Complete regression of advanced pancreatic ductal adenocarcinomas upon combined inhibition of EGFR and C-RAF
Open accessAbstract
Five-year survival for pancreatic ductal adenocarcinoma (PDAC) patients remains below 7% due to the lack of effective treatments. Here, we report that combined ablation of EGFR and c-RAF expression results in complete regression of a significant percentage of PDAC tumors driven by Kras/Trp53 mutations in genetically engineered mice. Moreover, systemic elimination of these targets induces toxicities that are well tolerated. Response to this targeted therapy correlates with transcriptional profiles that resemble those observed in human PDACs. Finally, inhibition of EGFR and c-RAF expression effectively blocked tumor progression in nine independent patient-derived xenografts carrying KRAS and TP53 mutations. These results open the door to the development of targeted therapies for PDAC patients.
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Combined inhibition of C-Raf and Egfr induced complete regression of pancreatic ductal adenocarcinomas in Kras/Trp53-driven GEM models and PDXs without apparent toxicity.
“combined inhibition of C-Raf and Egfr induced complete regression of pancreatic ductal adenocarcinomas in Kras/Trp53-driven GEM models and PDXs without apparent toxicity (77).”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [77]
C-Raf, but not B-Raf or A-Raf, may mediate the oncogenic signaling in KRAS-driven cancer.
“Together, these studies provided compelling evidence that C-Raf, but not B-Raf or A-Raf, may mediate the oncogenic signaling in KRAS-driven cancer.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [77]
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- Authors
- Blasco, M. T., Navas, C., Martín-Serrano, G., Graña-Castro, O., Lechuga, C. G., Martín-Díaz, L., Djurec, M., Li, J., Morales-Cacho, L., Esteban-Burgos, L., Perales-Patón, J., Bousquet-Mur, E., Castellano, E., Jacob, H. K. C., Cabras, L., Musteanu, M., Drosten, M., Ortega, S., Mulero, F., Sainz, B., Dusetti, N., Iovanna, J., Sánchez-Bueno, F., Hidalgo, M., Khiabanian, H., Rabadán, R., Al-Shahrour, F., Guerra, C., & Barbacid, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Centre National de la Recherche Scientifique (FR)
- Beth Israel Deaconess Medical Center (US)
- Columbia University Irving Medical Center (US)
- Corresponding author
- Guerra, Carmen
- Barbacid, Mariano
- ORCID
- Venue
- Cancer Cell
- Publisher
- Elsevier BV
- Published
- 2019-04
- Volume
- 35
- Issue
- 4
- Pages
- 573-587.e6
- ISSN
- 1535-6108 (ISSN-L)
- PMC
- PMC10132447
- OpenAlex
- W2937076225
- Cited by
- 115
- References
- 68
- Citations by year
- 2026: 12 · 2025: 8 · 2024: 13 · 2023: 17 · 2022: 12 · 2021: 24 · 2020: 21 · 2019: 8
- FWCI
- 6.78
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cancer Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- LA Referencia (Red Federada de Repositorios Institucionales de Publicaciones Científicas) (submittedVersion, cc-by-nc-sa)
- CEU Repositorio Institucional (Fundación Universitaria San Pablo CEU) (submittedVersion, cc-by-nc-nd)
- Funders
- Ligue Contre le Cancer (ERC-2014-ADG)
- Florida Polytechnic University
- European Research Council (ERC-AG/250297-RAS AHEAD, ERC-AG/695566-THERACAN)
- AXA Research Fund
- Ministerio de Educación, Cultura y Deporte
- Ministerio de Economía y Competitividad (SAF2014-59864-R)
- “la Caixa” Foundation
- National Institutes of Health (U54CA193313, U54CA209997)
- Topics
- Health Sciences › Medicine › Oncology › Pancreatic and Hepatic Oncology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- pancreatic ductal adenocarcinoma, EGFR inhibition, combination targeted therapy, tumor regression, KRAS mutation, Trp53 mutation, genetically engineered mouse models, patient-derived xenografts, gene expression profiling, drug toxicity
- MeSH terms
- Erlotinib Hydrochloride, Gefitinib, Animals, Humans, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Pancreatic Neoplasms, Signal Transduction, Gene Expression Regulation, Neoplastic, Tumor Suppressor Protein p53, Proto-Oncogene Proteins p21(ras), Apoptosis, Proto-Oncogene Proteins c-raf, Carcinoma, Pancreatic Ductal, Xenograft Model Antitumor Assays, Cell Line, Tumor, Tumor Burden, Protein Kinase Inhibitors, Cell Proliferation, Mice, 129 Strain, ErbB Receptors
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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