Evaluation of insulin-like growth factor (IGF-1) and retinol binding protein (RBP-4) levels in patients with newly diagnosed pancreatic adenocarcinoma (PDAC).
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.
The A16V (C→T) mutation in PRSS1, which encodes a cationic trypsinogen and has a mutation associated with hereditary pancreatitis and pancreatic adenocarcinoma, was observed in 40% (8/20) (7/17 of ETV6 translocation-positive and 1/3 of ETV6 translocation-negative secretory carcinomas).
Patients were more likely to undergo MIDP if they had lower ASA classification (P = 0.004) or BMI ≥ 30 (P < 0.001) and less likely if they had pancreatic adenocarcinoma (P < 0.001).
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.
The immunohistochemistry results revealed that RAB38 was upregulated and positively correlated with the grade of progression in pancreatic adenocarcinoma patients.
Pre-incubation with melatonin prevented the reduction in CD62L expression by CD8<sup>+</sup> T cells induced by the co-cultivation of peripheral blood mononuclear cells with human pancreatic adenocarcinoma cell line (MiaPaCa-2).
CUDC-907 displays potent antitumor activity against human pancreatic adenocarcinoma in vitro and in vivo through inhibition of HDAC6 to downregulate c-Myc expression.
To address this, we sought to determine if the HGF/Met and MSP/Ron systems produce overlapping or divergent contributions towards a malignant phenotype by performing a characterization of MSP and HGF driven signaling, behavioral, and transcriptomic responses in a primary pancreatic adenocarcinoma (PAAD) cell line in vitro.
However, demographic discrepancies, underpowered RDP sample and differences in oncological burden do not permit certain conclusions regarding the oncological safety of RDP and LDP for pancreatic adenocarcinoma.
This antigen, defined by two monoclonal antibodies recognising separate epitopes on a large glycoconjugate protein complex, is co-expressed with SOX9 by foregut ductal progenitors in the developing human liver and pancreas, and in pancreatic adenocarcinoma.
Functionally, loss-of function assays were carried out and the experimental results indicated that suppression of LINC01232 hindered the deterioration of PAAD by affecting cell proliferation and migration.
Protein-level analysis reveals that PKCα is fully phosphorylated at the PHLPP site in over 5,000 patient tumors, with higher PKC levels correlating (1) inversely with PHLPP1 levels and (2) positively with improved survival in pancreatic adenocarcinoma.
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.