ArticleCancer cell2012
EGF receptor signaling is essential for k-ras oncogene-driven pancreatic ductal adenocarcinoma.
Article in Cancer cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 237 papers, 1 of them a synthesis that pooled it.
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
237 citing papers in PubMed, 1 synthesis or guideline pooled it, 389 citations in OpenAlex.
- ANO1: More Than Just Calcium-Activated Chloride Channel in Cancer.Frontiers in oncology · 2022Pooled it
- Nimotuzumab combined with gemcitabine and nab-paclitaxel as first-line therapy for advanced pancreatic cancer: a single-arm, single-center Phase II prospective study.Frontiers in medicine · 2026Trial
- A Multicenter, Open-Label Phase II Clinical Trial of Combined MEK plus EGFR Inhibition for Chemotherapy-Refractory Advanced Pancreatic Adenocarcinoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2016Trial
- Molecular dynamics driving phenotypic divergence among KRAS mutants in pancreatic tumorigenesis.Developmental cell · 2026Article
- Absence of EGFR signalling in granulocytic cells relieves immunosuppression sensitising CRC metastases to immune checkpoint therapy.Cell death and differentiation · 2026Article
- Acinar-ductal metaplasia in pancreatitis and pancreatic ductal adenocarcinoma.Cellular oncology (Dordrecht, Netherlands) · 2026Review
- TBC1D23 drives lymphatic metastasis in pancreatic ductal adenocarcinoma by altering EGFR cell surface dynamics and signaling.Cellular oncology (Dordrecht, Netherlands) · 2026Article
- Article
- Oncogenic KRAS/ERK/JUNB signaling suppresses differentiation regulator GATA6 in pancreatic cancer.The Journal of clinical investigation · 2026Article
- Wilms Tumor 1-Expressing Stromal Cells Promote Pancreatic Cancer Progression.Cancer research · 2026Article
- Pancreatic cancer: molecular pathogenesis and emerging therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- SP1-Mediated Glycolytic Reprogramming Promotes Tumorigenesis and Progression in Pancreatic Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Hippo signaling pathway modulates pancreatic tissue homeostasis.Cell death discovery · 2025Review
- FGFR2 Abrogation Intercepts Pancreatic Ductal Adenocarcinoma Development.Cancer research · 2025Article
- EGFR controls transcriptional and metabolic rewiring in KRASEMBO molecular medicine · 2025Article
- Article
- Tumor-Intrinsic Kinome Landscape of Pancreatic Cancer Reveals New Therapeutic Approaches.Cancer discovery · 2025Article
- The Integrated Stress Response in Pancreatic Development, Tissue Homeostasis, and Cancer.Gastroenterology · 2024Review
- Consensus, debate, and prospective on pancreatic cancer treatments.Journal of hematology & oncology · 2024Review
- Article
177 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Clinical evidence indicates that mutation/activation of EGF receptors (EGFRs) is mutually exclusive with the presence of K-RAS oncogenes in lung and colon tumors. We have validated these observations using genetically engineered mouse models. However, development of pancreatic ductal adenocarcinomas driven by K-Ras oncogenes are totally dependent on EGFR signaling. Similar results were obtained using human pancreatic tumor cell lines. EGFRs were also essential even in the context of pancreatic injury and absence of p16Ink4a/p19Arf. Only loss of p53 made pancreatic tumors independent of EGFR signaling. Additional inhibition of PI3K and STAT3 effectively prevented proliferation of explants derived from these p53-defective pancreatic tumors. These findings may provide the bases for more rational approaches to treat pancreatic tumors in the clinic.
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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.