KrasG12D induces EGFR-MYC cross signaling in murine primary pancreatic ductal epithelial cells
Published 2015 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
KrasG12D induces EGFR-MYC cross signaling in murine primary pancreatic ductal epithelial cells
Authors
Keywords
-
Journal
ONCOGENE
Volume 35, Issue 29, Pages 3880-3886
Publisher
Springer Nature
Online
2015-11-23
DOI
10.1038/onc.2015.437
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Organoid Models of Human and Mouse Ductal Pancreatic Cancer
- (2015) Sylvia F. Boj et al. CELL
- Plasticity and Dedifferentiation within the Pancreas: Development, Homeostasis, and Disease
- (2015) Sapna Puri et al. Cell Stem Cell
- Lineage fate of ductular reactions in liver injury and carcinogenesis
- (2015) Simone Jörs et al. JOURNAL OF CLINICAL INVESTIGATION
- Detection of Tumor Suppressor Genes in Cancer Development by a Novel shRNA-Based Method
- (2015) J. von Burstin et al. MOLECULAR CANCER RESEARCH
- Combined inhibition of BET family proteins and histone deacetylases as a potential epigenetics-based therapy for pancreatic ductal adenocarcinoma
- (2015) Pawel K Mazur et al. NATURE MEDICINE
- Disclosure of Erlotinib as a Multikinase Inhibitor in Pancreatic Ductal Adenocarcinoma
- (2015) Laura Conradt et al. NEOPLASIA
- Oncogenic KRAS signalling in pancreatic cancer
- (2014) S Eser et al. BRITISH JOURNAL OF CANCER
- Loss of Fbw7 Reprograms Adult Pancreatic Ductal Cells into α, δ, and β Cells
- (2014) Rocio Sancho et al. Cell Stem Cell
- A modular and flexible ESC-based mouse model of pancreatic cancer
- (2014) M. Saborowski et al. GENES & DEVELOPMENT
- Activation and repression by oncogenic MYC shape tumour-specific gene expression profiles
- (2014) Susanne Walz et al. NATURE
- A next-generation dual-recombinase system for time- and host-specific targeting of pancreatic cancer
- (2014) Nina Schönhuber et al. NATURE MEDICINE
- MYC and EGR1 synergize to trigger tumor cell death by controlling NOXA and BIM transcription upon treatment with the proteasome inhibitor bortezomib
- (2014) Matthias Wirth et al. NUCLEIC ACIDS RESEARCH
- Analysis of the tumor-initiating and metastatic capacity of PDX1-positive cells from the adult pancreas
- (2014) Irene Ischenko et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Downstream of Mutant KRAS, the Transcription Regulator YAP Is Essential for Neoplastic Progression to Pancreatic Ductal Adenocarcinoma
- (2014) W. Zhang et al. Science Signaling
- The EGFR Family: Not So Prototypical Receptor Tyrosine Kinases
- (2014) M. A. Lemmon et al. Cold Spring Harbor Perspectives in Biology
- Dormant Cancer Cells Contribute to Residual Disease in a Model of Reversible Pancreatic Cancer
- (2013) W.-c. Lin et al. CANCER RESEARCH
- The Prrx1 homeodomain transcription factor plays a central role in pancreatic regeneration and carcinogenesis
- (2013) M. Reichert et al. GENES & DEVELOPMENT
- Inhibition of Myc family proteins eradicates KRas-driven lung cancer in mice
- (2013) L. Soucek et al. GENES & DEVELOPMENT
- Direct reprogramming by oncogenic Ras and Myc
- (2013) I. Ischenko et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Ready, Set, Go: The EGF Receptor at the Pancreatic Cancer Starting Line
- (2012) Rushika M. Perera et al. CANCER CELL
- Identification of Sox9-Dependent Acinar-to-Ductal Reprogramming as the Principal Mechanism for Initiation of Pancreatic Ductal Adenocarcinoma
- (2012) Janel L. Kopp et al. CANCER CELL
- Oncogenic Kras-Induced GM-CSF Production Promotes the Development of Pancreatic Neoplasia
- (2012) Yuliya Pylayeva-Gupta et al. CANCER CELL
- EGF Receptor Signaling Is Essential for K-Ras Oncogene-Driven Pancreatic Ductal Adenocarcinoma
- (2012) Carolina Navas et al. CANCER CELL
- EGF Receptor Is Required for KRAS-Induced Pancreatic Tumorigenesis
- (2012) Christine M. Ardito et al. CANCER CELL
- KRASG12D- and BRAFV600E-Induced Transformation of Murine Pancreatic Epithelial Cells Requires MEK/ERK-Stimulated IGF1R Signaling
- (2012) V. A. Appleman et al. MOLECULAR CANCER RESEARCH
- p53-dependent regulation of growth, epithelial-mesenchymal transition and stemness in normal pancreatic epithelial cells
- (2011) Andreia V. Pinho et al. CELL CYCLE
- Reviewing once more the c-myc and Ras collaboration
- (2011) Chenguang Wang et al. CELL CYCLE
- Acinar-to-ductal metaplasia accompanies c-myc-induced exocrine pancreatic cancer progression in transgenic rodents
- (2011) Paul J. Grippo et al. INTERNATIONAL JOURNAL OF CANCER
- Pancreatic ductal cells in development, regeneration, and neoplasia
- (2011) Maximilian Reichert et al. JOURNAL OF CLINICAL INVESTIGATION
- Oncogenic KRas Suppresses Inflammation-Associated Senescence of Pancreatic Ductal Cells
- (2010) Kyoung Eun Lee et al. CANCER CELL
- Adult pancreatic acinar cells dedifferentiate to an embryonic progenitor phenotype with concomitant activation of a senescence programme that is present in chronic pancreatitis
- (2010) A. V. Pinho et al. GUT
- Pancreatic Exocrine Duct Cells Give Rise to Insulin-Producing β Cells during Embryogenesis but Not after Birth
- (2009) Myriam Solar et al. DEVELOPMENTAL CELL
- PI3K signaling maintains c-myc expression to regulate transcription of E2F1 in pancreatic cancer cells
- (2009) Carolin Schild et al. MOLECULAR CARCINOGENESIS
- A robust and high-throughput Cre reporting and characterization system for the whole mouse brain
- (2009) Linda Madisen et al. NATURE NEUROSCIENCE
- Conditional inactivation of Myc impairs development of the exocrine pancreas
- (2008) H. Nakhai et al. DEVELOPMENT
- Pancreatic Inactivation of c-Myc Decreases Acinar Mass and Transdifferentiates Acinar Cells Into Adipocytes in Mice
- (2008) Claire Bonal et al. GASTROENTEROLOGY
- Modelling Myc inhibition as a cancer therapy
- (2008) Laura Soucek et al. NATURE
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExploreAsk a Question. Answer a Question.
Quickly pose questions to the entire community. Debate answers and get clarity on the most important issues facing researchers.
Get Started