ArticleNature chemical biology2016
Overcoming resistance to HER2 inhibitors through state-specific kinase binding.
Article in Nature chemical biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Modulating pseudokinase conformation from the ATP-binding site.Structure (London, England : 1993) · 2026Article
- Synthesis of new pyrazolo[3,4-d]pyrimidines as potential mutant EGFR/HER2 and Bcl2 inhibitors: anticancer evaluation, DFT, molecular docking and ADME studies.BMC chemistry · 2026Article
- The role of kinase domain dimerization in EGFR activation.Structure (London, England : 1993) · 2026Article
- Targeting cyclin-dependent kinase 2 (CDK2) interactions with cyclins and Speedy 1 (Spy1) for cancer and male contraception.Future medicinal chemistry · 2025Review
- Quantitative systems pharmacology modeling of HER2-positive metastatic breast cancer for translational efficacy evaluation and combination assessment across therapeutic modalities.Acta pharmacologica Sinica · 2024Article
- Distinct interactions stabilize EGFR dimers and higher-order oligomers in cell membranes.Cell reports · 2024Article
- Looking lively: emerging principles of pseudokinase signaling.Trends in biochemical sciences · 2022Review
- Understanding gilteritinib resistance to FLT3-F691L mutation through an integrated computational strategy.Journal of molecular modeling · 2022Article
- CD74-NRG1 Fusions Are Oncogenic In Vivo and Induce Therapeutically Tractable ERBB2:ERBB3 Heterodimerization.Molecular cancer therapeutics · 2022Article
- HER2 Mediates PSMA/mGluR1-Driven Resistance to the DS-7423 Dual PI3K/mTOR Inhibitor in PTEN Wild-type Prostate Cancer Models.Molecular cancer therapeutics · 2022Article
- Role of nano-lipid formulation of CARP-1 mimetic, CFM-4.17 to improve systemic exposure and response in osimertinib resistant non-small cell lung cancer.European journal of pharmaceutics and biopharmaceutics : official journal of Arbeitsgemeinschaft fur Pharmazeutische Verfahrenstechnik e.V · 2021Article
- Carotenoid-Enriched Fractions FromFrontiers in oncology · 2021Article
- Structural Insights into Pseudokinase Domains of Receptor Tyrosine Kinases.Molecular cell · 2020Article
- Article
- Understanding the Mechanisms by Which Epigenetic Modifiers Avert Therapy Resistance in Cancer.Frontiers in oncology · 2020Review
- p27 allosterically activates cyclin-dependent kinase 4 and antagonizes palbociclib inhibition.Science (New York, N.Y.) · 2019Article
- Selective Proteolysis to Study the Global Conformation and Regulatory Mechanisms of c-Src Kinase.ACS chemical biology · 2019Article
- KRASScience signaling · 2019Article
- Tracing the origin and evolution of pseudokinases across the tree of life.Science signaling · 2019Article
- Posttranscriptional upregulation of HER3 by HER2 mRNA induces trastuzumab resistance in breast cancer.Molecular cancer · 2018Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
The heterodimeric receptor tyrosine kinase complex formed by HER2 and HER3 can act as an oncogenic driver and is also responsible for rescuing a large number of cancers from a diverse set of targeted therapies. Inhibitors of these proteins, particularly HER2, have dramatically improved patient outcomes in the clinic, but recent studies have demonstrated that stimulating the heterodimeric complex, either via growth factors or by increasing the concentrations of HER2 and HER3 at the membrane, significantly diminishes the activity of the inhibitors. To identify an inhibitor of the active HER2-HER3 oncogenic complex, we developed a panel of Ba/F3 cell lines suitable for ultra-high-throughput screening. Medicinal chemistry on the hit scaffold resulted in a previously uncharacterized inhibitor that acts through preferential inhibition of the active state of HER2 and, as a result, is able to overcome cellular mechanisms of resistance such as growth factors or mutations that stabilize the active form of HER2.
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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.