ReviewFEBS letters2010
Oncogenic mutant forms of EGFR: lessons in signal transduction and targets for cancer therapy.
Review in FEBS letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
97 citing papers in PubMed, 180 citations in OpenAlex.
- Ligand-activated EGFR/MAPK signaling but not PI3K, are key resistance mechanisms to EGFR-therapy in colorectal cancer.Nature communications · 2025Trial
- Resistance to EGFR Inhibitors in NSCLC: Mechanistic Insights and Emerging Therapies.International journal of molecular sciences · 2026Review
- Extracellular and Membrane Protein: Structure, Biological Functions, Diseases, and an Emerging Modality for Drug Discovery.MedComm · 2026Review
- Targeting cancer expressed EGFR with a humanized monoclonal antibody.Scientific reports · 2026Article
- Downregulation of B7-H4 contributes to the synergistic effect of USP2a-targeted/anti-PD-1 combination therapy in EGFR mutant lung cancer.Cancer immunology, immunotherapy : CII · 2026Article
- Deciphering the cancer chemopreventive potential of phytochemicals: an integrative perspective on molecular targets and signaling networks.Cancer cell international · 2026Review
- Article
- EGFR-induced lncRNAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- 3,5-Disubstituted pyrazoline as a promising core for anticancer agents: mechanisms of action and therapeutic potentials.Future medicinal chemistry · 2025Review
- Discovery of STX-721, a Covalent, Potent, and Highly Mutant-Selective EGFR/HER2 Exon20 Insertion Inhibitor for the Treatment of Non-Small Cell Lung Cancer.Journal of medicinal chemistry · 2025Article
- Presence of EGF ligand restricts the binding ability of EgB4 nanobody to EGFR extracellular domain.Scientific reports · 2025Article
- Biased signaling by mutant EGFR underlies dependence on PKCα in lung adenocarcinoma.Cell reports · 2024Article
- Genomic, epigenomic and transcriptomic landscape of glioblastoma.Metabolic brain disease · 2024Review
- Anti-EGFR aptamer exhibits direct anti-cancer effects in NSCLC cells harboring EGFR L858R mutations.NPJ precision oncology · 2024Article
- PIM1 kinase and its diverse substrate in solid tumors.Cell communication and signaling : CCS · 2024Review
- Comparing the Efficacy of Two Generations of EGFR-TKIs: An Integrated Drug-Disease Mechanistic Model Approach in EGFR-Mutated Lung Adenocarcinoma.Biomedicines · 2024Article
- EGFR signaling and pharmacology in oncology revealed with innovative BRET-based biosensors.Communications biology · 2024Article
- Treatment of Non-Small Cell Lung Cancer with Atypical EGFR Mutations.Current treatment options in oncology · 2023Review
- Detection of EGFR gene polymorphisms in non-small cell lung cancer Egyptian patients: a case-control study.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2023Article
- Ring finger protein 12 activates AKT signalling to promote the progression of liver cancer by interacting with EGFR.Journal of cellular and molecular medicine · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The EGF-receptor is frequently mutated in a large variety of tumors. Here we review the most frequent mutations and conclude that they commonly enhance the intrinsic tyrosine kinase activity, or they represent loss-of-function of suppressive regulatory domains. Interestingly, the constitutive activity of mutant receptors translates to downstream pathways, which are subtly different from those stimulated by the wild-type receptor. Cancer drugs intercepting EGFR signaling have already entered clinical application. Both kinase inhibitors specific to EGFR, and monoclonal antibodies to the receptor are described, along with experimental approaches targeting the HSP90 chaperone. Deeper understanding of signaling pathways downstream to mutant receptors will likely improve the outcome of current EGFR-targeted therapies, as well as help develop new drugs and combinations.
Indexed as
Identifiers
What OpenQuestion holds
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.