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 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
Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
A new mathematical model for relative quantification in real-time RT-PCR
Pfaffl, M. W. (2001) · Nucleic Acids Research · doi:10.1093/nar/29.9.e45 · Cited by 34,610
Siegel, R. L., Miller, K. D., & Jemal, A. (2016) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21332 · Cited by 16,003
Genome engineering using the CRISPR-Cas9 system
Ran, F. A., Hsu, P. D., Wright, J., Agarwala, V., Scott, D. A., & Zhang, F. (2013) · Nature Protocols · doi:10.1038/nprot.2013.143 · Cited by 11,133
Mootha, V. K., Lindgren, C. M., Eriksson, K.-F., Subramanian, A., Sihag, S., Lehar, J., Puigserver, P., Carlsson, E., Ridderstråle, M., Laurila, E., et al. (2003) · Nature Genetics · doi:10.1038/ng1180 · Cited by 10,197
Comprehensive molecular profiling of lung adenocarcinoma
The Cancer Genome Atlas Research Network (2014) · Nature · doi:10.1038/nature13385 · Cited by 5,732
Pfaffl, M. W., Tichopad, A., Prgomet, C., & Neuvians, T. P. (2004) · Biotechnology Letters · doi:10.1023/b:bile.0000019559.84305.47 · Cited by 5,065
Pao, W., Miller, V., Zakowski, M., Doherty, J., Politi, K., Sarkaria, I., Singh, B., Heelan, R., Rusch, V., Fulton, L., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0405220101 · Cited by 4,338
EGFR Mutation and Resistance of Non–Small-Cell Lung Cancer to Gefitinib
Kobayashi, S., Boggon, T. J., Dayaram, T., Jänne, P. A., Kocher, O., Meyerson, M., Johnson, B. E., Eck, M. J., Tenen, D. G., & Halmos, B. (2005) · New England Journal of Medicine · doi:10.1056/nejmoa044238 · Cited by 3,964
Pao, W., Miller, V. A., Politi, K. A., Riely, G. J., Somwar, R., Zakowski, M. F., Kris, M. G., & Varmus, H. (2005) · PLoS Medicine · doi:10.1371/journal.pmed.0020073 · Cited by 3,527
Cited by
Sorted by citations
RAS-targeted therapies: is the undruggable drugged?
Moore, A. R., Rosenberg, S. C., McCormick, F., & Malek, S. (2020) · Nature Reviews Drug Discovery · doi:10.1038/s41573-020-0068-6 · Cited by 1,103
Choi, J., Park, J.-E., Tsagkogeorga, G., Yanagita, M., Koo, B., Han, N., & Lee, J. (2020) · Cell stem cell · doi:10.1016/j.stem.2020.06.020 · Cited by 580
The current state of the art and future trends in RAS-targeted cancer therapies
Punekar, S. R., Velcheti, V., Neel, B. G., & Wong, K.-K. (2022) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-022-00671-9 · Cited by 549
Vertical Pathway Inhibition Overcomes Adaptive Feedback Resistance to KRASG12C Inhibition
Ryan, M. B., Fece de la Cruz, F., Phat, S., Myers, D. T., Wong, E., Shahzade, H. A., Hong, C. B., & Corcoran, R. B. (2020) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-19-3523 · Cited by 496
“Previous studies have suggested that key RTKs may play dominant roles in driving adaptive feedback to inhibitors of the MAPK pathway, including EGFR in response to BRAF inhibition in BRAF colorectal cancer and EGFR/HER family kinases or FGFR in response to MEK inhibitors in KRAS-mutant lung cancers (13, 14, 21, 24).”
BackgroundHofmann, M. H., Gmachl, M., Ramharter, J., Savarese, F., Gerlach, D., Marszalek, J. R., Sanderson, M. P., Kessler, D., Trapani, F., Arnhof, H., et al. (2021) · Cancer Discovery · doi:10.1158/2159-8290.cd-20-0142 · Cited by 444
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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