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).
Extracellular lumican inhibits cancer cell replication and restrains growth of early-stage pancreatic adenocarcinoma (PDAC) such that patients with tumors containing stromal lumican experience a three-fold longer survival after treatment.
Evaluation of insulin-like growth factor (IGF-1) and retinol binding protein (RBP-4) levels in patients with newly diagnosed pancreatic adenocarcinoma (PDAC).
Four (hsa-mir-126, hsa-mir-3613, hsa-mir-424, and hsa-mir-4772) out of 17 differentially expressed miRNAs were associated to the OS of patients with PAAD.
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.
Finally, the combination of ATM silencing, radiotherapy, and PD-L1 blockade markedly improves <i>in vivo</i> murine tumor responses, supporting further investigation of this promising approach in pancreatic adenocarcinoma.<i>See related article by Zhang et al., p. 3940</i>.
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.
Four (hsa-mir-126, hsa-mir-3613, hsa-mir-424, and hsa-mir-4772) out of 17 differentially expressed miRNAs were associated to the OS of patients with PAAD.
The clinical relevance of these experiments is suggested by immunohistochemical, microarray, and quantitative RT-PCR studies of human colon and pancreatic tumors demonstrating significantly higher DUOX2, IL-4R, and IL-17RA expression in tumors than in adjacent normal tissues; in pancreatic adenocarcinoma, increased DUOX2 expression is adversely associated with overall patient survival.
In conclusion, the results of the present study suggested that suppressing PD-L1 in malignant cells during DC immunization may be a useful tool for immunotherapy in pancreatic adenocarcinoma.
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).