ArticleOncogene2016
Kras(G12D) induces EGFR-MYC cross signaling in murine primary pancreatic ductal epithelial cells.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 45 citations in OpenAlex.
- Ras-dependent activation of BMAL2 regulates hypoxic metabolism in pancreatic cancer.bioRxiv : the preprint server for biology · 2025Article
- Vitamin K-dependent gamma-carboxyglutamic acid protein 1 promotes pancreatic ductal adenocarcinoma progression through stabilizing oncoprotein KRAS and tyrosine kinase receptor EGFR.Clinical and translational medicine · 2025Article
- Target c-Myc to treat pancreatic cancer.Cancer biology & therapy · 2022Article
- Antibody-mediated blockade for galectin-3 binding protein in tumor secretome abrogates PDAC metastasis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The genetic landscape of pancreatic head ductal adenocarcinoma in China and prognosis stratification.BMC cancer · 2022Article
- CUX1 Enhances Pancreatic Cancer Formation by Synergizing with KRAS and Inducing MEK/ERK-Dependent Proliferation.Cancers · 2021Article
- Mutant Kras co-opts a proto-oncogenic enhancer network in inflammation-induced metaplastic progenitor cells to initiate pancreatic cancer.Nature cancer · 2021Article
- Analysis of the EGFR Amplification and CDKN2A Deletion Regulated Transcriptomic Signatures Reveals the Prognostic Significance ofFrontiers in oncology · 2021Article
- Targeting the ubiquitin-proteasome system in a pancreatic cancer subtype with hyperactive MYC.Molecular oncology · 2020Article
- Loss of Wasl improves pancreatic cancer outcome.JCI insight · 2020Article
- Differential impact of the ERBB receptors EGFR and ERBB2 on the initiation of precursor lesions of pancreatic ductal adenocarcinoma.Scientific reports · 2020Article
- MicroRNAs Targeting MYC Expression: Trace of Hope for Pancreatic Cancer Therapy. A Systematic Review.Cancer management and research · 2020Review
- Is there a CDKN2A-centric networkOncoTargets and therapy · 2020Review
- Pancreatic ductal adenocarcinoma: biological hallmarks, current status, and future perspectives of combined modality treatment approaches.Radiation oncology (London, England) · 2019Review
- ADAM9 contributes to vascular invasion in pancreatic ductal adenocarcinoma.Molecular oncology · 2019Article
- KRAS mutations in the parental tumour accelerate in vitro growth of tumoroids established from colorectal adenocarcinoma.International journal of experimental pathology · 2019Article
- Arsenite malignantly transforms human prostate epithelial cells in vitro by gene amplification of mutated KRAS.PloS one · 2019Article
- Oncogenic KRAS and the EGFR loop in pancreatic carcinogenesis-A connection to licensing nodes.Small GTPases · 2018Review
- MTOR inhibitor-based combination therapies for pancreatic cancer.British journal of cancer · 2018Article
- Report and Application of a Tool Compound Data Set.Journal of chemical information and modeling · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Epidermal growth factor receptor (EGFR) signaling has a critical role in oncogenic Kras-driven pancreatic carcinogenesis. However, the downstream targets of this signaling network are largely unknown. We developed a novel model system utilizing murine primary pancreatic ductal epithelial cells (PDECs), genetically engineered to allow time-specific expression of oncogenic Kras(G12D) from the endogenous promoter. We show that primary PDECs are susceptible to Kras(G12D)-driven transformation and form pancreatic ductal adenocarcinomas in vivo after Cdkn2a inactivation. In addition, we demonstrate that activation of Kras(G12D) induces an EGFR signaling loop to drive proliferation. Interestingly, pharmacological inhibition of EGFR fails to decrease Kras(G12D)-activated ERK or PI3K signaling. Instead our data provide novel evidence that EGFR signaling is needed to activate the oncogenic and pro-proliferative transcription factor c-MYC. EGFR and c-MYC have been shown to be essential for pancreatic carcinogenesis. Importantly, our data link both pathways and thereby explain the crucial role of EGFR for Kras(G12D)-driven carcinogenesis in the pancreas.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.