Disease relevance of Carcinoma, Pancreatic Ductal

• In contrast, hepatocellular carcinomas expressed the same keratin pattern as pancreatic acinar carcinomas with keratins 8 and 18, whereas cholangiocarcinomas expressed keratin 7, 8, 18, and 19, similar to pancreatic ductal carcinomas [1].
• Vascular endothelial growth factor mediated angiogenic potential of pancreatic ductal carcinomas enhanced by hypoxia: an in vitro and in vivo study [2].
• Three pancreatic ductal carcinomas and one chronic pancreatitis specimen demonstrated cytoplasmic staining with MUC2; the difference between the two groups was not found to be statistically significant [3].
• The authors previously reported that telomerase activity in pancreatic juice differentiates pancreatic ductal carcinoma from adenoma and pancreatitis [4].
• Even among patients with tubular adenocarcinoma, the most common type of pancreatic ductal carcinoma, if the patient is aged and has chronic pancreatitis, the main pancreatic duct and duct of Santorini may dilate to the same degree as in mucin-hypersecreting neoplasm [5].

High impact information on Carcinoma, Pancreatic Ductal

• A pancreatic ductal carcinoma, designated CBP, was established as a transplantable tumor line in the CB/SsLak inbred strain of Syrian golden hamsters [6].
• Oncogenic activation of the K-ras gene occurs in >90% of pancreatic ductal carcinoma and is found early in the PanIN-carcinoma sequence, but its functional roles remain poorly understood [7].
• Immunohistochemistry on tissue sections from human pancreatic ductal carcinoma also revealed iNOS expression in stromal cells and IL-1beta expression in tumor cells, thus supporting the in vitro findings [8].
• We investigated the prevalence of biallelic inactivation of BRCA2 in the presumed precursors to invasive pancreatic ductal carcinomas, pancreatic intraepithelial neoplasia (PanIN) [9].
• We have investigated the mRNA/protein expression of several tyrosine kinase receptors, growth factors, and p16INK4A cyclin inhibitor in cell lines derived from normal human pancreatic duct epithelium (HPDE) and compared them with those of five pancreatic ductal carcinoma cell lines [10].

Chemical compound and disease context of Carcinoma, Pancreatic Ductal

• Comparative molecular field analysis of the antitumor activity of 9H-thioxanthen-9-one derivatives against pancreatic ductal carcinoma 03 [11].
• Proteomic analysis of pancreatic ductal carcinoma cells treated with 5-aza-2'-deoxycytidine [12].
• Heterogeneic distribution of thymidine phosphorylase between primary tumors and metastatic lesions of human pancreatic ductal carcinoma: implications for the efficacy of chemotherapy with 5-FU or its derivatives [13].
• These results suggest that expression of group II PLA2 in human pancreatic ductal carcinomas is possibly involved in the proliferation of interstitial tissue directly or indirectly through prostaglandin production [14].
• BACKGROUND: The therapeutic efficacy of intratumoral instillation of genetically engineered, CYP2B1-expressing, microencapsulated cells in combination with ifosfamide had been previously demonstrated in xenografted human pancreatic ductal carcinomas [Gene Ther 1998;5:1070-1078] [15].

Biological context of Carcinoma, Pancreatic Ductal

• Mutations or alterations in the p53 tumor suppressor gene/protein are observed in 50-70% of these cancers, yet little information is available regarding the phenotypic effects of restoration of wild-type (wt) p53 function in pancreatic ductal carcinoma cells [16].
• In this study, we introduced a normal copy of chromosome 18 into some pancreatic ductal carcinoma cells with and without a complete inactivation of SMAD4 [17].
• Isolation of a pancreas-specific gene located on human chromosome 14q31: expression analysis in human pancreatic ductal carcinomas [18].
• Ki-ras and p53 gene mutations in pancreatic ductal carcinoma: a relationship with tumor phenotype and survival [19].
• Our data indicate that P27/Kip1 accumulation by Akt inactivation could induce cell cycle arrest in the G1 phase and suggest that the PI3K-Akt pathway plays an important role in cell proliferation in human pancreatic ductal carcinoma cells [20].

Anatomical context of Carcinoma, Pancreatic Ductal

• Injection of PC-1 cells into the homologous hamster pancreas resulted in tumor formation, histopathologically indistinguishable from the original primary pancreatic ductal carcinoma [21].

Gene context of Carcinoma, Pancreatic Ductal

• CONCLUSIONS: MUC1 is overexpressed in pancreatic ductal carcinoma with a predominantly membranous and variable cytoplasmic staining pattern [3].
• Conversely, MUC2 does not appear to be a useful marker for recognizing pancreatic ductal carcinoma in FNA specimens [3].
• Such genetic events on the CDKN2A gene may play an important role possibly at a later step in the progression of pancreatic ductal carcinoma [22].
• Human pancreatic ductal carcinoma cells express FGF-5 and FGFR-1IIIc, implying a potential for autocrine growth modulation [23].
• These results indicate the possible association of TRX and GRX with malignant potential of pancreatic ductal carcinoma [24].

Analytical, diagnostic and therapeutic context of Carcinoma, Pancreatic Ductal

• Detection of tumor cell dissemination in pancreatic ductal carcinoma patients by CK 20 RT-PCR indicates poor survival [25].
• Evaluation of blood flow in pancreatic ductal carcinoma using contrast-enhanced, wide-band Doppler ultrasonography: correlation with tumor characteristics and vascular endothelial growth factor [26].
• Terminally modified oligodeoxynucleotides directed against p53 in an orthotopic xenograft model: a novel adjuvant treatment strategy for pancreatic ductal carcinoma [27].

References