Comparison of the histologic risk assessment model between lower lip and oral squamous cell carcinoma.

INTRODUCTION: The histologic risk assessment (HRA) grading system was proposed as a practical measure to predict clinical outcome and its effectiveness has been shown in several studies. It has been suggested that the HRA model might exhibit differences among various oral subsites. The aim of the present study was to compare this system between squamous cell carcinomas (SCCs) of the lower lip (LL) and oral cavity. MATERIALS AND METHODS: All primary SCCs located in the LL and oral cavity were retrieved and graded using the HRA model. Data regarding risk score (RS), perineural invasion (PNI), lymphocytic infiltration (LI) and worst pattern of invasion (WPOI) were compared between LL and oral SCCs using χ2 analysis (P<0.05). RESULTS: There were a total of 33 LLSCCs, of which 15, 8 and 10 were categorized as low-risk (RS=0), intermediate-risk (RS=1-2) and high-risk (RS≥3) tumors, respectively. Corresponding values in the 48 oral SCCs were 7, 15 and 26 cases. Significant differences in RS (P=0.00), LI (P=0.01) and WPOI (P=0.01) were observed between LL and oral tumors. CONCLUSIONS: The HRA model could be included among the various factors suggested to be different between lip and oral SCCs. Low-risk tumors were more prevalent in the lip which corroborates the less aggressive nature of these cancers. Considering the significantly higher LI in LL SCCs, inflammation may be regarded as an important factor in regulating the invasive behavior of these tumors.

In vitro study on the effect of doxorubicin on the proliferation markers MCM3 and Ki-67.

PURPOSE: Aberrant proliferation is an essential feature of cancer cells, which can be caused by alterations in components of the cell cycle, such as minichromosome maintenance protein-3 (MCM3) and Ki-67. Doxorubicin is a cytotoxic/cytostatic anticancer agent commonly used in chemotherapy. We investigated the effect of this drug on MCM3 and Ki-67 in the KB cell line, which is considered a subline of HeLa cell line. METHODS: KB cells were treated with doxorubicin and its effect on apoptosis, mRNA levels and protein expression of MCM3 and Ki-67 was determined by flow cytometry (annexin V-FITC/PI assay), quantitative real-time RT-PCR (qRT-PCR) and immunocytochemistry, respectively. Cytotoxicity was assessed using the MTT assay. One-way analysis of variance (ANOVA) was used for comparing groups and differences were assessed by a Tukey's post hoc test. RESULTS: Protein expression of both biomarkers and MCM3 mRNA were not affected by doxorubicin, but Ki-67 mRNA significantly increased after treatment (p=0.049). CONCLUSIONS: Considering that doxorubicin can influence certain biochemical events that lead to modifications in Ki- 67, this factor might be useful in evaluating the impact of anthracycline-based chemotherapeutic agents. Changes in MCM3 following doxorubicin treatment require further investigation.

Head and neck non-Hodgkin's lymphoma: a 20-year demographic study of 381 cases.

Malignant lymphoma is a lymphoreticular malignancy with considerable geographic variation. The objective of the present study was to provide a preliminary report on patients with head and neck non-Hodgkin's lymphoma (NHL) in a selected Iranian population. In a retrospective review from 1981 through 2001, all cases of NHL occurring in the head and neck region were selected. Histological slides were reviewed and classified according to the Working Formulation. Clinical data including patients' age, sex, initial anatomic site of disease and presenting symptoms were also recorded. Information on 381 cases of NHL was retrieved from the archived medical records; 281 cases were nodal and 100 extranodal. The mean age of the patients with nodal and extranodal disease was 39.3 and 47.7 years, respectively. A significant difference in gender was noted in the nodal group (P<0.001), but not in the extranodal cases. The most common site of involvement in the extranodal subjects was Waldayer's ring. According to histopathologic evaluation, 72% of the specimens were intermediate-, 14% were high-, and 12% were low-grade malignancies. Considering the relative frequency of head and neck lymphoma, establishment of a uniform reporting method seems necessary in order to compare different reports from various populations.

Evaluation of myofibroblasts in oral epithelial dysplasia and squamous cell carcinoma.

BACKGROUND: Carcinogenesis is accompanied by a number of changes in the adjacent stroma including the appearance of myofibroblasts. The purpose of this study was to evaluate and compare the presence of myofibroblasts in normal mucosa, oral epithelial dysplasia, and different grades of oral squamous cell carcinoma. METHODS: The study sample consisted of three groups, including 40 oral squamous cell carcinomas, 15 dysplasias, and 15 sections of normal oral epithelium. Vimentin, desmin, and alpha-smooth muscle actin were used to identify myofibroblasts. RESULTS: The percentage and intensity of alpha-smooth muscle actin were examined, and positive immunostaining was observed in the myofibroblasts of all squamous cell carcinomas; however these cells did not stain in the dysplasias or normal epithelium specimens. The presence of myofibroblasts was significantly higher in oral squamous cell carcinomas compared to both, dysplasias and normal mucosa cases (P < 0.001). A significant difference was not observed between the different grades of oral squamous cell carcinoma (P = 0.2). CONCLUSIONS: These findings show the presence of myofibroblasts in the stroma of oral squamous cell carcinoma but not dysplasia and normal mucosa, suggesting further investigation to clarify the role of myofibroblasts in the carcinogenesis of this tumor.

Comparison of angiogenesis in keratocystic odontogenic tumours, dentigerous cysts and ameloblastomas.

OBJECTIVE: The aim of the present study was to evaluate and compare angiogenesis in keratocystic odontogenic tumours, dentigerous cysts (DCs) and ameloblasomas using monoclonal antibody against CD34. MATERIALS AND METHODS: Microvessel density was assessed in a total of 53 cases including 20 keratocystic odontogenic tumours, 13 DCs and 20 ameloblastomas (14 solid and six unicystic variants). Microvessel density was expressed as the mean number of microvessels per high-power-field. RESULTS: Statistically significant differences in mean microvessel density were observed between keratocystic odontogenic tumours, DCs and solid ameloblastomas (P < 0.001). Mean microvessel density was significantly higher in solid ameloblastomas compared with both keratocystic odontogenic tumours and DCs; and was also significantly higher in keratocystic odontogenic tumours than in DCs. CONCLUSION: Within the limitations of the present study, it can be suggested that angiogenesis may be one of the mechanisms possibly contributing to the different biological behaviours of keratocystic odontogenic tumours, DCs and solid ameloblastomas.

Comparative expression of calretinin in selected odontogenic tumours: a possible relationship to histogenesis.

AIMS: Calretinin, a calcium-binding protein, is expressed primarily in certain subtypes of neurons. It has also been reported to be present in mesotheliomas and other tumours. The aim was to determine the expression of calretinin in selected odontogenic neoplasms. METHODS AND RESULTS: Immunohistochemistry for calretinin was performed on 55 odontogenic tumours consisting of 20 solid ameloblastomas, five calcifying epithelial odontogenic tumours, 10 adenomatoid odontogenic tumours, 10 ameloblastic fibromas and 10 odontogenic myxomas. The distribution, intensity, pattern and localization of immunoreactive cells were determined by conventional light microscopy. chi(2) test was used for statistical analysis and P < 0.05 was considered to be significant. All 20 ameloblastomas showed intense immunopositivity with a diffuse distribution pattern. None of the other neoplasms was reactive with calretinin. Differences in the proportion of calretinin expression between groups were statistically significant at P < 0.001. CONCLUSIONS: Considering that ameloblastomas, in contrast to the other studied tumours, were consistently reactive for calretinin, this protein may have a role in the pathogenesis of this aggressive neoplasm.