Current Therapeutic Advances Targeting EGFR and EGFRvIII in Glioblastoma

Padfield, Emily; Ellis, Hayley Patricia; Kurian, Kathreena M.

doi:10.3389/fonc.2015.00005

Cited by 209 publications

(169 citation statements)

References 88 publications

(118 reference statements)

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“…This previous study described the phosphorylation of Beclin-1 by active EGFR in NSCLC cells (13). If EGFR in GBM cells also regulates Beclin-1, this is of note as EGFR is frequently amplified or mutated in GBM (35). In the current study, Beclin-1 was not phosphorylated by inactive or active EGFR independently of TMZ treatment in LN18 and LN18 vIII .…”

Section: Discussionmentioning

confidence: 51%

Temozolomide induces autophagy in primary and established glioblastoma cells in an EGFR independent manner

et al. 2017

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Abstract. Despite major contributions to the current molecular understanding of autophagy, a recycling process for intracellular components to maintain homeostatic balance, relatively little is known about the interacting networks. To address this issue, the current study investigated the role of autophagy in primary and established glioblastoma multiforme (GBM) cells and its interplay with the epidermal growth factor receptor (EGFR) and the standard chemotherapeutic agent temozolomide (TMZ). TMZ treatment leads to an upregulation of autophagy, predominantly in primary GBM cells. The interaction between EGFR and Beclin-1, an important protein in initiating autophagy, was assessed using a cancer cell line transfected with EGFR vIII , and by stimulation with EGF. The results of the current study suggest that Beclin-1 and EGFR do not interact directly in either primary or established GBM cells. To enable the limited efficacy of patient treatment strategies of GBM to potentially be enhanced through the application of autophagy regulators, the multiple cellular interactions of autophagy require further elucidation.

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Section: Discussionmentioning

confidence: 51%

Temozolomide induces autophagy in primary and established glioblastoma cells in an EGFR independent manner

et al. 2017

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“…EGFR, amplification/mutation of which has been observed in ∼57% of GBM patients (27), is recognized as an attractive target for targeted therapy (28). Several EGFR inhibitors have been explored in clinical trials for the treatment of GBM (29); however, poor response and development of resistance have been almost invariably observed.…”

Section: Discussionmentioning

confidence: 99%

Noninvasive brain cancer imaging with a bispecific antibody fragment, generated via click chemistry

Luo

Hernandez

Hong

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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Early diagnosis remains a task of upmost importance for reducing cancer morbidity and mortality. Successful development of highly specific companion diagnostics targeting aberrant molecular pathways of cancer is needed for sensitive detection, accurate diagnosis, and opportune therapeutic intervention. Herein, we generated a bispecific immunoconjugate [denoted as Bs-F(ab) Cu-NOTA-Bs-F(ab) 2 was able to visualize small U87MG tumor nodules (<5 mm in diameter), owing to high tumor uptake (31.4 ± 10.8%ID/g at 36 h postinjection) and a tumor/muscle ratio of 76.4 ± 52.3, which provided excellent sensitivity for early detection. Finally, we successfully confirmed the feasibility of a ZW800-1-labeled Bs-F(ab) 2 for nearinfrared fluorescence imaging and image-guided surgical resection of U87MG tumors. More importantly, our rationale can be used in the construction of other disease-targeting bispecific antibody fragments for early detection and diagnosis of small malignant lesions.

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“…In one study, GNPs were used for radiofrequency ablation of pancreatic and colorectal adenocarcinomas in animal models [33]. Although the high levels of EGFR in some forms of GBM also make it an accurate and desirable therapeutic target, current therapies targeting EGFR, including tyrosine kinase inhibitors and RNA interference, have proved to be ineffective [7,8,34]. Therefore, attention is being addressed to other means: the delivery of novel antitumor agents across the blood-brain barrier, gene therapy, and brain tumor vaccines [35][36][37].…”

Section: Discussionmentioning

confidence: 99%

Identification of Postoperative Margins of Glioblastoma Multiforme Using Gold Nanoparticles Conjugated to Epidermal Growth Factor Antibodies

Hazon¹,

Marianayagam²,

Barinfeld³

et al. 2017

Nano Res Appl

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Background: Glioblastoma multiforme (GBM) is the most common primary malignant brain tumor in adults. Complete resection is impossible. Overexpression of epidermal growth factor receptor (EGFR) by the tumor has been associated with the level of malignancy and possibly with prognosis. Monoclonal antibodies may be used to identify tumor borders. The aim of the present study was to investigate the value of immunostaining with anti-EGFR antibodies conjugated to gold nanoparticles (GNPs) for detecting tumor infiltration into adjacent tissue.

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Current Therapeutic Advances Targeting EGFR and EGFRvIII in Glioblastoma

Cited by 209 publications

References 88 publications

Temozolomide induces autophagy in primary and established glioblastoma cells in an EGFR independent manner

Temozolomide induces autophagy in primary and established glioblastoma cells in an EGFR independent manner

Noninvasive brain cancer imaging with a bispecific antibody fragment, generated via click chemistry

Identification of Postoperative Margins of Glioblastoma Multiforme Using Gold Nanoparticles Conjugated to Epidermal Growth Factor Antibodies

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