Expression of survivin, PTEN and p27 in normal, hyperplastic, and carcinomatous endometrium

Abstract

We aimed to investigate if expressions of survivin and p27 proteins are involved in the development of endometrioid carcinoma, along with whether there are any correlations between these proteins and loss of wild-type PTEN that is found in up to 80% of endometrial carcinomas. We also studied their correlations with classical prognostic factors and survival in endometrial carcinoma. To our knowledge, this is the first time survivin expression is investigated in endometrial hyperplasia along with endometrioid adenocarcinoma. For immunohistochemical analysis, 29 endometrioid adenocarcinoma, 38 endometrial hyperplasia, and 10 proliferative endometrium tissue samples were selected in the pathology archives. Staining of cells was scored as +2 if >50%, +1 if <50%, and negative if none were stained positive. Survivin expression increased from proliferative to hyperplasia to carcinoma cases. PTEN and p27 expressions decreased in hyperplasia and carcinoma cases with respect to proliferative endometrium. All these differences were statistically significant (P < 0.05). PTEN positively correlated to p27 (P < 0.05); however, neither was correlated with survivin. None of these genes were correlated with classical prognostic factors such as grade and myometrial invasion in endometrioid adenocarcinoma. However, mean survival was statistically significantly higher in PTEN-positive cases (46.6 vs 16.4 months) (P < 0.05). Survivin overexpression might be one of the important mechanisms in the development of endometrioid adenocarcinoma along with lost or decreased activity of PTEN and p27. However, survivin seems to exert its role in ways different from those of PTEN or p27 in the development of endometrioid adenocarcinoma. These findings on the role of survivin in endometrioid adenocarcinoma should be confirmed and the pathways through which survivin acts in endometrioid adenocarcinoma studied further with a larger sample size.

DNA methylation inhibits p53-mediated survivin repression

“…This suggests that survivin overexpression is selective toward high-grade, poorly differentiated tumors. This finding is consistent with reverse transcriptase PCR and immunohistochemistry data from other laboratories (Lehner et al, 2002;Takai et al, 2002;Erkanli et al, 2006Erkanli et al, , 2007.…”

Oral Cavity Carcinogenesis Modeled in Carcinogen-Treated Mice

“…In normal control epithelium, represented by the control group, survivin protein was absent in all specimens. This was consistent with pu bli shed p ap ers sho win g the lack o f survivin immunoreactivity in normal adult tissues 43) . The present study found the survivin expression rate was 30 % (24/80) in the oral mucosal dysplasia, and it was 57.1 % (12 / 21) in oral squamous cell carcinoma.…”

Inhibition of Apoptosis in Cryptosporidium parvum -Infected Intestinal Epithelial Cells Is Dependent on Survivin

“…In vivo, C. parvum appears to replicate in the basal crypt cells (52), and parasite development has a significant preference for mitotic cells in S/G 2 /M phase cells (65). Survivin also has a role in cell cycle progression (1,6,34), and its expression is controlled by cell cycle pathway components such as Myc and PTEN that are active only in the undifferentiated cells (12,19). If C. parvum can turn on survivin to manage apoptosis, it is also possible that this same mechanism operates to lock the host cell in a relatively undifferentiated state.…”