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Cancer: Adenocarcinoma
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Total 16 results found since Jan 2013.
Abstract IA05: Regulation of Ras proteins and their effectors
Ras proteins regulate multiple phenotypes, including proliferation, contact inhibition, cell motility, metabolism, and genome integrity. This range of phenotypes may relate to the number of different effector pathways that Ras activates. The best validated of these is the Raf/MAPK pathway. Ras proteins can activate PI 3-kinase pathways directly, though this seems to vary between tissue types. Ras proteins bind and activate RalGDS, but this pathway is less well understood. In addition to these three major pathways, Ras proteins in their GTP state interact directly with several other potential effectors.Analysis of the contr...
Source: Cancer Research - March 13, 2017 Category: Cancer & Oncology Authors: Tina Yuan, Frank McCormick Tags: Oncogenic Signals Translate the Cancer Genome Source Type: research
Abstract B08: ER chaperone GRP78 increases chemoresistance in pancreatic ductal adenocarcinoma
Conclusions: Collectively, our data show that GRP78 expression promotes chemoresistance in PDAC and therapeutic strategies blocking the activity of GRP78 increase the efficacy of currently available therapies.Citation Format: Jenifer B. Gifford, Wei Huang, Ann E. Zeleniak, Antreas Hindoyan, Hong Wu, Timothy R. Donahue, Reginald Hill.{Authors}. ER chaperone GRP78 increases chemoresistance in pancreatic ductal adenocarcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr B08.
Source: Cancer Research - December 13, 2016 Category: Cancer & Oncology Authors: Jenifer B. Gifford, Wei Huang, Ann E. Zeleniak, Antreas Hindoyan, Hong Wu, Timothy R. Donahue, Reginald Hill Tags: Molecular Drivers of Pancreatic Cancer Biology and Metastasis Source Type: research
Abstract A35: SOX9 induces chemo-resistance in pancreatic cancer cells and its high expression predicts poor prognosis
Conclusions: These data indicate that Sox9 plays an important role in chemo-resistance by the induction of stemness in pancreatic cancer cells.Citation Format: Shingo Kagawa, Taku Higasihara, Hideyuki Yoshitomi, Shigetsugu Takano, Hiroaki Shimizu, Masayuki Ohtsuka, Atsushi Kato, Katsunori Furukawa, Masaru Miyazaki.{Authors}. SOX9 induces chemo-resistance in pancreatic cancer cells and its high expression predicts poor prognosis. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 S...
Source: Cancer Research - December 13, 2016 Category: Cancer & Oncology Authors: Shingo Kagawa, Taku Higasihara, Hideyuki Yoshitomi, Shigetsugu Takano, Hiroaki Shimizu, Masayuki Ohtsuka, Atsushi Kato, Katsunori Furukawa, Masaru Miyazaki Tags: Early Detection Source Type: research
Abstract A67: TFF (Trefoil Factor Family) is a novel tumor suppressor and can be the therapeutic target for pancreatic cancer
Conclusion: TFF1 and TFF2 act as tumor suppressor in pancreatic carcinogenesis in a different manner, and they can be a novel therapeutic target for PDAC.Citation Format: Junpei Yamaguchi, Yukihiro Yokoyama, Toshio Kokuryo, Masato Nagino.{Authors}. TFF (Trefoil Factor Family) is a novel tumor suppressor and can be the therapeutic target for pancreatic cancer. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Advances in Science and Clinical Care; 2016 May 12-15; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2016;76(24 Suppl):Abstract nr A67.
Source: Cancer Research - December 13, 2016 Category: Cancer & Oncology Authors: Junpei Yamaguchi, Yukihiro Yokoyama, Toshio Kokuryo, Masato Nagino Tags: Early Detection Source Type: research
Abstract PR01: Role of mitochondrial folate transporter in metabolism of tumor cells
The objective of the present study is to identify modulators of cellular metabolism among transportome genes which could potentially be exploited as targets in pancreatic ductal adenocarcinoma (PDAC). Indeed cancer cells have the ability to adapt in order to survive stressful environment where oxygen and nutrients are limited due to the poor vasculature and outgrowth of stromal component. Thus, disrupting mechanisms of metabolic adaptation could inhibit tumor proliferation or sensitize tumor cells to treatment. Ion channels and transporters provide the link between cancer cells, stroma and matrix. Additionally these protei...
Source: Molecular Cancer Research - January 15, 2016 Category: Cancer & Oncology Authors: Kovalenko, I., Schockel, L., Glasauer, A., Haegebarth, A., Christian, S. Tags: Therapeutic Targets From Cancer: Oral Presentations - Proffered Abstracts Source Type: research
Abstract C156: GPCRs as potential therapeutic targets in pancreatic cancer-associated fibroblasts
Pancreatic ductal adenocarcinoma (PDAC) is characterized by a dense fibrotic stromal matrix, composed of activated fibroblasts (PFs)/stellate cells (PSCs), immune/inflammatory cells and other cell types. This unique tumor microenvironment is increasingly recognized as a key mediator of PDAC progression and drug resistance. Targeting the tumor stroma may thus be a therapeutic approach for PDAC. Pancreatic cancer-associated fibroblasts (CAFs), myofibroblast-like cells that produce extracellular matrix proteins, are responsible for the desmoplasia in PDAC. PSCs and PFs are the key progenitors of CAFs. Blocking the activity of...
Source: Molecular Cancer Therapeutics - January 7, 2016 Category: Cancer & Oncology Authors: Zhou, S., Chang, S., McCann, T., French, R., Lowy, A. M., Insel, P. A. Tags: Target Identification and Validation: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A2-18: The challenges of using large-scale genomics data to identify novel drivers of lung cancer
Lung cancer is one of the major causes of cancer deaths worldwide and only 30% of patients survive the disease for at least one year after diagnosis. Patients are often too frail to receive systemic chemotherapy and there is an urgent need for less toxic, efficacious, targeted therapies. Despite recent efforts with large-scale genomics data we still lack knowledge about driver mutations for the majority of lung cancers.Increasingly, cancer researchers are using online cancer genomic databases to identify novel targets to investigate. A comparison of two prominent databases from different institutes (CCLE and COSMIC) reveal...
Source: Cancer Research - November 15, 2015 Category: Cancer & Oncology Authors: Hudson, A. M., Yates, T., Wirth, C., Li, Y., Trotter, W., Fawdar, S., Miller, C., Brognard, J. Tags: Genomics and Target Discovery Source Type: research
Abstract A30: A genome-wide siRNA screen in mammalian cells for regulators of S6 phosphorylation
To identify the cellular components that participate in the regulation of mTOR complex 1 (mTORC1), the amino acid-dependent, rapamycin-inhibitable complex, we carried out a genome-wide RNAi depletion screen. We employed a rabbit monoclonal antibody specific for RPS6 [Ser235P/Ser236P] and high content microscopy to quantify rpS6 phosphorylation in the pancreatic ductal adenocarcinoma cancer cell line (PDAC) MiaPaCa-2. Applying a stringent selection, we retrieved over 600 genes wherein at least two RNAi gave significant reduction in S6 phosphorylation. This cohort is significantly enriched in genes whose depletion affects th...
Source: Molecular Cancer Therapeutics - July 6, 2015 Category: Cancer & Oncology Authors: Papageorgiou, A., Tamayo, P., Mesirov, J., Avruch, J., Rapley, J. Tags: PI3K-mTOR Activation in Human Cancer: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A112: Eradication of cancer stem-like cells in PDAC
Conclusion: These data indicate that p21 maintains chemotherapy induced CSLCs quiescence and drug resistance such that targeting p21 in combination with cytotoxic therapies is beneficial in eradicating both basal and Gem transformed CSLCs.Note: This abstract was not presented at the conference.Citation Format: Thiruvengadam Arumugam, Vijaya Ramachandran, Craig Logsdon. Eradication of cancer stem-like cells in PDAC. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2015;75(13 Suppl):Abstract nr A112.
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Arumugam, T., Ramachandran, V., Logsdon, C. Tags: New Therapies Source Type: research
Abstract B114: c-Rel is a critical mediator of NF-{kappa}B dependent TRAIL resistance of pancreatic cancer cells
In conclusion, we were able to delineate a novel c-Rel, NFATc2 and COX-2 dependent anti-apoptotic signalling pathway in PDAC with broad clinical implications for pharmaceutical intervention strategies.Citation Format: Claudia Geismann, Frauke Grohmann, Robert Häsler, Philip Rosenstiel, Günter Schneider, Sebastian Zeissig, Stefan Schreiber, Heiner Schäfer, Alexander Arlt. c-Rel is a critical mediator of NF-κB dependent TRAIL resistance of pancreatic cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer: Innovations in Research and Treatment; May 18-21, 2014; New Orleans, LA. Phila...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Geismann, C., Grohmann, F., Hasler, R., Rosenstiel, P., Schneider, G., Zeissig, S., Schreiber, S., Schafer, H., Arlt, A. Tags: Other Topics Source Type: research
Abstract A13: Mechanisms of E47 induced quiescence and acinar cell differentiation in human pancreatic cancer cells
Pancreatic ductal adenocarcinoma (PDA) initiates from quiescent acinar cells that attain a Kras mutation, undergo acinar-ductal metaplasia and rapidly acquire increased growth potential. During this process several transcription factors from the basic helix-loop-helix (bHLH) family are downregulated while expression of their inhibitor Id3 is induced. Previously we showed that Id3 knockdown with siRNA resulted in growth arrest in PDA cells. Here we queried whether aggressive PDA cells can be reprogrammed to revert to their original quiescent acinar cell phenotype by shifting bHLH transcription programs. In order to mitigate...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Kim, S., Yang, C., Riha, C., Lamy, R., Jakubison, B. L., Konieczny, S. F., Itkin-Ansari, P. Tags: Development Source Type: research
Abstract A39: The activation of {beta}1-integrin by type i collagen coupling with the Hedgehog pathway promotes the epithelial-mesenchymal transition in pancreatic cancer cells
In this study, we demonstrated that pancreatic cancer cells exhibited increased proliferation and decreased apoptosis in response to type I collagen. In addition, exposed to type I collagen, PDAC cells lost the expression of E-cadherin and increased expression of mesenchymal markers, including N-cadherin and vimentin, which was correlated with enhanced cell migration and invasiveness. Conversely, the knockdown of β1-integrin abolished the effects induced by type I collagen. Further investigation revealed that type I collagen activates β1-integrin accompanied with significant up-regulation of Gli-1. siRNA specific to Gli-...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Duan, W., Ma, Q., Ma, J., Xu, Q., Lei, J., Wu, E. Tags: Development Source Type: research
Abstract A71: Post-transcriptional regulation of the proto-oncogene PIM1 by the mRNA stability factor HuR: implications for pancreatic cancer therapeutic response and cell survival
Pancreatic ductal adenocarcinoma (PDA) is an aggressive malignancy characterized by its insidious development and resistance to conventional and targeted therapies. As a result of selective pressures imposed by cytotoxic agents and the tumor microenvironment, PDA cells orchestrate a potent and elusive chemoresistant mechanism. Recently, the serine-threonine kinase PIM1 has emerged as a key regulator of PDA cell survival under cancer-associated stress (e.g: cytotoxic DNA-damaging agents, hypoxia). However, the molecular mechanism behind PIM1 overexpression in PDAs is unknown. Here, we demonstrate that cis-acting AU-rich ele...
Source: Cancer Research - June 30, 2015 Category: Cancer & Oncology Authors: Blanco, F. F., Meisner-Kober, N., Londin, E., Rigoutsos, I., Winter, J., Yeo, C., Brody, J. Tags: Heterogeneity in Tumor Progression Source Type: research
Abstract B47: Therapeutic KRAS silencing in lung and colon cancer models
This study highlights the potential translational impact of therapeutic RNA interference, which may have broad applications in oncology, especially for traditional "undruggable" targets.Citation Format: Chad Pecot, Sherry Wu, Seth Bellister, Rajat Bhattacharya, Anshumaan Maharaj, Cristian Rodriguez-Aguayo, Vianey Gonzalez-Villasana, Rajesha Rupaimoole, Gabriel Lopez-Berestein, Lee M. Ellis, Anil Sood. Therapeutic KRAS silencing in lung and colon cancer models. [abstract]. In: Proceedings of the AACR Special Conference on RAS Oncogenes: From Biology to Therapy; Feb 24-27, 2014; Lake Buena Vista, FL. Philadelphia (PA): AACR;...
Source: Molecular Cancer Research - February 5, 2015 Category: Cancer & Oncology Authors: Pecot, C., Wu, S., Bellister, S., Bhattacharya, R., Maharaj, A., Rodriguez-Aguayo, C., Gonzalez-Villasana, V., Rupaimoole, R., Lopez-Berestein, G., Ellis, L. M., Sood, A. Tags: RAS Targeting: Poster Presentations - Proffered Abstracts Source Type: research
Abstract A55: KRAS gene amplification is a distinct molecular subgroup of gastroesophageal adenocarcinoma that may benefit from combined RAS/RAF/MEK/ERK and PI3K/PTEN/AKT/mTOR pathway inhibition
Conclusions: In this series, we observed KRAS wild type gene amp+ to be present in a subset (16%) of GEC patients at diagnosis, correlating with very high protein expression. KRAS amp+ was present after treatment with trastuzumab in HER2+ patients, and also after anti-MET therapy. These data suggest that KRAS amp+ represents a molecular subset with advanced disease at diagnosis. The observation of acquired KRAS amp+ after targeted therapies may be a resistance mechanism to anti-HER and anti-MET inhibitors. Inhibition using combined MEK/AKT pathway inhibitors, and proof-of-principle siRNA, warrants further investigation for...
Source: Molecular Cancer Research - February 5, 2015 Category: Cancer & Oncology Authors: Henderson, L., Xu, P., Rambo, B., Liao, W.-L., Hembrough, T., Catenacci, D. Tags: Role of WT RAS and RAS Isoforms: Poster Presentations - Proffered Abstracts Source Type: research
