Role of apoptotic, autophagic and senescence pathways in minor salivary gland adenoid cystic carcinoma.

BACKGROUND: Adenoid cystic carcinoma (ACC) is a salivary gland malignancy with poor long-term survival, which warrants studies aimed at clarifying the pathogenesis of this disease in order to widen the scope of therapeutic options currently available. Alterations in regulatory mechanisms relating to vascular support, cell death and autophagy are important pathways for tumor growth in cancer. Thus, the present study aimed to access vascular supply, apoptosis, autophagy and cell senescence in ACC of minor salivary glands. METHODS: We analyzed 25 cases of minor salivary gland ACC by immunohistochemistry using anti-CD34, anti-CD105, anti-D2-40, anti-Bax, anti-Bcl-2, anti-Beclin-1, anti-LC3B, anti-p21 and anti-p16. RESULTS: Microvessel density was low and based on anti-CD34, anti-CD105 and anti-D2-40 immunostaining. There was positivity for anti-CD34, anti-Bcl-2, anti-Beclin, anti-LC3B and anti-p21 and a positive correlation between Bcl-2 and Beclin (p = 0.014). CONCLUSIONS: Our results showed that ACC does not depend on neo-angiogenesis and is probably associated to anti-apoptotic, autophagic and anti-senescence events.

Microvessel density and cell proliferation in juvenile ossifying fibroma: A comparative study with central ossifying fibroma.

Considered as an aggressive counterpart of central ossifying fibroma (OF), juvenile ossifying fibroma (JOF) is a benign fibro-osseous neoplasm characterized by an unpredictable destructive behavior, elevated morbidity, mutilating treatment and high potential for local recurrences. The aim of this study is to compare the analysis for cell proliferation and vascular markers between JOF and OF. Cell proliferation index was measured by Ki-67 and Mcm-2 expression and microvessel density (MVD) was obtained by the immunoexpression of CD34/CD105. We observed a reduced expression of vascular markers, where MVD for CD34 was significantly higher in JOF than in OF (p = 0.009), but no statistical difference was found for CD105. JOF and OF showed low expression for Ki-67 and Mcm-2 and no difference was noted between both, suggesting that other mechanisms such as anti-apoptotic and/or pro-autophagic pathways or even increased expression of matrix metalloproteinases may be responsible for the aggressiveness of JOF.

Immunoexpression of cyclooxygenase-2 and p53 in oral squamous cell carcinoma.

PURPOSE: Cyclooxygenase-2 (COX-2) is an induced proinflammatory enzyme involved in various steps of carcinogenesis such as cell proliferation, reduction in apoptosis rates, and promotion of tumor angiogenesis. Mutation or inactivation of the tumor suppressor gene p53 is frequently observed in malignant neoplasms and is known to be involved in the early stages of carcinogenesis. Recent studies reveal a possible correlation between COX-2 and p53 expression in several malignant neoplasms. The present study analyzed the correlation between the expression of COX-2 and p53 in oral squamous cell carcinoma (OSCC) and evaluated the differences in the expression of these 2 proteins according to the histologic grade of malignancy of the tumor. MATERIALS AND METHODS: Thirty-four cases of OSCC were graded according to the histologic grading system proposed by Bryne [Oral Dis 4(2) (1998) 70-77]. Immunoexpression of COX-2 and p53 was analyzed by counting 1000 neoplastic cells in 5 different fields at the deep invasive front of the tumor under a light microscope. On the basis of the number of immunopositive cells, the labeling index expressed as the percentage of positively stained cells was established for each marker. RESULTS: Increased COX-2 expression in most specimens was observed, although no significant correlation was observed between COX-2 and p53 labeling indices (P > .05). Moreover, there were no significant differences in the expression of these proteins between high- and low-grade tumors (P > .05). CONCLUSION: The increased expression of COX-2 in OSCC suggests a role for this protein in the pathogenesis and progression of oral cancer.

Hiperplasia endotelial papilar intravascular oral: uma entidade rara / Intravascular papillary endothelial hyperplasia: a rare entity

A hiperplasia endotelial papilar intravascular (HEPI) é uma lesão vascular reativa caracterizada pela proliferação endotelial excessiva localizada no interior de vasos sangüíneos comumente dilatados, associada a trombos em organização, ou secundária a outras lesões vasculares, como hemangiomas e granulomas piogênicos. A HEPI é um achado incomum na cavidade oral, onde os lábios são o principal sítio de acometimento, e surge clinicamente sob a forma de nódulos azulados de aspecto clínico semelhante ao de lesões como hemangioma, mucocele e varicosidades. Sob o aspecto histopatológico, observam-se projeções papilares de tecido conjuntivo fibroso revestidas por uma ou duas camadas de células endoteliais no interior de um lúmen vascular. A principal peculiaridade da HEPI reside em sua semelhança histológica com o angiossarcoma e na possível interpretação errônea como neoplasia maligna. Neste artigo, os autores descrevem um caso de HEPI oral e realizam uma breve revisão da literatura, enfatizando suas características histopatológicas e o diagnóstico diferencial.