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Immunohistochemical expression of Basic fibroblast growth factor-2 and Heparanase in oral squamous cell carcinoma

Authors: Karrar N. Shareef كرار شريف --- Ahlam H. Majeed احلام مجيد
Journal: Journal of baghdad college of dentistry مجلة كلية طب الاسنان بغداد ISSN: 16800087 Year: 2013 Volume: 25 Issue: 1 Pages: 94-98
Publisher: Baghdad University جامعة بغداد

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Abstract

Back ground: The aim of this study was to evaluate the expression of fibroblast growth factor-2 and Heparanase inoral squamous cell carcinoma, and to correlate the two studied marker with each other and withclinicopathologicalfinding including grade, stage.Methods: Sections of 30 formalin-fixed paraffin embedded blocks specimens of oral squamous cell carcinoma wereimmunostained to assess the expression of fibroblast growth factor-2 and Heparanse in oral squamous cellcarcinoma cases.Results: The expression of fibroblast growth factor-2 and Heparanase were positive in all oral squamous cellcarcinoma cases (100%). The positive expression of fibroblast growth factor-2 was significantly correlated with tumorsite (p=0.016),and clinical presentation(p-value =0.003).The positive expression of Heparanse was significantlycorrelated with tumor grade(p-value =0.002) .On other hand there was non-significant correlation between fibroblastgrowth factor-2 ,Heparanase and other clinicopathological parameters .Statistically significant correlation was foundbetween the expressions of fibroblast growth factor-2 and Heparanase(p-value= 0.021).Conclusion: The fibroblast growth factor-2 and Heparanase positive expression was noted in all cases of oralsquamous cell carcinomasignifying their important role in the angiogenesis and lymph node metastasis in oralsquamous cell carcinoma, furthermore they cooperate in promoting vascularization, suggesting that fibroblastgrowth factor-2 and heparanase are promising targets for the development of anticancer therapeutics for headand neck malignancies


Article
Detection of ERBB2 (Her2/neu) and P16 (INK4A) genes in oral squamous cell carcinoma using fluorescent in situ hybridization (FISH)

Authors: Hiba A. Abdulameer هبة عبد الامير --- Ahlam H. Majeed احلام مجيد
Journal: Journal of baghdad college of dentistry مجلة كلية طب الاسنان بغداد ISSN: 16800087 Year: 2012 Volume: 24 Issue: 4 Pages: 46-51
Publisher: Baghdad University جامعة بغداد

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Abstract

Background Head and neck cancers account for approximately 5% of all carcinomas in industrialized countries, witha worldwide incidence of 500,000 new cases annually. Nearly all head and neck cancers (90%) are squamous cellcarcinomas (SCCs), and >50% of tumors arise in the oral cavity. It is important to know what prognostic factors canfacilitate diagnosis, optimize therapeutic decisions, and improve the survival of these patients. A member of theepidermal growth factor receptor (EGFR) family, HER2/neu, has received much attention because of its therapeuticimplications. The p16 gene produces P16 protein, which in turn inhibits phosphorylation of Rb, thus inhibiting the Rbinducedrelease of transcription factor EF1 and cell cycle progression. Genetic aberration analyzed by fluorescence(FISH) to measure the gene copy number. The aims of the present study are to detect HER2/neu amplification andP16 deletion in oral squamous cell carcinoma and correlate them with various clinicopathological parameters (age,sex, clinical presentation, tumor site, tumor stage, tumor grade).Materials and Methods Thirty formalin-fixed paraffin embedded tissue blocks of oral squamous cell carcinoma whichwere collected from laboratories archives included in this study. H&E stain was done for each block for reassessmentof histological examination. DNA probes were used to detect copy numbers of the HER2/neu and P16 genes usingfluorescent in situ hybridization technique (FISH).Results FISH evaluation showed that HER2/neu gene amplification was found in 12 cases (40%), while 18 cases (60%)showed no amplification. Among the cases in which amplification was not found, 8 cases (44.45%) showed polysomyof chromosome 17.P16 gene deletion was found in 20 cases (66.7%) while 10 cases (33.3%) showed no deletion.Conclusions: HER2/neu amplification and P16 deletion were observed in studied oral squamous cell carcinomasamples using FISH, however, statistically non significant correlation with all clinicopathological findings (age, sex,clinical presentation, tumor site, tumor stage, tumor grade) and also between both genes were found in the presentstudy. It is premature to conclude that HER-2/neu and P16 alterations may have prognostic significance, but it is alsotoo early to dismiss that possibility without a larger, perhaps multicenter study


Article
Immunohistochemical evaluation of actin expression in basal cell carcinoma and oral squamous cell carcinoma

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Abstract

Background: Basal cell carcinomas (BCCs) are generally slow-growing tumours. They have been classified as aggressive (A-BCC) and non-aggressive (NA-BCC).Oral squamous cell carcinoma (OSCC) is a major cause of cancer morbidity worldwide, this is due to the characteristics of invasion. The microenviroment or stroma of neoplastic tissues plays an active role in tumour progression. Trans-differentiation of fibroblast to myofibroblast is a crucial and early event in tumourigensis. Alterations of contractile tension generated by the actin–myosin complex are of central importance in the development of the phenotype of morphologically transformed neoplastic cells with invasive behavior. Actin is the predominant component of contractile microfillament and it may be associated with increase contractility and invasiveness of tumour cells.Objective: This study aimed to investigate the presence of myofibroblasts in the stroma of basal cell carcinoma and oral squamous cell carcinoma, evaluated by the immunohistochemical expression of actin.Materials and methods: Twenty four formalin –fixed, paraffin -embedded tissue blocks (14 cases basal cell carcinoma, 10 cases oral squamous cell carcinoma) were included in this study. An immunohistochemical analysis was performed using anti alpha - smooth muscle actin (α- SMA) monoclonal antibody.

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