ArticleNature communications2019
Identification of metabolic vulnerabilities of receptor tyrosine kinases-driven cancer.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 1 of them a synthesis that pooled it.
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Who cites it
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 140 citations in OpenAlex.
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Targeting receptor tyrosine kinases: from molecular mechanisms to clinical therapeutics.Signal transduction and targeted therapy · 2026Review
- α-ketoglutarate accumulation orchestrates immunosuppressive metabolic remodeling to drive cetuximab resistance in metastatic colorectal cancer.Cell death & disease · 2026Article
- Lactylation and lactate: insights into muscle cell epigenetic regulators in exercise.Molecular medicine (Cambridge, Mass.) · 2026Review
- Solute carrier transporters as metabolic gatekeepers in tumor-microenvironment crosstalk.Acta pharmacologica Sinica · 2026Review
- Explore the Heterogeneity of Glioblastoma Based on Genes Related to Glutamine Metabolism.Cancer informatics · 2026Article
- The role of fibroblast growth factors in cell and cancer metabolism.FEBS letters · 2026Review
- Integrative multi-omics analysis proposes a metabolic classification of gliomas: distinct metabolic states, immune infiltration, and prognosis.Journal of translational medicine · 2025Article
- NDUFS3 promotes proliferation via glucose metabolism reprogramming inducing AMPK phosphorylating PRPS1 to increase the purine nucleotide synthesis in melanoma.Cell death and differentiation · 2025Article
- SOX2 drives esophageal squamous carcinoma by reprogramming lipid metabolism and histone acetylation landscape.Nature communications · 2025Article
- Cancer-associated fibroblasts promote drug resistance in ALK-driven lung adenocarcinoma cells by upregulating lipid biosynthesis.Cancer & metabolism · 2025Article
- SCNN1A expression in triple-negative breast cancer: clinical implications for prognosis and neoadjuvant therapy response.World journal of surgical oncology · 2025Article
- Emerging roles of lysine lactyltransferases and lactylation.Nature cell biology · 2025Review
- Metformin sensitizes triple-negative breast cancer to histone deacetylase inhibitors by targeting FGFR4.Journal of biomedical science · 2025Article
- A Comprehensive Review of Advanced Lactate Biosensor Materials, Methods, and Applications in Modern Healthcare.Sensors (Basel, Switzerland) · 2025Review
- The Inhibitory Effects of NCT503 and Exogenous Serine on High-Selenium Induced Insulin Resistance in Mice.Nutrients · 2025Article
- Eye on the horizon: The metabolic landscape of the RPE in aging and disease.Progress in retinal and eye research · 2025Review
- Lactylation-Driven IGF2BP3-Mediated Serine Metabolism Reprogramming and RNA m6A-Modification Promotes Lenvatinib Resistance in HCC.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Understanding serine and glycine metabolism in cancer: a path towards precision medicine to improve patient's outcomes.Discover oncology · 2024Review
- Inhibitory effect of 1,4,5,6-tetrahydroxy-7,8-diprenylxanthone against NSCLC with L858R/T790M/C797S mutant EGFR.Scientific reports · 2024Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
23 authors at 4 institutions in 2 countries.
Funding
Abstract
One of the biggest hurdles for the development of metabolism-targeted therapies is to identify the responsive tumor subsets. However, the metabolic vulnerabilities for most human cancers remain unclear. Establishing the link between metabolic signatures and the oncogenic alterations of receptor tyrosine kinases (RTK), the most well-defined cancer genotypes, may precisely direct metabolic intervention to a broad patient population. By integrating metabolomics and transcriptomics, we herein show that oncogenic RTK activation causes distinct metabolic preference. Specifically, EGFR activation branches glycolysis to the serine synthesis for nucleotide biosynthesis and redox homeostasis, whereas FGFR activation recycles lactate to fuel oxidative phosphorylation for energy generation. Genetic alterations of EGFR and FGFR stratify the responsive tumors to pharmacological inhibitors that target serine synthesis and lactate fluxes, respectively. Together, this study provides the molecular link between cancer genotypes and metabolic dependency, providing basis for patient stratification in metabolism-targeted therapies.
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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.