over time. For multiple or recurrent lesions the presence or history of ulcers on the skin, genital areas, or eyes should be evaluated along with any accompanying systemic symptoms such as fever, arthritis, or other signs of underlying systemic disease. Biopsy may be indicated in many ulcerative lesions of the oral cavity although some are more suitable for clinical diagnosis. Neoplastic ulcerated lesions are notorious in the oral cavity for their ability to mimic benign ulcerative lesions, highlighting the essential nature of biopsy to establish a diagnosis in cases that are not clinically identifiable or do not respond as expected to treatment. Adjunctive tests may be required for final diagnosis of some ulcerated lesions especially autoimmune lesions. Laboratory tests or evaluation to rule out systemic disease may be also required for recurrent or severe ulcerations especially when accompanied by other symptoms. This discussion will describe the clinical and histopathologic characteristics of a variety of ulcerated lesions found in the oral cavity. KeywordsOral ulcer • Herpetic gingivostomatitis • Aphthous stomatitis • Oral erythema multiforme • Oral medication related ulcer • Oral lichen planus • Oral vesiculobullous lesions • Traumatic oral ulcer • Oral squamous cell carcinoma • Oral lymphoma

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Nornicotine, AGE, and upregulation of RAGE may be involved in the pathogenesis of periodontal disease associated with smoking.

miR-375 interacts with five conserved target sites in the CIP2A coding region, whereas the CIP2A 3′ UTR is not conserved across mammalian species. Reexpression of the tumor suppressor miR-375 in cancer cells represses the expression of CIP2A, resulting in a decrease in the MYC protein level and leading to reduced cell proliferation, migration, and invasion.

Recent reports have demonstrated that Dicer, an RNase III endonuclease required for microRNA (miRNA) maturation, is aberrantly expressed in different types of cancer. Furthermore, Dicer has been reported to be regulated by the let-7 family of miRNA genes. We hypothesize that Dicer is aberrantly expressed in oral cancer cells due to altered expressions of let-7, and that Dicer contributes to the development and progression of the disease. Western blot examination of Dicer protein levels in four head and neck squamous cell carcinoma (HNSCC) cell lines, including two oral cancer cell lines, demonstrated that Dicer had between 4 to 24 fold higher expression levels when compared to normal human primary gingival epithelial cells. Furthermore, five of six oral cancer tissues analyzed by indirect immunofluorescence had increased Dicer protein expression, compared to normal gingival epithelial tissue. The Dicer mRNA levels were not found to correlate well with protein expression in the HNSCC cell lines, suggesting that Dicer protein expression was post-transcriptionally regulated. Analysis of let-7a and let-7b levels in HNSCC cell lines by real-time PCR demonstrated that let-7b, but not let-7a, was significantly reduced in the HNSCC cell lines compared to control cells. Lastly, transfection of oral cancer cells with chemically synthesized let-7b and small interfering RNAs targeting Dicer significantly inhibited cell proliferation up to 83% and >100%, respectively, as early as three days post-transfection.Together, these data demonstrate that elevated expression levels of Dicer in oral cancer cells correlate with down-regulation of let-7b and increased cell proliferation.

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