Coactivation of Receptor Tyrosine Kinases Affects the Response of Tumor Cells to Targeted Therapies

By Jayne M. Stommel, Alec C. Kimmelman, Haoqiang Ying, R. Nabioullin, Aditya H. Ponugoti, R. Wiedemeyer, A. Stegh, James E. Bradner, K. Ligon, C. Brennan and 2 more. Science, 2007

962 citations recorded by the source corpus.

Subfields: Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/a1af882318cfd9af31a3cbdbd6ab588c7c47c466

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Citations in the corpus

Malignant astrocytic glioma: genetics, biology, and paths to treatment. (2007, background): “…provides a rational explanation for the feeble ability of RTK inhibitor monotherapy to effect durable clinical responses in GBM patients, in that the inhibition of a single RTK is insufficient to block signaling through critical growth and survival pathways (Huang et al. 2007; Stommel et al. 2007).”
Comprehensive genomic characterization defines human glioblastoma genes and core pathways (2008, neutral): “Weisenberger(49), Fei Pan(49), David Van Den Berg(49), Leander Van Neste(44), Joo Mi Yi(42), Kornel E.”
Broad targeting of resistance to apoptosis in cancer (2015, background): “Two other receptors, platelet-derived growth factor receptor (PDGFR) and c-Met or hepatocyte growth factor receptor (HGFR), are also involved in EGFR function and in maintaining downstream pathway activation [175].”
Mesenchymal Transition and PDGFRA Amplification/Mutation Are Key Distinct Oncogenic Events in Pediatric Diffuse Intrinsic Pontine Gliomas (2012, background): “Combinatorial targeted approaches may also be valid given the observation of multiple oncogenic alterations activating the same downstream signaling cascades [76].”
Single-cell RNA-seq highlights intratumoral heterogeneity in primary glioblastoma (2014, background): “Mosaic RTK amplification and redundant signaling pathways contribute to targeted therapy resistance in glioblastoma (11, 30, 31).”
Cancer stem cells in glioblastoma (2015, background): “The abnormal activation of RTKs involves many pathways that are redundant and can initiate and maintain downstream signaling, making tumors refractory to treatment (Stommel et al. 2007).”
PI3K pathway alterations in cancer: variations on a theme (2008, positive): “Stommel et al. (2007) show that expression of EGFRvIII and constitutive MET in glioblastoma cell lines renders cells resistant to EGFR, MET and PDGFRa inhibitors alone, but not in combination.”
AKT inhibition relieves feedback suppression of receptor tyrosine kinase expression and activity (2011, neutral): “These RTK arrays detect phosphorylation of 42 RTKs (Stommel et al., 2007).”
P53 and Pten control neural and glioma stem/progenitor cell renewal and differentiation (2008, positive): “Multi-RTK co-activation in human primary GBM 12 was also evident in the murine tumors with robust PDGFR α expression overlapping with strong regional activation of EGFR (Supplementary Fig.”