Asymmetrical proliferative pattern loss linked to cyclin D1 overexpression during malignant transformation of the lip epithelium.

BACKGROUND: There is inadequate knowledge on the involvement of oncogenic mechanisms linked to the cyclin (CCND1) gene in lip squamous cell carcinoma (LSCC). OBJECTIVE: The aim of this study was to analyse the implication of cyclin D1 in the malignant transformation of lip lesions. METHODS: We immunohistochemically studied 45 actinic cheilitis cases (15 mild dysplasia, 15 moderate dysplasia, 15 severe dysplasia/carcinoma in situ), 30 LSCC cases with adjacent non-tumour epithelium and 15 normal oral epithelium samples for detection of cyclin D1, ß-catenin and Ki-67. RESULTS: Cyclin D1 and Ki-67 expressions were significantly increased in the basal layer of premalignant epithelia and peripheral layers of tumour nests vs. CONTROLS: Premalignant epithelia had lost their asymmetrical proliferative pattern. CONCLUSION: Lip carcinogenesis was associated with loss of the asymmetrical proliferative pattern, a preventive mechanism against lip oncogenesis, and with cyclin D1 overexpression.

Expression of proliferative markers in ameloblastomas and malignant odontogenic tumors.

OBJECTIVE: To compare the proliferative activity in ameloblastoma and malignant odontogenic tumors, as assessed by Ki-67 immunostaining and determine whether expression of substance P (SP) and NK-1 receptor (NK-1R) is related to cell proliferation in these tumors. MATERIALS AND METHODS: Immunohistochemistry was used to evaluate protein expression in 44 benign and malignant odontogenic tumors from 39 patients. Immunohistochemistry was performed with anti-SP, anti-NK-1R, and anti-Ki-67 monoclonal antibodies, and the clinical and pathological data of the patients with odontogenic tumor were evaluated. RESULTS: Expression of Ki-67 in malignant odontogenic tumors was significantly higher than in ameloblastomas (P < 0.001), and the expression level was associated with higher expression of NK-1R. Among the ameloblastomas, there was significantly higher expression of Ki-67 in peripheral ameloblastic-like cells (3.3 ± 4.1) than in stellate reticulum-like cells (2.6 ± 3.7) (P = 0.04). In the majority of tissue locations of the malignant tumors, expression of SP and NK-1R was positively correlated with higher expression of Ki-67. CONCLUSION: These findings show that the expression level of Ki-67 in ameloblastomas was positively correlated with the rate of growth of odontogenic tumors. Overexpression of NK-1R complex in malignant odontogenic tumors could be part of the trigger stimulus that results in higher proliferative activity of the tumor.

Cell apoptosis and proliferation in salivary glands of Sjögren's syndrome.

BACKGROUND: Sjögren's syndrome (SS) occurs associated with parotid neoplasm, non-Hodgkin's B-cell lymphoma, which could impair the condition or be life-threatening for patients. The aim of this work was to analyze cell proliferation and apoptosis modifications in acinar, ductal and inflammatory infiltrate in salivary glands (SG) in patients with Sjögren Syndrome, keratoconjunctivitis, or stomatitis sicca or in healthy subjects, to establish parameters that indicate the likelihood of malignancy of the disease in populations at risk. METHODS: A study was performed with n = 58 histological samples of lower lip SG from patients diagnosed with SS, keratoconjunctivitis, or stomatitis sicca (SICCA) and from healthy subjects (C). Ki67 and caspase-3 immunolabeling were performed. RESULTS: The most important result was significant differences between the three study groups in Ki67 and caspase-3 markers (P < 0.0001) in infiltrated lymphocytes. CONCLUSION: The results of this work are indicative of a high degree of proliferation (85%) in infiltrated lymphocytes (IL) associated with SS which, according the literature, could be considered a risk. Furthermore, the markers used in this work are widely known and represent a lower cost than others and can be used to determine risk groups within the population of SS patients, enabling their follow-up.