ArticleCancers2011
Analysis of Somatic Mutations in Cancer: Molecular Mechanisms of Activation in the ErbB Family of Receptor Tyrosine Kinases.
Article in Cancers, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 24 citations in OpenAlex.
- Screening and Docking Molecular Studies of Natural Products Targeting overexpressed Receptors HER-2 in Breast Cancer.Archives of Razi Institute · 2025Article
- HER3 receptor and its role in the therapeutic management of metastatic breast cancer.Journal of translational medicine · 2024Review
- Determinants of resistance and response to melanoma therapy.Nature cancer · 2024Review
- Neural-specific alterations in glycosphingolipid biosynthesis and cell signaling associated with two human ganglioside GM3 synthase deficiency variants.Human molecular genetics · 2023Article
- Discovery of potent and selective HER2 inhibitors with efficacy against HER2 exon 20 insertion-driven tumors, which preserve wild-type EGFR signaling.Nature cancer · 2022Article
- Computational studies of anaplastic lymphoma kinase mutations reveal common mechanisms of oncogenic activation.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Article
- Antitumour immunity regulated by aberrant ERBB family signalling.Nature reviews. Cancer · 2021Review
- Evaluation of EGFR mutations in NSCLC with highly sensitive droplet digital PCR assays.Molecular medicine reports · 2019Article
- Computational algorithms for in silico profiling of activating mutations in cancer.Cellular and molecular life sciences : CMLS · 2019Review
- Prostate cancer health disparities: An immuno-biological perspective.Cancer letters · 2018Article
- Review
- A novel multi-target inhibitor harboring selectivity of inhibiting EGFR T790M sparing wild-type EGFR.American journal of cancer research · 2017Article
- Article
- Molecular modeling of ErbB4/HER4 kinase in the context of the HER4 signaling network helps rationalize the effects of clinically identified HER4 somatic mutations on the cell phenotype.Biotechnology journal · 2013Article
- Article
- Multiscale Cancer Modeling and In Silico Oncology: Emerging Computational Frontiers in Basic and Translational Cancer Research.Journal of bioengineering & biomedical science · 2013Article
- Structural systems biology and multiscale signaling models.Annals of biomedical engineering · 2012Review
- A multiscale modeling approach to investigate molecular mechanisms of pseudokinase activation and drug resistance in the HER3/ErbB3 receptor tyrosine kinase signaling network.Molecular bioSystems · 2011Article
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 ErbB/EGFR/HER family of kinases consists of four homologous receptor tyrosine kinases which are important regulatory elements in many cellular processes, including cell proliferation, differentiation, and migration. Somatic mutations in, or over-expression of, the ErbB family is found in many cancers and is correlated with a poor prognosis; particularly, clinically identified mutations found in non-small-cell lung cancer (NSCLC) of ErbB1 have been shown to increase its basal kinase activity and patients carrying these mutations respond remarkably to the small tyrosine kinase inhibitor gefitinib. Here, we analyze the potential effects of the currently catalogued clinically identified mutations in the ErbB family kinase domains on the molecular mechanisms of kinase activation. Recently, we identified conserved networks of hydrophilic and hydrophobic interactions characteristic to the active and inactive conformation, respectively. Here, we show that the clinically identified mutants influence the kinase activity in distinctive fashion by affecting the characteristic interaction networks.
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.