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https://www.readbyqxmd.com/read/28282719/pharmacogenetics-and-personalized-medicine-in-pancreatic-cancer
#1
Ali Hosseini Bereshneh, Fatemeh Morshedi, Mahsa Hematyar, Arastoo Kaki, Masoud Garshasbi
 Pancreatic cancer (PC) is a progressive, fatal disease with a high degree of malignancy. More than 40000 peoplediefrom this cancer annually in the United States. As a multifactorial condition, PC has a complex nature, and there are several genes and signalingpathwaysimplicated in PC pathogenesis and progression. There are diffèrent mutations in master genesincludingtumorsuppressors and oncogenesthat lead to Pancreaticintraepithelialneoplasia (PanIN) whichis the mostcommon non-invasive precursorlesion of pancreatic cancer...
March 2017: Acta Medica Iranica
https://www.readbyqxmd.com/read/28272465/reconstituting-development-of-pancreatic-intraepithelial-neoplasia-from-primary-human-pancreas-duct-cells
#2
Jonghyeob Lee, Emily R Snyder, Yinghua Liu, Xueying Gu, Jing Wang, Brittany M Flowers, Yoo Jung Kim, Sangbin Park, Gregory L Szot, Ralph H Hruban, Teri A Longacre, Seung K Kim
Development of systems that reconstitute hallmark features of human pancreatic intraepithelial neoplasia (PanINs), the precursor to pancreatic ductal adenocarcinoma, could generate new strategies for early diagnosis and intervention. However, human cell-based PanIN models with defined mutations are unavailable. Here, we report that genetic modification of primary human pancreatic cells leads to development of lesions resembling native human PanINs. Primary human pancreas duct cells harbouring oncogenic KRAS and induced mutations in CDKN2A, SMAD4 and TP53 expand in vitro as epithelial spheres...
March 8, 2017: Nature Communications
https://www.readbyqxmd.com/read/28260136/cells-of-origin-of-pancreatic-neoplasms
#3
REVIEW
Junpei Yamaguchi, Yukihiro Yokoyama, Toshio Kokuryo, Tomoki Ebata, Masato Nagino
Pancreatic ductal adenocarcinoma (PDAC) is a lethal malignant disease associated with poor prognosis, despite recent medical advances. It is of great importance to understand the initial events and cells of origin of pancreatic cancer to prevent the development and progression of PDAC. There are three distinct precursor lesions that develop into PDAC: pancreatic intraepithelial neoplasms (PanINs), intraductal papillary mucinous neoplasms (IPMNs), and mucinous cystic neoplasms (MCNs). Studies on genetically engineered mouse models have revealed that the initiation and development of these lesions largely depend on genetic alterations...
March 4, 2017: Surgery Today
https://www.readbyqxmd.com/read/28249896/lipocalin-2-promotes-pancreatic-ductal-adenocarcinoma-by-regulating-inflammation-in-the-tumor-microenvironment
#4
Sobeyda Gomez-Chou, Agnieszka Swidnicka-Siergiejko, Niharika Badi, Myrriah Chavez-Tomar, Gregory B Lesinski, Tanios Bekaii-Saab, Matthew R Farren, Thomas A Mace, Carl Schmidt, Yan Liu, Defeng Deng, Rosa F Hwang, Liran Zhou, Todd T Moore, Deyali Chatterjee, Huamin Wang, Xiaohong Leng, Ralph B Arlinghaus, Craig D Logsdon, Zobeida Cruz-Monserrate
Lipocalin-2 (LCN2) promotes malignant development in many cancer types. LCN2 is upregulated in patients with pancreatic ductal adenocarcinoma (PDAC) and in obese individuals, but whether it contributes to PDAC development is unclear. In this study, we investigated the effects of Lcn2 depletion on diet-induced obesity, inflammation and PDAC development. Mice with acinar cell-specific expression of KrasG12D were crossed with Lcn2-depleted animals and fed isocaloric diets with varying amounts of fat content. Pancreas were collected and analyzed for inflammation, pancreatic intraepithelial neoplasia (PanIN) and PDAC...
March 1, 2017: Cancer Research
https://www.readbyqxmd.com/read/28246467/familial-pancreatic-cancer-concept-management-and-issues
#5
REVIEW
Hiroyuki Matsubayashi, Kyoichi Takaori, Chigusa Morizane, Hiroyuki Maguchi, Masamichi Mizuma, Hideaki Takahashi, Keita Wada, Hiroko Hosoi, Shinichi Yachida, Masami Suzuki, Risa Usui, Toru Furukawa, Junji Furuse, Takamitsu Sato, Makoto Ueno, Yoshimi Kiyozumi, Susumu Hijioka, Nobumasa Mizuno, Takeshi Terashima, Masaki Mizumoto, Yuzo Kodama, Masako Torishima, Takahisa Kawaguchi, Reiko Ashida, Masayuki Kitano, Keiji Hanada, Masayuki Furukawa, Ken Kawabe, Yoshiyuki Majima, Toru Shimosegawa
Familial pancreatic cancer (FPC) is broadly defined as two first-degree-relatives with pancreatic cancer (PC) and accounts for 4%-10% of PC. Several genetic syndromes, including Peutz-Jeghers syndrome, hereditary pancreatitis, hereditary breast-ovarian cancer syndrome (HBOC), Lynch syndrome, and familial adenomatous polyposis (FAP), also have increased risks of PC, but the narrowest definition of FPC excludes these known syndromes. When compared with other familial tumors, proven genetic alterations are limited to a small proportion (< 20%) and the familial aggregation is usually modest...
February 14, 2017: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/28173980/expression-of-polymeric-immunoglobulin-receptor-and-stromal-activity-in-pancreatic-ductal-adenocarcinoma
#6
Prabhu Arumugam, Satyajit Bhattacharya, Joanne Chin-Aleong, Melania Capaso, Hemant M Kocher
BACKGROUND/OBJECTIVES: Polymeric immunoglobulin receptor (pIgR) traffics Immunoglobulins (IgA and IgM) through epithelial cells in normal mucosae but neither are expressed in the normal pancreas. Recent work from our laboratory suggested pIgR may be upregulated in pancreatic ductal adenocarcinoma (PDAC). Our aim was to assess the role of pIgR in human PDAC. METHODS: pIgR expression was manipulated (siRNA and shRNA) in cell lines to evaluate its subsequent effect on cell behaviour in 2D assays as well as 3D organotypics models...
February 1, 2017: Pancreatology: Official Journal of the International Association of Pancreatology (IAP) ... [et Al.]
https://www.readbyqxmd.com/read/27980052/clinicopathological-significance-of-necl-4-expression-in-pancreatic-ductal-adenocarcinoma
#7
Aya Kawanishi, Kenichi Hirabayashi, Misuzu Yamada, Yumi Takanashi, Atsuko Hadano, Yoshiaki Kawaguchi, Toshio Nakagohri, Naoya Nakamura, Tetsuya Mine
AIMS: The loss, or decreased expression, of nectin-like molecule 4 (Necl-4; an immunoglobulin-like cell adhesion molecule) is reported to be associated with the development and progression of certain types of cancer. We investigated the clinicopathological significance of Necl-4 expression in patients with pancreatic ductal adenocarcinoma (PDAC). METHODS: Immunohistochemical analyses of Necl-4 (n=258) and E-cadherin (n=256) expression were performed using tissue microarray blocks of PDAC samples...
December 15, 2016: Journal of Clinical Pathology
https://www.readbyqxmd.com/read/27941872/er-stress-protein-agr2-precedes-and-is-involved-in-the-regulation-of-pancreatic-cancer-initiation
#8
L Dumartin, W Alrawashdeh, S M Trabulo, T P Radon, K Steiger, R M Feakins, M P di Magliano, C Heeschen, I Esposito, N R Lemoine, T Crnogorac-Jurcevic
The mechanisms of initiation of pancreatic ductal adenocarcinoma (PDAC) are still largely unknown. In the present study, we analysed the role of anterior gradient-2 (AGR2) in the earliest stages of pancreatic neoplasia. Immunohistochemical analysis of chronic pancreatitis (CP) and peritumoral areas in PDAC tissues showed that AGR2 was present in tubular complexes (TC) and early pancreatic intraepithelial neoplasia (PanINs). Moreover, AGR2 was also found in discrete subpopulations of non-transformed cells neighbouring these pre-neoplastic lesions...
December 12, 2016: Oncogene
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
#9
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...
December 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27783689/epithelial-to-stromal-re-distribution-of-primary-cilia-during-pancreatic-carcinogenesis
#10
Simon Schimmack, Sarah Kneller, Nigora Dadabaeva, Frank Bergmann, Andrew Taylor, Thilo Hackert, Jens Werner, Oliver Strobel
BACKGROUND: The Hedgehog (HH) pathway is a mediator in pancreatic ductal adenocarcinoma (PDAC). Surprisingly, previous studies suggested that primary cilia (PC), the essential organelles for HH signal transduction, were lost in PDAC. The aim of this study was to determine the presence of PC in human normal pancreas, chronic pancreatitis, and during carcinogenesis to PDAC with focus on both epithelia and stroma. METHODS: PC were analyzed in paraffin sections from normal pancreas, chronic pancreatitis, intraductal papillary-mucinous neoplasia, and PDAC, as well as in primary human pancreatic stellate cells (PSC) and pancreatic cancer cell lines by double immunofluorescence staining for acetylated α-tubuline and γ-tubuline...
2016: PloS One
https://www.readbyqxmd.com/read/27775692/quantitative-assessment-of-pancreatic-cancer-precursor-lesions-in-ihc-stained-tissue-with-a-tissue-image-analysis-platform
#11
Famke Aeffner, Nathan T Martin, Mirza Peljto, Joshua C Black, Justin K Major, Maryam Jangani, Michael O Ports, Joseph S Krueger, G David Young
Tissue image analysis (tIA) is emerging as a powerful tool for quantifying biomarker expression and distribution in complex diseases and tissues. Pancreatic ductal adenocarcinoma (PDAC) develops in a highly complex and heterogeneous tissue environment and, generally, has a very poor prognosis. Early detection of PDAC is confounded by limited knowledge of the pre-neoplastic disease stages and limited methods to quantitatively assess disease heterogeneity. We sought to develop a tIA approach to assess the most common PDAC precursor lesions, pancreatic intraepithelial neoplasia (PanIN), in tissues from Kras(LSL-G12D/+); Trp53(LSL-R172H/+); Pdx-Cre (KPC) mice, a validated model of PDAC development...
October 24, 2016: Laboratory Investigation; a Journal of Technical Methods and Pathology
https://www.readbyqxmd.com/read/27764699/fbxw7-deletion-accelerates-kras-g12d-driven-pancreatic-tumorigenesis-via-yap-accumulation
#12
Qiang Zhang, Yaqing Zhang, Joshua D Parsels, Ines Lohse, Theodore S Lawrence, Marina Pasca di Magliano, Yi Sun, Meredith A Morgan
Pancreatic cancers driven by KRAS mutations require additional mutations for tumor progression. The tumor suppressor FBXW7 is altered in pancreatic cancers, but its contribution to pancreatic tumorigenesis is unknown. To determine potential cooperation between Kras mutation and Fbxw7 inactivation in pancreatic tumorigenesis, we generated P48-Cre;LSL-Kras(G12D);Fbxw7(fl/fl) (KFC(fl/fl)) compound mice. We found that KFC(fl/fl) mice displayed accelerated tumorigenesis: all mice succumbed to pancreatic ductal adenocarcinoma (PDA) by 40 days of age, with PDA onset occurring by 2 weeks of age...
November 2016: Neoplasia: An International Journal for Oncology Research
https://www.readbyqxmd.com/read/27748943/c-fos-erk-promotes-the-progression-from-pancreatic-intraepithelial-neoplasia-to-pancreatic-ductal-adenocarcinoma
#13
Lei You, Xiaoxia Ren, Yongxing Du, Wenjing Zhao, Ming Cui, Ge Chen, Yupei Zhao
Pathogenesis of pancreatic ductal adenocarcinoma (PDAC) is thought to develop through the progression of precursor lesions, known as pancreatic intraepithelial neoplasias (PanIN). In the present study, we showed that c-Fos promoted proliferation, cell cycle and migration in pancreatic cancer cells. Caerulein was used to accelerate the pathogenesis of Pdx-cre; KrasG12D mice. During PanIN formation and development of PDAC, the expression of ERK and c-Fos increased concomitantly. When ERK activity was inhibited by U0126, the expression of c-Fos also decreased...
December 2016: Oncology Reports
https://www.readbyqxmd.com/read/27732578/a-renewed-model-of-pancreatic-cancer-evolution-based-on-genomic-rearrangement-patterns
#14
Faiyaz Notta, Michelle Chan-Seng-Yue, Mathieu Lemire, Yilong Li, Gavin W Wilson, Ashton A Connor, Robert E Denroche, Sheng-Ben Liang, Andrew M K Brown, Jaeseung C Kim, Tao Wang, Jared T Simpson, Timothy Beck, Ayelet Borgida, Nicholas Buchner, Dianne Chadwick, Sara Hafezi-Bakhtiari, John E Dick, Lawrence Heisler, Michael A Hollingsworth, Emin Ibrahimov, Gun Ho Jang, Jeremy Johns, Lars G T Jorgensen, Calvin Law, Olga Ludkovski, Ilinca Lungu, Karen Ng, Danielle Pasternack, Gloria M Petersen, Liran I Shlush, Lee Timms, Ming-Sound Tsao, Julie M Wilson, Christina K Yung, George Zogopoulos, John M S Bartlett, Ludmil B Alexandrov, Francisco X Real, Sean P Cleary, Michael H Roehrl, John D McPherson, Lincoln D Stein, Thomas J Hudson, Peter J Campbell, Steven Gallinger
Pancreatic cancer, a highly aggressive tumour type with uniformly poor prognosis, exemplifies the classically held view of stepwise cancer development. The current model of tumorigenesis, based on analyses of precursor lesions, termed pancreatic intraepithelial neoplasm (PanINs) lesions, makes two predictions: first, that pancreatic cancer develops through a particular sequence of genetic alterations (KRAS, followed by CDKN2A, then TP53 and SMAD4); and second, that the evolutionary trajectory of pancreatic cancer progression is gradual because each alteration is acquired independently...
October 20, 2016: Nature
https://www.readbyqxmd.com/read/27725904/presentation-of-underglycosylated-mucin-1-in-pancreatic-adenocarcinoma-pdac-at-early-stages
#15
Su-Tang Lo, Pamela Pantazopouos, Zdravka Medarova, Anna Moore
Underglycosylated mucin 1 antigen (uMUC1) is a proven biomarker of cancer progression relevant to many malignancies including pancreatic ductal adenocarcinoma (PDAC). However, while ample evidence exists of the expression of total MUC1, little is known about the abundance of the underglycolsylated form of the antigen and its significance in disease progression. Such knowledge is important because the underglycosylated form of MUC1 is intimately linked to metastatic potential. Here, we investigated the expression uMUC1 at various stages of PDAC including pancreatic intraepithelial neoplasia (PanIN)...
2016: American Journal of Cancer Research
https://www.readbyqxmd.com/read/27712835/utility-of-18-fludeoxyglucose-in-preoperative-positon-emission-tomography-computed-tomography-pet-ct-in-the-early-diagnosis-of-exocrine-pancreatic-cancer-a-study-of-139-resected-cases
#16
Francisco Sánchez-Bueno, Rocío García-Pérez, María Antonia Claver Valderas, Jesús de la Peña Moral, Laura Frutos Esteban, Eduardo Ortiz Ruiz, Matilde Fuster Quiñonero, Pascual Parrilla Paricio
INTRODUCTION: In pancreatic ductal adenocarcinoma (PDA), surgical resection is the only curative treatment, but due to its late clinical presentation only 15-25% patients are candidates for curative resection. The aim of this prospective, single-center study is to determine the diagnostic utility of preoperative PET-CT for early detection of PDA and early panIN lesions. METHODS: We studied the histopathological features of PDA and different panIN lesions in 139 surgical samples from patients undergoing pancreatic resection (from 2010-2014), comparing these results with preoperative PET-CT and MDCT study...
November 2016: Cirugía Española
https://www.readbyqxmd.com/read/27667193/satellite-rnas-promote-pancreatic-oncogenic-processes-via-the-dysfunction-of-ybx1
#17
Takahiro Kishikawa, Motoyuki Otsuka, Takeshi Yoshikawa, Motoko Ohno, Hideaki Ijichi, Kazuhiko Koike
Highly repetitive tandem arrays at the centromeric and pericentromeric regions in chromosomes, previously considered silent, are actively transcribed, particularly in cancer. This aberrant expression occurs even in K-ras-mutated pancreatic intraepithelial neoplasia (PanIN) tissues, which are precancerous lesions. To examine the biological roles of the satellite RNAs in carcinogenesis, we construct mouse PanIN-derived cells expressing major satellite (MajSAT) RNA and show increased malignant properties. We find an increase in frequency of chromosomal instability and point mutations in both genomic and mitochondrial DNA...
2016: Nature Communications
https://www.readbyqxmd.com/read/27617308/adipocytes-promote-pancreatic-cancer-cell-proliferation-via-glutamine-transfer
#18
Kevin A Meyer, Christopher K Neeley, Nicki A Baker, Alexandra R Washabaugh, Carmen G Flesher, Barbara S Nelson, Timothy L Frankel, Carey N Lumeng, Costas A Lyssiotis, Michelle L Wynn, Andrew D Rhim, Robert W O'Rourke
Adipocytes promote progression of multiple cancers, but their role in pancreatic intraepithelial neoplasia (PanIN) and ductal adenocarcinoma (PDAC) is poorly defined. Nutrient transfer is a mechanism underlying stromal cell-cancer crosstalk. We studied the role of adipocytes in regulating in vitro PanIN and PDAC cell proliferation with a focus on glutamine metabolism. Murine 3T3L1 adipocytes were used to model adipocytes. Cell lines derived from PKCY mice were used to model PanIN and PDAC. Co-culture was used to study the effect of adipocytes on PanIN and PDAC cell proliferation in response to manipulation of glutamine metabolism...
September 2016: Biochemistry and Biophysics Reports
https://www.readbyqxmd.com/read/27610015/therapeutic-potential-of-targeting-acinar-cell-reprogramming-in-pancreatic-cancer
#19
REVIEW
Chi-Hin Wong, You-Jia Li, Yang-Chao Chen
Pancreatic ductal adenocarcinoma (PDAC) is a common pancreatic cancer and the fourth leading cause of cancer death in the United States. Treating this life-threatening disease remains challenging due to the lack of effective prognosis, diagnosis and therapy. Apart from pancreatic duct cells, acinar cells may also be the origin of PDAC. During pancreatitis or combined with activating KRas(G12D) mutation, acinar cells lose their cellular identity and undergo a transdifferentiation process called acinar-to-ductal-metaplasia (ADM), forming duct cells which may then transform into pancreatic intraepithelial neoplasia (PanIN) and eventually PDAC...
August 21, 2016: World Journal of Gastroenterology: WJG
https://www.readbyqxmd.com/read/27602757/pancreatic-stellate-cell-secreted-il-6-stimulates-stat3-dependent-invasiveness-of-pancreatic-intraepithelial-neoplasia-and-cancer-cells
#20
Nagaraj S Nagathihalli, Jason A Castellanos, Michael N VanSaun, Xizi Dai, Mahogany Ambrose, Qiaozhi Guo, Yanhua Xiong, Nipun B Merchant
Pancreatic ductal adenocarcinoma (PDAC) is a dynamic tumor supported by several stromal elements such as pancreatic stellate cells (PSC). Significant crosstalk exists between PSCs and tumor cells to stimulate oncogenic signaling and malignant progression of PDAC. However, how PSCs activate intercellular signaling in PDAC cells remains to be elucidated. We have previously shown that activated signal transducer and activator of transcription 3 (STAT3) signaling is a key component in the progression of pancreatic neoplasia...
October 4, 2016: Oncotarget
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