Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors.

By I. Mellinghoff, Maria Y Wang, I. Vivanco, D. Haas-Kogan, Shaojun Zhu, Ederlyn Q Dia, K. Lu, K. Yoshimoto, Julie Huang, D. Chute and 14 more. New England Journal of Medicine, 2005

1,471 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/5cedf1581db82b78277b88306d77039f27914726

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Citations in the corpus

PI3K pathway alterations in cancer: variations on a theme (2008, neutral): “Like PTEN ; HER2þ breast cancers that are resistant to trastuzumab, PTEN ;EGFRvIII glioblastomas are resistant to the EGFR inhibitors, erlotinib and gefitinib, due to the persistence of EGFR-independent PI3K signaling (Mellinghoff et al., 2005).”
Exciting New Advances in Neuro-Oncology (2010, background): “In malignant gliomas, PI3K/Akt/mTOR signaling is frequently increased because of receptor tyrosine kinase overactivity (EGFR, PDGFR, and mesenchymal-epithelial transition factor [MET]), mutated oncogenic PI3K subunits, and/or loss of PTEN tumor suppressor activity (Fig.”
Identification and characterization of NVP-BEZ235, a new orally available dual phosphatidylinositol 3-kinase/mammalian target of rapamycin inhibitor with potent in vivo antitumor activity (2008, background): “function in glioblastoma multiforme has been correlated with resistance to epidermal growth factor receptor– targeted therapies (37), radiotherapy, and alkylating agents such as temozolomide (38).”
Exosomes in Tumor Microenvironment Influence Cancer Progression and Metastasis (2013, background): “The expression of this EGFRvIII mutant/variant is decisive in determining the therapeutic approach for such patients [59].”
Glioblastoma microvesicles transport RNA and protein that promote tumor growth and provide diagnostic biomarkers (2008, background): “One study showed that EGFRvIII-positive gliomas respond 50 times better than EGFRvIII-negative cells to treatment with EGFR inhibitors, such as erlotinib or gefitini”
A Patient-Derived Glioblastoma Organoid Model and Biobank Recapitulates Inter- and Intra-tumoral Heterogeneity. (2019, background): “, 2011), but showed a survival benefit in patients with mutated EGFR in the absence of downstream PTEN mutation (Arif et al., 2018; Mellinghoff et al., 2005).”
Hexokinase 2 is a key mediator of aerobic glycolysis and promotes tumor growth in human glioblastoma multiforme (2011, background): “In addition, GBMs are known to have aberrant activation of growth factor receptors and/or loss of PTEN activity (Mellinghoff et al., 2005) with subse quent activation of the PI3K–AKT pathway.”
Targeting brain cancer: advances in the molecular pathology of malignant glioma and medulloblastoma (2010, neutral): “gov/drugdictionary/?CdrID=38428">erlotinib when PTEN expression is retaine”
Model organisms: The mighty mouse: genetically engineered mouse models in cancer drug development (2006, neutral): “As the specific genetic profile can alter a tumour's response to a drug (for example, PTEN (phosphatase and tensin homologue deleted on chromosome 10) mutation status in anti-epidermal growth factor receptor (EGFR) trial”
Targeting PI3K signalling in cancer: opportunities, challenges and limitations (2009, background): “Indeed, for an RTK inhibitor to be an effective therapy, it must lead to downregulation of PI3K signallin”
Diffuse glioma growth: a guerilla war (2007, background): “those in which the glioma cells coexpressed EGFRvIII and PTEN) [115].”
The cancer biomarker problem (2008, background): “And, in glioblastoma multiforme, distinct mutations in the genetic region encoding the extracellular domain of EGFR predict sensitivity to EGFR inhibitors but only in cases in which the tumour-suppressor protein PTEN is also intac”
Targeting the cancer kinome through polypharmacology (2010, neutral): “This can result from the activation of multiple, redundant kinase signalling pathways 29 or the presence of activating mutations in downstream pathway components, such as KRAS or PTEN , which enable the tumour to bypass the drug target 20,21,30 .”