The DOI matches its Crossref record; 51 of the 52 references it cites were found in a registry or an index.
KRAS as a druggable target in NSCLC: Rising like a phoenix after decades of development failures
Abstract
Cancers of nearly all lineages harbor alterations that deregulate mitogen-activated protein kinase signaling, a crucial signaling pathway for tumor formation and maintenance. Of these, KRAS mutations are the most frequent gain-of-function alterations found in patients with cancer. In particular they represents the most common molecular alteration detected in non-small cell lung cancer (NSCLC) accounting for up to 25% of all oncogenic mutations. They were identified decades ago and prior efforts to target these proteins have been unsuccessful. KRAS mutation profiles (i.e. frequency of specific codon substitutions) in smokers and never-smokers are distinct and not all KRAS alterations are driver mutations. KRAS has evolved from a mutation with possible predictive value to a therapeutic target with great promise. Here, we will discuss the biology of KRAS in lung cancer and its clinical implications in oncology today and in the foreseeable future.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“G12C and G12V mutations are shown to preferentially activate RAL signaling and G12D-mutant cell lines are shown to have high levels of phosphorylated AKT, suggesting preferential activation of PI3K-AKT-mTOR pathway [46, 47].”
From Drugging KRAS: Current perspectives and state-of-art review (2022) · cites this paper as [47]
Citations
Cites
Bray, F., Ferlay, J., Soerjomataram, I., Siegel, R. L., Torre, L. A., & Jemal, A. (2018) · CA: A Cancer Journal for Clinicians · doi:10.3322/caac.21492 · Cited by 84,109
UCSF Chimera—A visualization system for exploratory research and analysis
Pettersen, E. F., Goddard, T. D., Huang, C. C., Couch, G. S., Greenblatt, D. M., Meng, E. C., & Ferrin, T. E. (2004) · Journal of Computational Chemistry · doi:10.1002/jcc.20084 · Cited by 45,882
PD-1 and PD-L1 Immune Checkpoint Blockade to Treat Breast Cancer
Hartkopf, A. D., Taran, F., Wallwiener, M., Walter, C. B., Krämer, B., Grischke, E., & Brucker, S. Y. (2016) · Breast Care · doi:10.1159/000453569 · Cited by 30,989
Adverse Renal Effects of Immune Checkpoint Inhibitors: A Narrative Review
Wanchoo, R., Karam, S., Uppal, N. N., Barta, V. S., Deray, G., Devoe, C., Launay‐Vacher, V., Jhaveri, K. D., & on behalf of Cancer and Kidney International Network Workgroup on Immune Checkpoint Inhibitors (2017) · American Journal of Nephrology · doi:10.1159/000455014 · Cited by 15,318
Calcium's Role in Mechanotransduction during Muscle Development
Damm, T. B., & Egli, M. (2014) · Cellular Physiology and Biochemistry · doi:10.1159/000356667 · Cited by 14,552
Nivolumab versus docetaxel in advanced nonsquamous non-small-cell lung cancer
Borghaei, H., Paz-Ares, L., Horn, L., Spigel, D. R., Steins, M., Ready, N. E., Chow, L. Q., Vokes, E. E., Felip, E., Holgado, E., et al. (2015) · New England Journal of Medicine · doi:10.1056/nejmoa1507643 · Cited by 9,335
Mutational landscape determines sensitivity to PD-1 blockade in non–small cell lung cancer
Rizvi, N. A., Hellmann, M. D., Snyder, A., Kvistborg, P., Makarov, V., Havel, J. J., Lee, W., Yuan, J., Wong, P., Ho, T. S., et al. (2015) · Science · doi:10.1126/science.aaa1348 · Cited by 7,802
Oncology meets immunology: the cancer-immunity cycle.
Chen, D. S., & Mellman, I. (2013) · Immunity · doi:10.1016/j.immuni.2013.07.012 · Cited by 6,929
Seger, R., & Krebs, E. G. (1995) · The FASEB Journal · doi:10.1096/fasebj.9.9.7601337 · Cited by 3,631
K-Ras(G12C) inhibitors allosterically control GTP affinity and effector interactions
Ostrem, J. M., Peters, U., Sos, M. L., Wells, J. A., & Shokat, K. M. (2013) · Nature · doi:10.1038/nature12796 · Cited by 2,557
Flagged first, then by citations
1 of the 52 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Renaud, 2018, KRAS-specific amino acid substitutions are associated with different responses to chemotherapy in advanced non–small-cell lung cancer, Clin Lung Cancer, 19, e919, 10.1016/j.cllc.2018.08.005 · DOI
Cited by
Sorted by citations
Oncogenic driver mutations in non-small cell lung cancer: Past, present and future
Chevallier, M., Borgeaud, M., Addeo, A., & Friedlaender, A. (2021) · World Journal of Clinical Oncology · doi:10.5306/wjco.v12.i4.217 · Cited by 332
Self-citationRodak, O., Peris‐Díaz, M. D., Olbromski, M., Podhorska‐Okołów, M., & Dzięgiel, P. (2021) · Cancers · doi:10.3390/cancers13184705 · Cited by 246
Drugging KRAS: Current perspectives and state-of-art review
Parikh, K., Banna, G., Liu, S. V., Friedlaender, A., Desai, A., Subbiah, V., & Addeo, A. (2022) · Journal of Hematology & Oncology · doi:10.1186/s13045-022-01375-4 · Cited by 164
Self-citationOncogenic alterations in advanced NSCLC: a molecular super-highway
Friedlaender, A., Pérol, M., Banna, G. L., Parikh, K., & Addeo, A. (2024) · Biomarker Research · doi:10.1186/s40364-024-00566-0 · Cited by 150
Self-citationHuang, M.-Y., Jiang, X.-M., Wang, B.-L., Sun, Y., & Lu, J.-J. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2020.107694 · Cited by 136
Metadata
- Authors
- Friedlaender, A., Drilon, A., Weiss, G. J., Banna, G. L., & Addeo, A.
- Affiliations
- University Hospital of Geneva (CH)
- Memorial Sloan Kettering Cancer Center (US)
- United Lincolnshire Hospitals NHS Trust (GB)
- Corresponding author
- Addeo, Alfredo
- Venue
- Cancer Treatment Reviews
- Publisher
- Elsevier BV
- Published
- 2020-04
- Volume
- 85
- Pages
- 101978
- ISSN
- 0305-7372 (ISSN-L)
- OpenAlex
- W3004931546
- Cited by
- 118
- References
- 52
- Citations by year
- 2026: 6 · 2025: 10 · 2024: 17 · 2023: 20 · 2022: 24 · 2021: 22 · 2020: 19
- FWCI
- 2.99
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Treatment Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (P30CA008748)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer Genomics and Diagnostics
- Keywords
- KRAS mutation, non-small cell lung cancer, druggable targets, MAPK signaling, gain-of-function mutations, smoking status, driver mutations, KRAS inhibitors, cancer therapeutics
- MeSH terms
- Antineoplastic Agents, Carcinoma, Non-Small-Cell Lung, Female, Forecasting, Humans, Immunotherapy, Lung Neoplasms, Male, Mutation, Gene Expression Regulation, Neoplastic, Survival Analysis, Proto-Oncogene Proteins p21(ras), Treatment Outcome, Molecular Targeted Therapy
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 ›
Are you an author, or do you see a problem with this page? Request a review
