@article {7777,
	title = {Immunohistochemical study of PTEN and phosphorylated mTOR proteins in familial and sporadic invasive breast carcinomas},
	journal = {Histopathology},
	volume = {56},
	year = {2010},
	note = {Cited By :24Export Date: 21 February 2017},
	month = {2010},
	pages = {876 - 882},
	abstract = {Aims: Loss of phosphatase and tensin homologue (PTEN) leads to activation of several kinases, including mammalian target of rapamycin (mTOR), which promotes cell cycle progression. The aim was to study the expression of PTEN and phosphorylated (p)-mTOR in familial and sporadic invasive breast carcinomas and their relation to clinicopathological features, molecular indices (Wnt1) and patients{\textquoteright} survival. Methods and results: PTEN and p-mTOR were detected immunohistochemically in 215 sections of invasive breast carcinomas (112 with a familial history of breast cancer). Image analysis was used and univariate and multivariate analyses employed for statistical evaluation of results. PTEN was detecte5d in the nucleus (73.5\%) and p-mTOR in the cytoplasm (44.2\%) of cancer cells. Loss of PTEN protein was more frequently detected in women with a familial history of breast cancer (72\%) (P < 0.0001), while its expression was negatively correlated with Wnt1, in total (P = 0.049). p-mTOR showed a positive association with lymph node status (P = 0.010) and was found to have a negative impact on patients{\textquoteright} overall survival (P = 0.016). Conclusions: Loss of PTEN protein expression appears to occur more frequently in women with a family history of breast cancer, whereas activation of mTOR protein seems to be related to a more aggressive phenotype. {\textcopyright} 2010 Blackwell Publishing Limited.},
	keywords = {breast cancer, Familial, mTOR, PTEN, Sporadic},
	url = {https://www.scopus.com/inward/record.uri?eid=2-s2.0-77953195355\&doi=10.1111\%2fj.1365-2559.2010.03570.x\&partnerID=40\&md5=9d77cfb28cdd69a01ac55e675518dc61},
	author = {Bakarakos, P. and Theohari, I. and Nomikos, A. and Mylona, E. and Papadimitriou, C. and Dimopoulos, A.-M. and Nakopoulou, L.}
}
