In patients with adenocarcinoma (AC), high PTEN expression (n = 9) was associated with significantly longer survival than low PTEN expression (mean survival 23.50 vs. 15.54 months, log rank P = 0.043).
Further, we found that a significant fraction of ERG-positive, PTEN-negative HGPIN and intraductal carcinoma (IDC-P) lesions are most likely clonally derived from adjacent PTEN-negative adenocarcinomas, indicating that such PTEN-negative HGPIN and IDC-P lesions arise from, rather than give rise to, the nearby invasive adenocarcinoma.
Significantly more squamous cell carcinomas compared with adenocarcinomas demonstrated loss of (negative) PTEN staining (26 of 44 [59%] versus 32 of 94 [34%]; p = 0.009).
There were no significant differences in the menstruation status and the expression levels of TFF-1 and PTEN mRNAs between adenocarcinoma and squamous carcinoma (p > 0.05).
Among 11 HPV-negative adenocarcinomas, 40.0% (2/5) endometrioid cases and 33.3% (2/6) mucinous cases were shown to be PTEN mutated, while no cases (0/21) were PTEN-mutant in the remainder (i.e. adenosquamous carcinomas and HPV-positive adenocarcinomas).
While PTEN inactivation leads to PC, it is not sufficient for metastasis, the loss of PTEN concurrently with the inactivation of both TP53 and RB1 empower lineage plasticity in PC cells, which substantially promotes PC metastasis and the conversion to PC adenocarcinoma to neuroendocrine PC (NEPC), demonstrating the essential function of TP53 and RB1 in the suppression of PCSCs.
In addition, microsatellite instability (MSI) leading to the functional inactivation of the PTEN gene has also been reported for ovarian adenocarcinomas with frequencies varying from 6 to 37%.
186 adenocarcinomas and 16 adenomas from the EPIC Norfolk study were tested for PTEN and PIK3CA mutations by DNA sequencing and PTEN expression changes by immunohistochemistry.
The aim of this study was to assess the involvement of PTEN and other putative 10q tumor suppressors in endometrioid-type adenocarcinomas characterized by loss of 10q sequences.
Noteworthy clinicopathologic correlations between PTEN transcriptional up/down-regulation and young age (p=0.0081, 61.7+/-8.7years versus 66.1+/-8.1years), smoking (p=0.032) and less differentiated adenocarcinomas (p=0.013) were identified.
Epidermal growth factor receptor, phosphatidylinositol-3-kinase catalytic subunit/PTEN, and KRAS/NRAS/BRAF in primary resected esophageal adenocarcinomas: loss of PTEN is associated with worse clinical outcome.
Protein tyrosine phosphatase (PTPase) activity was examined in two cell lines: human umbilical vein endothelial (HUVE) cells, which display contact inhibition of cell growth, and A427 human adenocarcinoma cells, which have lost this ability.
PTEN expression was significantly correlated with gender, smoking history, histology (adenocarcinoma [ADC] vs. squamous cell carcinoma), tumor node metastasis stage (I-II vs. III-IV), N status (N0 vs. N1-N3), and distant metastasis (M0 vs. M1).
The aim of this study was to investigate the role of MMAC1 protein in the relationship between ovarian endometriosis and clear cell and endometrioid-type ovarian adenocarcinomas.
PTEN loss was higher in lung ADC than in the adenocarcinoma component of ASC and significantly higher in lung SCC than in the squamous component of ASC.
In addition, microsatellite instability (MSI) leading to the functional inactivation of the PTEN gene has also been reported for ovarian adenocarcinomas with frequencies varying from 6 to 37%.