Biomedical subjects
Publications and source records attributed to A Mitselou.
A 67 year old man developed "status epilepticus" and died with acute respiratory failure. An autopsy and concomitant histological examination, revealed intravascular infiltrate of lymphoid cells throughout the body. Immunohistochemical studies showed intense positive staining for leukocyte common antigen (LCA), L26 and CD20 and negative staining for Factor VIII- related antigen, and CD5, demonstrated that the neoplastic cells were of B-cell lineage.
PURPOSE OF INVESTIGATION: This study aimed to investigate the immunohistochemical expression of cyclins D1 and E in normal, hyperplastic and neoplastic endometrium, and their correlation with proliferative activity and clinicopathological features. METHODS: We carried out immunohistochemical techniques on archived material of formalin-fixed paraffin-embedded tissues using the antibodies against the cyclins D1 and E, PR-ER, p53, Ki67 (MIB1) and pRb with the streptavidin-biotin-peroxidase method in a total of 20 cases of normal endometrium, 32 cases of hyperplastic endometrium and 66 cases of endometrial carcinomas. RESULTS: Cyclin D1 and E immunoreactivity was observed in the nuclei of tumour cells in 18.2% and 39.1%, respectively, of the cases of endometrial carcinomas. Cyclin D1 labelling index was not significantly correlated with any of the clinicopathologic parameters examined. However, there was a significant correlation between the cyclin E labelling index and histological grade of carcinoma (p = 0.00096), which increased significantly with histological grades of malignancy. We also detected a significant correlation between cyclin E and PCNA (p < 0.0001) as well as with the tumor suppressor genes p53 and pRb (p = 0.052 and 0.0002, respectively) in endometrioid endometrial carcinoma. CONCLUSION: Our results indicate that cyclin E overexpression may be involved in the development and/or proliferation and differentiation of human endometrioid endometrial carcinoma. Immunoexpression of cyclin D1 does not appear to be associated with cell-cycle progression in the benign or malignant endometrium.
Heat shock protein 27 (HSP27) is a relatively small protein produced in response to pathophysiological stress. In the current prospective study the presence and localization of HSP27 was associated with other potential prognostic factors such as: estrogen and progesterone receptors, p53 and proliferative associated indices (MIB1, PCNA). One hundred and twenty-two samples of endometrial tissues (65 endometrial carcinomas, 28 adenomatous hyperplasias, 31 normal endometrium) were studied. Patient records were examined for FIGO stage, grade, and depth of myometrial invasion, histology and lympho-vascular space invasion. HSPp27 expression was lower in the group of carcinomas when compared with the cases of adenomatous hyperplasias (p < 0.0001), normal proliferative (p < 0.0001) and secretory endometrium (p = 0.02). HSP27 expression was higher in carcinomas from premenopausal women in comparison with women in menopausal status and postmenopausal status. Multivariate tests showed no statistical significance of HSP27 expression according to tumor grade and stage. A positive relationship between the expression of HSP27 expression and estrogen receptors (p = 0.0018) as well as with progesterone receptor (p = 0.0012) was found with linear regression analysis of variance. Our data showed that the lower HSP27 expression in endometrial carcinomas in comparison with hyperplastic and normal endometrium may indicate a decreased endogenous protection mechanism against the various stressful stimuli. This expression could be under hormonal control and does not seem to be correlated with other conventional or possible prognostic parameters.
PURPOSE OF INVESTIGATION: We have studied by immunohistochemistry the presence and localization of CD44, estrogen and progesterone receptors, p53 and proliferative associated indices (MIB1, PCNA) in archival endometrial tissue, in order to determine their diagnostic and prognostic value as well as the possible correlations between them. METHODS: We examined 186 samples of endometrial tissue (100 endometrial carcinomas of endometrioid type, 40 cases of hyperplasia and 46 of normal endometrium). Patient records were examined for FIGO stage, grade, and depth of myometrial invasion, histology, and lympho-vascular space invasion. RESULTS: Strong membranous immunostaining (> 10% of neoplastic cells) was observed in 45% of the carcinomas. A statistically significant correlation was found in the expression of protein in stromal cells, when compared with epithelial cells (p < 0.0001). Immunohistochemical expression of CD44 was significantly lower in cancer cases than in normal endometrium, mainly in the secretory phase (p < 0.0001). CD44 positive cases by immunohistochemistry failed to show any statistical correlation with tumor grade or with vessel invasion. The expression of the protein was lower in FIGO Stage II compared with Stage I (p = 0.03). A positive relation of CD44 expression with progesterone receptor status (p = 0.02) was detected. CD44 expression was also positively associated with the proliferation associated with the proliferative index MIB1 (p = 0.001). CONCLUSION: CD44 is closely related to the secretory phase of the normal menstrual cycle and its expression is decreased in hyperplasia (simple or complex with or without atypia) and in cancer cases. These observations suggest that decreased CD44 expression might be functionally involved in the multiple mechanisms of the development and progression of endometrial lesions.
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The immunohistochemical expression of cathepsin D was performed in paraffin embedded tissue from 79 endometrial carcinomas, 35 cases of hyperplasia, and 32 normal endometrium using the streptavidin-biotin method to investigate the role of cathepsin D (CD) in these lesions and its possible relationship with other potential and established prognostic markers. The association between CD and the other markers was assessed by univariate analysis. Tumor cell CD expression was lower in the group of carcinomas compared to the normal proliferative (P = 0.022) and secretory endometrium (P = 0.0005). In addition, hyperplastic cell CD expression was lower compared with epithelial cell CD expression in the secretory phase of normal endometrium (P = 0.009). Malignant cell CD expression was inversely correlated with tumor stromal cells (P = 0.007). A positive relationship of stromal cell CD expression with pRb (P = 0.046) and PCNA score (P < 0.0001) was detected in the group of carcinomas. In the proliferative phase of normal endometrium, epithelial CD expression was positively correlated with estrogen status (P = 0.015). The data show that down-regulation of CD expression is an early event in endometrial carcinogenesis. In addition, stromal cell CD expression may be involved in cell growth process in endometrial carcinomas.
BACKGROUND: Cell cycle progression and transition of cells from the first gap phase (G1) to the DNA replication phase (S) depend on a finely tuned balance between the levels of cyclins, cyclin-dependent kinases (CDKs) and cyclin-dependent kinase inhibitors (CDKIs). MATERIALS AND METHODS: We analyzed 57 squamous cell invasive carcinomas of the larynx, 10 in situ carcinomas, 56 cases of dysplasia, 11 papillomas and 26 keratosis. We investigated: a) the immunohistochemical expression of CDKIs, p21 and p27, b) any possible relation between normal and abnormal immunoprofiles of these proteins and p53 protein and proliferation status as determined by the expression of Ki67 and PCNA, and c) their presence in pre-malignant and malignant laryngeal lesions. RESULTS: Expression of p21 and p27 was observed in 58.9% and 89.5% of the laryngeal carcinomas, respectively. High levels of p21 were significantly correlated with increased cyclin D (p=0.001), cyclin E (p<0.001) and Ki67 (p<0.001), while increased expression levels of p27 were associated with p53 accumulation (p=0.02) and with increased proliferation status as expressed by Ki67 (p=0.05). CONCLUSION: Due to the increased expression levels of CDKIs in laryngeal carcinomas, we suggest the existence of a mechanism by which tumor cells tolerate the inhibitory effect of these proteins on cell cycle progression.