The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Afatinib restrains K-RAS–driven lung tumorigenesis
Open accessAbstract
K-RAS –mutated lung adenocarcinomas depend on ERBB signaling, and pan-ERBB inhibitors impair K-RAS–driven lung tumorigenesis.
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In the citing paper
“In NSCLCs and CRCs, KRASG12C inhibition leads to an accumulation of activated upstream EGFR and/or other ERBB family members, which facilitates escape from KRASG12C-inhibitor monotherapy110,121–124.”
From The current state of the art and future trends in RAS-targeted cancer therapies (2022) · cites this paper as [124]
In the citing paper
“afatinib blocked compensatory ERBB2 and ERBB3 activation, whereas erlotinib and gefitinib did not.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“Genetic mouse models revealed that EGFR deletion attenuates mutant KRAS activity and transiently reduces tumor growth.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“Notably, both studies revealed a requirement for simultaneous inhibition of multiple ERBB while targeting a single member of the family was not effective.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“EGFR inhibition initiated a rapid resistance mechanism involving non-EGFR ERBB family members, which triggered a tumor escape mechanism.”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“recent studies have challenged this paradigm, which instead demonstrated that the activation of ERBB signaling was required for KRASG12D-driven lung tumorigenesis in preclinical mice models and that pan-ERBB inhibition other than EGFR inhibition alone was strikingly effective to inhibit KRAS-mutant tumor growth and progression (61, 62).”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“an independent study by Moll et al. demonstrated a requirement for ERBB signaling to support the progression of KRASG12D-driven lung cancer (62).”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
In the citing paper
“targeting of MEK alone is frequently hampered by adaptive resistance, which is complex and context-dependent, and can involve activation of various RTKs, including ERBB family, AXL, PDGFR-α, or FGFR1 (26, 53, 59–62).”
From New Horizons in KRAS-Mutant Lung Cancer: Dawn After Darkness (2019) · cites this paper as [62]
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Cites
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Self-citation
Metadata
- Authors
- Moll, H. P., Pranz, K., Musteanu, M., Grabner, B., Hruschka, N., Mohrherr, J., Aigner, P., Stiedl, P., Brcic, L., Laszlo, V., Schramek, D., Moriggl, R., Eferl, R., Moldvay, J., Dezso, K., Lopez-Casas, P. P., Stoiber, D., Hidalgo, M., Penninger, J., Sibilia, M., Győrffy, B., Barbacid, M., Dome, B., Popper, H., & Casanova, E.
- Affiliations
- Comprehensive Cancer Center Vienna (AT)
- Ludwig Boltzmann Institute for Cancer Research (AT)
- Spanish National Cancer Research Centre, E-28029 Madrid, Spain.
- Institute of Pathology, Medical University of Graz, AT-8036 Graz, Austria.
- Division of Thoracic Surgery, Department of Surgery and CCC, Medical University of Vienna, AT-1090 Vienna, Austria.
- Institute of Molecular Biotechnology (AT)
- University of Veterinary Medicine Vienna (AT)
- Semmelweis University (HU)
- First Department of Pathology and Experimental Cancer Research, Semmelweis University, HU-1122 Budapest, Hungary.
- Spanish National Cancer Research Centre (ES)
- Medical University of Graz (AT)
- Corresponding author
- Casanova, Emilio
- ORCID
- Venue
- Science Translational Medicine
- Published
- 2018-06-20
- Volume
- 10
- Issue
- 446
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- PMC
- PMC7610658
- OpenAlex
- W2808999647
- Cited by
- 125
- References
- 51
- Citations by year
- 2026: 4 · 2025: 8 · 2024: 8 · 2023: 11 · 2022: 18 · 2021: 21 · 2020: 22 · 2019: 23 · 2018: 9
- FWCI
- 14.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- Repository of the Academy's Library (Library of the Hungarian Academy of Sciences) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Semmelweis University Repository (Semmelweis University) (submittedVersion)
- Funders
- Austrian Science Fund (FWF-P25599-B19, SFB-F4707, SFB-F06105)
- Fellinger Krebsforschungsverein
- National Research, Development and Innovation Office, Hungary (NVKP_16-1-2016-0037)
- Hungarian NRDI Office (K109626, K108465, KNN121510, SNN114490)
- Hungarian Academy of Science
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Lung Cancer Treatments and Mutations
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Health Sciences › Medicine › Oncology › HER2/EGFR in Cancer Research
- Keywords
- afatinib, KRAS mutation, lung adenocarcinoma, lung carcinogenesis, ErbB signaling, pan-ErbB inhibitor, EGFR, HER2, HER3, ErbB4, tyrosine kinase inhibitors
- MeSH terms
- Erlotinib Hydrochloride, Gefitinib, Adenocarcinoma of Lung, Afatinib, Humans, Lung Neoplasms, Mutation, Signal Transduction, Proto-Oncogene Proteins p21(ras), Drug Resistance, Neoplasm, Cell Line, Tumor, Cell Proliferation, Carcinogenesis, ErbB Receptors
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