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https://www.readbyqxmd.com/read/27910856/acquired-resistance-of-pancreatic-cancer-cells-to-cisplatin-is-multifactorial-with-cell-context-dependent-involvement-of-resistance-genes
#1
R Mezencev, L V Matyunina, G T Wagner, J F McDonald
Pancreatic ductal adenocarcinoma (PDAC) is one of the most lethal of malignancies, in large measure, due to the propensity of PDAC cells to acquire resistance to chemotherapeutic agents. A better understanding of the molecular basis of acquired resistance is a major focus of contemporary PDAC research. We report here the results of a study to independently develop cisplatin resistance in two distinct parental PDAC cell lines, AsPC1 and BxPC3, and to subsequently examine the molecular mechanisms associated with the acquired resistance...
December 2, 2016: Cancer Gene Therapy
https://www.readbyqxmd.com/read/27904769/disruption-of-actin-filaments-and-suppression-of-pancreatic-cancer-cell-viability-and-migration-following-treatment-with-polyisoprenylated-cysteinyl-amides
#2
Augustine T Nkembo, Olufisayo Salako, Rosemary A Poku, Felix Amissah, Elizabeth Ntantie, Hernan Flores-Rozas, Nazarius S Lamango
Pancreatic cancer is characterized by K-Ras mutations in over 90% of the cases. The mutations make the tumors aggressive and resistant to current therapies resulting in very poor prognoses. Valiant efforts to drug mutant K-Ras and related proteins for the treatment of cancers with Ras mutations have been elusive. The need thus persists for therapies to target and suppress the hyperactive K-Ras mutant proteins to normal levels of activity. Polyisoprenylated cysteinyl amide inhibitors (PCAIs) of polyisoprenylated methylated protein methyl esterase (PMPMEase) were designed to disrupt polyisoprenylated protein metabolism and/or functions...
2016: American Journal of Cancer Research
https://www.readbyqxmd.com/read/27903970/ion-channels-in-control-of-pancreatic-stellate-cell-migration
#3
Hannah Storck, Benedikt Hild, Sandra Schimmelpfennig, Sarah Sargin, Nikolaj Nielsen, Angela Zaccagnino, Thomas Budde, Ivana Novak, Holger Kalthoff, Albrecht Schwab
Pancreatic stellate cells (PSCs) play a critical role in the progression of pancreatic ductal adenocarcinoma (PDAC). Once activated, PSCs support proliferation and metastasis of carcinoma cells. PSCs even co-metastasise with carcinoma cells. This requires the ability of PSCs to migrate. In recent years, it has been established that almost all "hallmarks of cancer" such as proliferation or migration/invasion also rely on the expression and function of ion channels. So far, there is only very limited information about the function of ion channels in PSCs...
November 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27895743/diagnosis-of-pancreatic-lesions-collected-by-endoscopic-ultrasound-guided-fine-needle-aspiration-using-next-generation-sequencing
#4
Eri Kameta, Kazuya Sugimori, Takashi Kaneko, Tomohiro Ishii, Haruo Miwa, Takeshi Sato, Yasuaki Ishii, Soichiro Sue, Tomohiko Sasaki, Yuki Yamashita, Wataru Shibata, Naomichi Matsumoto, Shin Maeda
Endoscopic ultrasound-guided fine-needle aspiration (EUF-FNA) has improved the diagnosis of pancreatic lesions. Next-generation sequencing (NGS) facilitates the production of millions of sequences concurrently. Therefore, in the current study, to improve the detectability of oncogenic mutations in pancreatic lesions, an NGS system was used to diagnose EUS-FNA samples. A total of 38 patients with clinically diagnosed EUS-FNA specimens were analyzed; 27 patients had pancreatic ductal adenocarcinoma (PDAC) and 11 had non-PDAC lesions...
November 2016: Oncology Letters
https://www.readbyqxmd.com/read/27895409/two-cases-of-pancreatic-ductal-adenocarcinoma-with-intrapancreatic-metastasis
#5
Yusuke Fujita, Minoru Kitago, Yohei Masugi, Osamu Itano, Masahiro Shinoda, Yuta Abe, Taizo Hibi, Hiroshi Yagi, Yoko Fujii-Nishimura, Michiie Sakamoto, Yuko Kitagawa
There are no standardized diagnostic criteria for intrapancreatic metastasis of pancreatic ductal adenocarcinoma (PDAC). Here, we report two cases of patients with PDAC who were pathologically diagnosed as harboring intrapancreatic metastasis. In both cases, the main lesions were located in the pancreatic body, and no other lesion was detected preoperatively. The patients were diagnosed with pancreatic body cancers and distal pancreatectomy was performed. Pathological findings revealed microscopic cancer nests, which had connections to neither the main lesion nor the premalignant lesion in the pancreatic tail parenchyma...
November 7, 2016: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/27895310/tgf%C3%AE-1-overexpression-is-associated-with-improved-survival-and-low-tumor-cell-proliferation-in-patients-with-early-stage-pancreatic-ductal-adenocarcinoma
#6
Evan S Glazer, Eric Welsh, Jose M Pimiento, Jamie K Teer, Mokenge P Malafa
The role of transforming growth factor beta-type-1 (TGFβ1) in pancreatic ductal adenocarcinoma (PDAC) progression is stage-dependent. We hypothesized that TGFβ1 expression is associated with survival and proliferation markers in patients with early-stage PDAC. We acquired clinicopathologic, treatment, and mRNA expression data from The Cancer Genome Atlas data set for 106 patients identified with stage I/II PDAC who underwent pancreaticoduodenectomy. Patients were categorized as high expression when mRNA expression was ≥75th percentile for each gene...
November 23, 2016: Oncotarget
https://www.readbyqxmd.com/read/27895106/saliva-exosomes-from-pancreatic-tumor-bearing-mice-modulate-nk-cell-phenotype-and-antitumor-cytotoxicity
#7
Stergios Katsiougiannis, David Chia, Yong Kim, Ram P Singh, David T W Wong
Tumor exosomes are emerging as antitumor immunity regulators; however, their effects on secondary exosome secretion by distal organs have not been explored. We have previously demonstrated that suppression of exosomes at the distal tumor site of pancreatic ductal adenocarcinoma (PDAC) ablated the development of salivary biomarker profile. Here, we explore the function of salivary exosomes from tumor-bearing mice in immune surveillance. We provide evidence that salivary exosomes from mice with PDAC exhibit a suppressive effect that results in reduced tumor-killing capacity by NK cells...
November 28, 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27894105/histone-deacetylase-inhibitors-provoke-a-tumor-supportive-phenotype-in-pancreatic-cancer-associated-fibroblasts
#8
Andrew H Nguyen, Irmina A Elliott, Nanping Wu, Cynthia Matsumura, Maria Vogelauer, Narsis Attar, Amanda Dann, Razmik Ghukasyan, Paul A Toste, Sanjeet G Patel, Jennifer L Williams, Luyi Li, David W Dawson, Caius Radu, Siavash K Kurdistani, Timothy R Donahue
Although histone deacetylase inhibitors (HDACi) are a promising class of anti-cancer drugs, thus far, they have been unsuccessful in early phase clinical trials for pancreatic ductal adenocarcinoma (PDAC). One potential reason for their poor efficacy is the tumor stroma, where cancer-associated fibroblasts (CAFs) are a prominent cell type and a source of resistance to cancer therapies. Here, we demonstrate that stromal fibroblasts contribute to the poor efficacy of HDACi's in PDAC. HDACi-treated fibroblasts show increased biological aggressiveness and are characterized by increased secretion of pro-inflammatory tumor-supportive cytokines and chemokines...
November 24, 2016: Oncotarget
https://www.readbyqxmd.com/read/27893718/foxo3-is-essential-for-cd44-expression-in-pancreatic-cancer-cells
#9
M Kumazoe, M Takai, J Bae, S Hiroi, Y Huang, K Takamatsu, Y Won, M Yamashita, S Hidaka, S Yamashita, S Yamada, M Murata, S Tsukamoto, H Tachibana
Pancreatic ductal adenocarcinoma (PDAC) is one of the most fatal types of cancer and the 5-year survival rate is only 5%. Several studies have suggested that cancer stem cells (CSCs) are thought to be involved in recurrence and metastasis and so it is essential to establish an approach targeting CSCs. Here we have demonstrated that cyclic guanosine monophosphate (cGMP) suppressed CD44 expression and the properties of CSCs in PDAC. Microarray analysis suggested that cGMP inhibited Forkhead box O3 (FOXO3), which is known as a tumor suppressor...
November 28, 2016: Oncogene
https://www.readbyqxmd.com/read/27893715/tgf%C3%AE-promotes-mesenchymal-phenotype-of-pancreatic-cancer-cells-in-part-through-epigenetic-activation-of-vav1
#10
P-H Huang, P-J Lu, L-Y Ding, P-C Chu, W-Y Hsu, C-S Chen, C-C Tsao, B-H Chen, C-T Lee, Y-S Shan, C-S Chen
The highly homeostasis-resistant nature of cancer cells leads to their escape from treatment and to liver metastasis, which in turn makes pancreatic ductal adenocarcinoma (PDAC) difficult to treat, especially the squamous/epithelial-to-mesenchymal transition (EMT)-like subtype. As the molecular mechanisms underlying tumour heterogeneity remain elusive, we investigated whether epigenetic regulation might explain inter-individual differences in the progression of specific subtypes. DNA methylation profiling performed on cancer tissues prior to chemo/radiotherapy identified one hypermethylated CpG site (CpG6882469) in the VAV1 gene body that was correlated with demethylation of two promoter CpGs (CpG6772370/CpG6772811) in both PDAC and peripheral blood...
November 28, 2016: Oncogene
https://www.readbyqxmd.com/read/27892481/autophagy-is-required-for-pdac-glutamine-metabolism
#11
Ju-Won Seo, Jungwon Choi, So-Yeon Lee, Suhyun Sung, Hyun Ju Yoo, Min-Ji Kang, Heesun Cheong, Jaekyoung Son
Macroautophagy (autophagy) is believed to maintain energy homeostasis by degrading unnecessary cellular components and molecules. Its implication in regulating cancer metabolism recently started to be uncovered. However, the precise roles of autophagy in cancer metabolism are still unclear. Here, we show that autophagy plays a critical role in glutamine metabolism, which is required for tumor survival. Pancreatic ductal adenocarcinoma (PDAC) cells require both autophagy and typical glutamine transporters to maintain intracellular glutamine levels...
November 28, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27889647/activation-of-wnt-%C3%AE-catenin-signaling-enhances-pancreatic-cancer-development-and-the-malignant-potential-via-up-regulation-of-cyr61
#12
Makoto Sano, David R Driscoll, Wilfredo E DeJesus-Monge, Brian Quattrochi, Victoria A Appleman, Jianhong Ou, Lihua Julie Zhu, Nao Yoshida, Shintaro Yamazaki, Tadatoshi Takayama, Masahiko Sugitani, Norimichi Nemoto, David S Klimstra, Brian C Lewis
Pancreatic ductal adenocarcinoma (PDAC), a poor prognostic cancer, commonly develops following activating mutations in the KRAS oncogene. Activation of WNT signaling is also commonly observed in PDAC. To ascertain the impact of postnatal activation of WNT-stimulated signaling pathways in PDAC development, we combined the Elastase-tva-based RCAS-TVA pancreatic cancer model with the established LSL-Kras(G12D), Ptf1a-cre model. Delivery of RCAS viruses encoding β-catenin(S37A) and WNT1 stimulated the progression of premalignant pancreatic intraepithelial neoplasias (PanIN) and PDAC development...
November 24, 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27889645/suppression-of-tumor-growth-and-muscle-wasting-in-a-transgenic-mouse-model-of-pancreatic-cancer-by-the-novel-histone-deacetylase-inhibitor-ar-42
#13
Sally E Henderson, Li-Yun Ding, Xiaokui Mo, Tanios Bekaii-Saab, Samuel K Kulp, Ching-Shih Chen, Po-Hsien Huang
PURPOSE: Pancreatic ductal adenocarcinoma (PDAC) is the third leading cause of cancer death in the United States. This study was aimed at evaluating the efficacy of AR-42 (formerly OSU-HDAC42), a novel histone deacetylase (HDAC) inhibitor currently in clinical trials, in suppressing tumor growth and/or cancer-induced muscle wasting in murine models of PDAC. EXPERIMENTAL DESIGN: The in vitro antiproliferative activity of AR-42 was evaluated in six human pancreatic cancer cell lines (AsPC-1, COLO-357, PANC-1, MiaPaCa-2, BxPC-3, SW1990)...
November 24, 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27889393/triple-amirna-vegfrs-inhibition-in-pancreatic-cancer-improves-the-efficacy-of-chemotherapy-through-emt-regulation
#14
Jianfei Huang, Haijun Mei, Zhiyuan Tang, Jieying Li, Xiaojing Zhang, Yixiang Lu, Fang Huang, Qin Jin, Zhiwei Wang
Pancreatic ductal adenocarcinoma (PDAC) is a devastating disease with dismal outcome. Both novel prognostic markers and therapeutic targets are needed to improve the overall outcome of patients. Although single or double VEGFRs have been studied in PDAC, little is known about the role of triple combination of VEGFRs (VEGFR1, 2, and 3) in prognosis and therapy. We determined VEGFRs protein expression in 241 pancreatic tissues by tissue microarray immunohistochemistry (TMA-IHC), and correlated with patients' clinical characteristics and overall survival...
November 23, 2016: Journal of Controlled Release: Official Journal of the Controlled Release Society
https://www.readbyqxmd.com/read/27888145/critical-role-of-hnrnp-a1-in-activating-kras-transcription-in-pancreatic-cancer-cells-a-molecular-mechanism-involving-g4-dna
#15
REVIEW
Susanna Cogoi, Valentina Rapozzi, Sabina Cauci, Luigi E Xodo
KRAS is one of the most mutated genes in human cancer. Its crucial role in the tumourigenesis of pancreatic ductal adenocarcinoma (PDAC) has been widely demonstrated. As this deadly cancer does not sufficiently respond to conventional chemotherapies, it is important to increase our knowledge of pancreatic cancer biology, in particular how oncogenic KRAS is regulated. The promoter of KRAS contains a GA-element composed of runs of guanines that fold into a G4 structure. This unusual DNA conformation is recognized by several nuclear proteins, including MAZ and hnRNP A1...
November 22, 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27886609/utility-of-virtual-touch-quantification-in-the-diagnosis-of-pancreatic-ductal-adenocarcinoma
#16
Takumi Onoyama, Masahiko Koda, Yuki Fujise, Tomoaki Takata, Soichiro Kawata, Toshiaki Okamoto, Kennichi Miyoshi, Tomomitsu Matono, Takaaki Sugihara, Kazuya Matsumoto, Koichiro Kawaguchi, Kenichi Harada, Kazuo Yashima, Hajime Isomoto
This study aimed to compare the tissue stiffness of pancreatic ductal adenocarcinoma (PDAC) with that of pancreatic parenchyma using virtual touch quantification (VTQ). SWV was measured in 34 PDAC lesions and in pancreatic parenchyma of both controls and patients. SWVs in PDAC lesions were significantly higher than in pancreatic parenchyma in both healthy controls and in patients with PDAC. The area under the ROC for diagnosis of PDAC was 0.94 for pancreatic parenchyma in healthy controls, and 0.85 for pancreatic parenchyma in patients with PDAC...
November 17, 2016: Clinical Imaging
https://www.readbyqxmd.com/read/27885893/tumor-vessel-relationships-in-pancreatic-ductal-adenocarcinoma-at-multidetector-ct-different-classification-systems-and-their-influence-on-treatment-planning
#17
Ahmed M Zaky, Christopher L Wolfgang, Matthew J Weiss, Ammar A Javed, Elliot K Fishman, Atif Zaheer
Treatment of pancreatic ductal adenocarcinoma (PDAC) remains a challenge, given its propensity for early systemic spread and growth into the adjacent vital vascular structures. With the advent of newer surgical techniques and chemoradiation therapies, multidetector computed tomography (CT) plays a crucial role in the identification of patients with borderline resectable disease who may benefit from such treatments. Stage III PDAC is divided into two categories-locally advanced, defined by arterial encasement or nonreconstructible portovenous axis involvement; and borderline resectable, defined by limited arterial involvement and/or reconstructible portovenous involvement...
November 25, 2016: Radiographics: a Review Publication of the Radiological Society of North America, Inc
https://www.readbyqxmd.com/read/27881452/arginine-methylation-of-mdh1-disrupts-pdac-metabolism-and-growth
#18
(no author information available yet)
Hypomethylation of MDH1 enhances glutamine metabolism and cellular proliferation in PDAC.
November 23, 2016: Cancer Discovery
https://www.readbyqxmd.com/read/27877222/hedgehog-signaling-non-canonical-activated-by-pro-inflammatory-cytokines-in-pancreatic-ductal-adenocarcinoma
#19
Yuqiong Wang, Gang Jin, Quanjiang Li, Zhiping Wang, Weimin Hu, Ping Li, Shude Li, Hongyu Wu, Xiangyu Kong, Jun Gao, Zhaoshen Li
Hedgehog(HH) pathway is found to be activated through a manner of canonical, or the non-canonical HH pathways. Distinct hyperplasia stroma around tumor cells is supposed to express pro-inflammatory cytokines abundantly, such as tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), etc. in pancreatic ductal adenocarcinoma (PDAC) tissues. In this study we observed the effects of TNF-α and IL-1β on HH pathway activation in PDAC cells, and explored their activation manners. Our results showed that pro-inflammatory cytokines, TNF-α and IL-1β, could up-regulate the expression of GLI1 gene, increase its nuclear protein expression and promote malignant cell behaviors including migration, invasion, epithelial-mesenchymal transition (EMT) and drug resistance as well...
2016: Journal of Cancer
https://www.readbyqxmd.com/read/27877217/pregnancy-specific-%C3%AE-1-glycoprotein-1-is-expressed-in-pancreatic-ductal-adenocarcinoma-and-its-subcellular-localization-correlates-with-overall-survival
#20
Jasmin H Shahinian, Hannah Fuellgraf, Stefan Tholen, Justin Mastroianni, Julia Daniela Knopf, Markus Kuehs, Bettina Mayer, Manuel Schlimpert, Birte Kulemann, Simon Kuesters, Jens Hoeppner, Ulrich F Wellner, Martin Werner, Ulrich T Hopt, Robert Zeiser, Peter Bronsert, Oliver Schilling
Proteins of the pregnancy specific β-1 glycoprotein (PSG) family are renowned for their elevated expression during pregnancy. Only few reports have investigated their expression in adenocarcinomas. We studied the expression of PSG1 in pancreatic adenocarcinoma (PDAC). In a cohort of 104 patient samples, immunohistochemical analysis determined PSG1 expression in every specimen. PSG1 was found at apical and cytoplasmic localization or solely at cytoplasmic localization, with the latter case being correlated to shortened median survival (25 vs 11 months, logrank p-value < 0...
2016: Journal of Cancer
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