Oral Leukoplakia Related to Malignant Transformation

AbstractOral leukoplakia and its malignant transformation are reviewed in this article. Oral leukoplakia is defined as a predominantly white lesion of the oral mucosa that can not be characterized as any other definable lesion; however, the lesion must be confirmed histopathologically by biopsy in order to discuss malignant transformation of oral leukoplakia. Malignant transformation rates of oral leukoplakia range from 0.13 to 17.5%, while the rates of five-year cumulative malignant transformation range from 1.2 to 14.5%. Some reports found a high incidence of malignant transformation in older patients. Chewing tobacco and smoking are distinct risk factors particularly among males in certain countries; however, other countries have noted that females or non-smokers may be at risk of malignant transformation. HPV has been detected in oral dysplasia lesions and cancer in non-smokers. Conflicting reports have been presented regarding the malignant transformation of oral leukoplakia with epithelial dysplasia; however, we and some authors believe that epithelial dysplasia is an important factor in the malignant transformation of oral leukoplakia. The majority of researchers showed non-homogenous leukoplakia as a risk factor, although different terms have been used to describe these lesions. There may be several routes to malignant transformation of oral leukoplakia, including transformations induced by carcinogenesis due to betel quid chewing or smoking, or by HPV infection. While no definite treatment modalities for oral leukoplakia have been established, we suggest surgical therapy with an adequate safety-margin and well-timed evaluation as an appropriate treatment in preventing malignant transformation

Prognostic utility of chromosomal instability detected by fluorescence in situ hybridization in fine-needle aspirates from oral squamous cell carcinomas

<p>Abstract</p> <p>Background</p> <p>Although chromosomal instability (CIN) has been detected in many kinds of human malignancies by means of various methods, there is no practical assessment for small clinical specimens. In this study, we evaluated CIN in fine-needle aspiration (FNA) biopsied oral squamous cell carcinomas (SCCs) using fluorescence <it>in situ </it>hybridization (FISH) analysis, and investigated its prognostic significance.</p> <p>Methods</p> <p>To evaluate CIN status of tumors, FISH with genomic probes for the centromeres of chromosomes 7, 9, and 11 was performed on specimens obtained by FNA from 77 patients with primary oral SCCs.</p> <p>Results</p> <p>High-grade CIN (CIN3) was observed in 11.7% (9/77) of patients with oral SCCs and was associated significantly with reduced disease-free survival (<it>p </it>= .008) and overall survival (<it>p </it>= .003). Multivariate Cox proportional hazards analysis showed that CIN status was significantly correlated with disease-free survival (<it>p </it>= .035) and overall survival (<it>p </it>= .041).</p> <p>Conclusion</p> <p>Analysis of CIN status using FISH on FNA biopsy specimens may be useful in predicting of recurrence and poor prognosis in patients with oral SCCs.</p

SURFACE ROUGHNESS OF SQUAMOUS CELL CARCINOMA OF THE ORAL MUCOSA

The surface rough ness value of 39 oral squamous cell carcinomas was measured by the Rmax method. The means of the eight measurement values of each carcinoma ranged from 87 µm to 1176 µm. The average value of all 39 lesions was 341 µm. The average value of the lesions of the papillomatous and granulomatous types was larger than that of the leukoplakic and erosive types. The lesions with the size of more than 2 cm in diameter were rougher than those of less than 2 cm. The lesions of the gingiva were rougher than those on the tongue. There was an inclination that the surface of the verrucous carcinoma was rougher than that of the invasive squamous cell carcinoma and that the surface of early carcinoma was smoother than that of the invasive squamous cell carcinoma

ULTRASONIC EVALUATION OF CERVICAL LYMPH NODE METASTASIS OF SQUAMOUS CELL CARCINOMA IN ORAL CAVITY

Forty-four patients with oral cancer were examined by ultrasonography to detect cervical lymph nodal metastases. The lymph nodes, which were histopathologically or clinically confirmed to have cancer metastases, showed the following characteristic echogram findings: distinctive nodal boundary, posterior echo enhancement and an increased ratio of the shortest and the longest diameters of the node.It is suggested that these three peculiar ultrasonographic findings are considered to be important items for the differential diagnosis of benign nodes from the cervical metastasis of oral cance

Identification of a Novel Human Immunodeficiency Virus Type 1 Integrase Interactor, Gemin2, That Facilitates Efficient Viral cDNA Synthesis In Vivo

Retroviral integrase (IN) catalyzes the integration of viral cDNA into a host chromosome. Additional roles have been suggested for IN, including uncoating, reverse transcription, and nuclear import of the human immunodeficiency virus type 1 (HIV-1) genome. However, the underlying mechanism is largely unknown. Here, using a yeast two-hybrid system, we identified a survival motor neuron (SMN)-interacting protein 1 (Gemin2) that binds to HIV-1 IN. Reduction of Gemin2 with small interfering RNA duplexes (siGemin2) dramatically reduced HIV-1 infection in human primary monocyte-derived macrophages and also reduced viral cDNA synthesis. In contrast, siGemin2 did not affect HIV-1 expression from the integrated proviral DNA. Although Gemin2 was undetectable in cell-free viral particles, coimmunoprecipitation experiments using FLAG-tagged Gemin2 strongly suggested that Gemin2 interacts with the incoming viral genome through IN. Further experiments reducing SMN or other SMN-interacting proteins suggested that Gemin2 might act on HIV-1 either alone or with unknown proteins to facilitate efficient viral cDNA synthesis soon after infection. Thus, we provide the evidence for a novel host protein that binds to HIV-1 IN and facilitates viral cDNA synthesis and subsequent steps that precede integration in vivo