Epidermal growth factor receptor in glioblastoma

Xu, Hongsheng; Zong, Hailiang; Ma, Chao; Ming, Xing; Shang, Ming; Li, Kai; He, Xiaoguang; Du, Huarui; Cao, Lei

doi:10.3892/ol.2017.6221

Cited by 112 publications

(82 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…EGFR gene amplification is observed in approximately 50% of GBMs, whereas EGFRvIII (Figure 1 ), a constitutively active truncated form of the EGFR protein that lacks the extracellular domain, occurs in 20–30% of cases ( 11 , 17 – 19 ). Indeed, targeted inhibition of EGFR or the tumor-specific EGFRvIII holds therapeutic promise and several clinical trials with specific tyrosine kinases as well as monoclonal antibodies are ongoing ( 20 , 21 ).…”

Section: Introductionmentioning

confidence: 99%

Epstein–Barr Virus in Gliomas: Cause, Association, or Artifact?

et al. 2018

View full text Add to dashboard Cite

Gliomas are the most common malignant brain tumors and account for around 60% of all primary central nervous system cancers. Glioblastoma multiforme (GBM) is a grade IV glioma associated with a poor outcome despite recent advances in chemotherapy. The etiology of gliomas is unknown, but neurotropic viruses including the Epstein–Barr virus (EBV) that is transmitted via salivary and genital fluids have been implicated recently. EBV is a member of the gamma herpes simplex family of DNA viruses that is known to cause infectious mononucleosis (glandular fever) and is strongly linked with the oncogenesis of several cancers, including B-cell lymphomas, nasopharyngeal, and gastric carcinomas. The fact that EBV is thought to be the causative agent for primary central nervous system (CNS) lymphomas in immune-deficient patients has led to its investigations in other brain tumors including gliomas. Here, we provide a review of the clinical literature pertaining to EBV in gliomas and discuss the possibilities of this virus being simply associative, causative, or even an experimental artifact. We searched the PubMed/MEDLINE databases using the following key words such as: glioma(s), glioblastoma multiforme, brain tumors/cancers, EBV, and neurotropic viruses. Our literature analysis indicates conflicting results on the presence and role of EBV in gliomas. Further comprehensive studies are needed to fully implicate EBV in gliomagenesis and oncomodulation. Understanding the role of EBV and other oncoviruses in the etiology of gliomas, would likely open up new avenues for the treatment and management of these, often fatal, CNS tumors.

show abstract

Section: Introductionmentioning

confidence: 99%

Epstein–Barr Virus in Gliomas: Cause, Association, or Artifact?

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Several growth factors, including platelet-derived growth factor ( 111 ), fibroblast growth factor ( 112 ), insulin-like growth factor ( 113 ), and epidermal growth factor (EGF) ( 114 ), induce NF-κB activation through receptors that are members of the RTK family. EGF and the EGF receptor EGFR (HER1) have been extensively studied in cancer, with EGFR amplification implicated in the pathogenesis of lung cancer ( 115 ), glioblastoma ( 116 ), and breast cancer ( 117 ), among others. Indeed, EGFR itself is the target of several therapeutics: either RTK inhibitors such as gefitinib, used in lung cancer, or monoclonal antibody inhibitors such as cetuximab, employed against colon cancer ( 118 ).…”

Section: Receptor Tyrosine Kinases (Rtks) Also Signal Via mentioning

confidence: 99%

CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis

et al. 2018

View full text Add to dashboard Cite

The CARMA–Bcl10–MALT1 (CBM) signalosome is an intracellular protein complex composed of a CARMA scaffolding protein, the Bcl10 linker protein, and the MALT1 protease. This complex was first recognized because the genes encoding its components are targeted by mutation and chromosomal translocation in lymphoid malignancy. We now know that the CBM signalosome plays a critical role in normal lymphocyte function by mediating antigen receptor-dependent activation of the pro-inflammatory, pro-survival NF-κB transcription factor, and that deregulation of this signaling complex promotes B-cell lymphomagenesis. More recently, we and others have demonstrated that a CBM signalosome also operates in cells outside of the immune system, including in several solid tumors. While CARMA1 (also referred to as CARD11) is expressed primarily within lymphoid tissues, the related scaffolding protein, CARMA3 (CARD10), is more widely expressed and participates in a CARMA3-containing CBM complex in a variety of cell types. The CARMA3-containing CBM complex operates downstream of specific G protein-coupled receptors (GPCRs) and/or growth factor receptor tyrosine kinases (RTKs). Since inappropriate expression and activation of GPCRs and/or RTKs underlies the pathogenesis of several solid tumors, there is now great interest in elucidating the contribution of CARMA3-mediated cellular signaling in these malignancies. Here, we summarize the key discoveries leading to our current understanding of the role of CARMA3 in solid tumor biology and highlight the current gaps in our knowledge.

show abstract

“…Intraoperatively, fluorescence intensity could guide the surgeon to resect tumor tissue together with a safe margin. Epidermal growth factor receptor (EGFR) is known to be overexpressed on the cell surface of various types of malignant tumors, including breast and lung adenocarcinomas (40% of cases) [8,9], anal cancers [10], glioblastoma (50%) [11] and epithelial tumors of the head and neck (80-100%) [12]. Recently, we reported N-(2-hydroxypropyl)methacrylamide (HPMA)-based polymer probes for fluorescence-guided surgery targeted to EGFR with the oligopeptide YHWYGYTPQNVI (GE-11) [13].…”

Section: Introductionmentioning

confidence: 99%

Targeted Polymer-Based Probes for Fluorescence Guided Visualization and Potential Surgery of EGFR-Positive Head-and-Neck Tumors

et al. 2020

View full text Add to dashboard Cite

This report describes the design, synthesis and evaluation of tumor-targeted polymer probes to visualize epidermal growth factor receptor (EGFR)-positive malignant tumors for successful resection via fluorescence guided endoscopic surgery. Fluorescent polymer probes of various molecular weights enabling passive accumulation in tumors via enhanced permeability and retention were prepared and evaluated, showing an optimal molecular weight of 200,000 g/mol for passive tumor targeting. Moreover, poly(N-(2-hydroxypropyl)methacrylamide)-based copolymers labeled with fluorescent dyes were targeted with the EGFR-binding oligopeptide GE-11 (YHWYGYTPQNVI), human EGF or anti-EGFR monoclonal antibody cetuximab were all able to actively target the surface of EGFR-positive tumor cells. Nanoprobes targeted with GE-11 and cetuximab showed the best targeting profile but differed in their tumor accumulation kinetics. Cetuximab increased tumor accumulation after 15 min, whereas GE 11 needed at least 4 h. Interestingly, after 4 h, there were no significant differences in tumor targeting, indicating the potential of oligopeptide targeting for fluorescence-navigated surgery. In conclusion, fluorescent polymer probes targeted by oligopeptide GE-11 or whole antibody are excellent tools for surgical navigation during oncological surgery of head and neck squamous cell carcinoma, due to their relatively simple design, synthesis and cost, as well as optimal pharmacokinetics and accumulation in tumors.

show abstract

Epidermal growth factor receptor in glioblastoma

Cited by 112 publications

References 45 publications

Epstein–Barr Virus in Gliomas: Cause, Association, or Artifact?

Epstein–Barr Virus in Gliomas: Cause, Association, or Artifact?

CARMA3 Is a Critical Mediator of G Protein-Coupled Receptor and Receptor Tyrosine Kinase-Driven Solid Tumor Pathogenesis

Targeted Polymer-Based Probes for Fluorescence Guided Visualization and Potential Surgery of EGFR-Positive Head-and-Neck Tumors

Contact Info

Product

Resources

About