This study was conducted to determine patients' outcome according to the expressions of CXCR4, CXCR7 and HIF-1alpha after resection of PA. Immunohistochemistry for CXCR4, CXCR7 and HIF-1alpha expressions as well as cell proliferative index (Ki-67) was conducted in 71 resected (R0) PA and their 48 related lymph nodes (LN) using tissue microarray.
Alterations in K-ras were detected in 73% of PC cases and 57% of CP cases, respectively. beta-Actin mRNA was expressed in >3.0 x 10(1) copies/microl in all but two PC cases in which hTERT mRNA was not detected.
Bioinformatic analysis was carried for driver gene prediction, and we proved that AHNAK was a driver gene of pancreatic adenocarcinoma and a predictor of poor outcomes of PDAC by clinical characteristics analysis and in vitro experiments.
FA-6 cells, which are derived from a pancreatic adenocarcinoma that secretes a parathyroid hormone related peptide, exhibit only very low levels of p38 MAPK expression, relative to T3M-4 cells.
Comparison of the BxPC-3 (derived from a primary tumor) and HPAF-II (derived from a metastasis) demonstrates a reciprocal relationship between cav-1 expression and p42/p44 Erk activation with PC cell migration, invasion, RhoC GTPase and p38 MAPK activation.
FA-6 cells, which are derived from a pancreatic adenocarcinoma that secretes a parathyroid hormone related peptide, exhibit only very low levels of p38 MAPK expression, relative to T3M-4 cells.
Comparison of the BxPC-3 (derived from a primary tumor) and HPAF-II (derived from a metastasis) demonstrates a reciprocal relationship between cav-1 expression and p42/p44 Erk activation with PC cell migration, invasion, RhoC GTPase and p38 MAPK activation.
As development of pancreatic cancer is firmly linked to smoking, the aim of the present study was to examine the expression and oncogenic role of AKR1B10 in pancreatic adenocarcinoma.
These data indicate that inhibiting AKT with CTMP may be of therapeutic benefit in the treatment of pancreatic adenocarcinoma and, when combined with established therapies, may result in an increase in tumor cell death.
Targeting and imaging of ALCAM-positive tumors using (64)Cu-DOTA-CysDb were evaluated in mice bearing human pancreatic adenocarcinoma xenografts (HPAF-II or BxPC-3).
In the present study, 5-LOX was found to be overexpressed not only in pancreatic cancer cell lines but also in tissue samples of patients suffering from pancreatic adenocarcinoma.
We pay particular attention to pancreatic adenocarcinoma, an aggressive tumor that has a 5-year survival rate of 3-5%, and is the fourth leading cause of cancer mortality in the US. and IAP.
We pay particular attention to pancreatic adenocarcinoma, an aggressive tumor that has a 5-year survival rate of 3-5%, and is the fourth leading cause of cancer mortality in the US. and IAP.
Microarray data showed that Ang-2 was upregulated in neuroendocrine tumors ( approximately 8 times more than normal) and adenocarcinoma of the pancreas ( approximately 5 times more than normal) although Ang-1 and Tie-2 were not differentially expressed.
Immunohistochemistry showed tumor-specific staining of Ang-2 in 10 of 15 matched adenocarcinoma of the pancreas (67%) and 6 of 8 neuroendocrine tumors (75%).
We investigated expression levels of AIB1 protein and mRNA in pancreatic cancer cell lines and in a series of archival pancreatic adenocarcinoma (n=78), pancreatic intraepithelial neoplasia (n=93), pancreatitis (n=28), and normal pancreas tissues (n=52).
In this study, we performed an immunostaining assay to evaluate ANXA10 expression in 155 primary human tissue specimens, including normal pancreas, chronic pancreatitis (CP), pancreatic adenocarcinoma (PDAC), pancreatic intraepithelial neoplasia (PanIN, the most important precursor of PDAC), and intraductal papillary mucinous neoplasm (IPMN).
In addition, we identified six genes in common (i.e., <i>ANXA2</i> [annexin A2], <i>EPHA2</i> [erythropoietin-producing hepatocellular class A2], <i>ITGB4</i> [integrin beta 4], <i>KRT19</i> [keratin type I cytoskeletal 19], <i>LGALS3</i> [galectin-3], and <i>S100A14</i> [S100 calcium binding protein A14]) between the protein-protein interaction and gene co-expression networks that may have critical functions in PAAD.