| Changshu KE. Epidermal growth factor receptor: a key manipulator in molecular pathways of malignant glioma. Oncol Transl Med, 2016, 2: 99-103. |
| Epidermal growth factor receptor: a key manipulator in molecular pathways of malignant glioma |
| Epidermal growth factor receptor: a key manipulator in molecular pathways of malignant glioma |
| Received:January 25, 2016 Revised:May 20, 2016 |
| DOI：10.1007/s10330-016-0135-y |
| 中文关键词: epidermal growth factor receptor (EGFR); molecular pathways; malignant glioma |
| 英文关键词: epidermal growth factor receptor (EGFR); molecular pathways; malignant glioma |
| 基金项目:WJ2015MB067 湖北省卫计委一般项目 人恶性胶质瘤PBK/TOPK 磷酸化与c-myc 基因的调控机制 |
| Author Name | Affiliation | E-mail | | Changshu KE* | Dept. of Pathology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China | kecs@hust.edu.cn |
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| 中文摘要: |
| The epidermal growth factor receptor (EGFR) is a member of the ErbB/EGFR family, including EGFR/Her1,
ErbB2/Her2, ErbB-3/Her3, and ErbB-4/Her4. EGFR exerts its effects through the receptor tyrosine kinase
phosphorylation and activation of important downstream signaling pathways in normal and neoplastic cells,
mainly the Ras GTPase/MAP kinase (MAPK), STAT3, and phosphatidylinositide 3 kinase-AKT pathways.
EGFR deregulation is common in malignant glioma, especially primary glioblastoma, and exists in three
forms: gene overexpression (amplification), autocrine effects of EGFR activation, and activating receptor
mutation (EGFRvIII). However, some EGFR abnormalities have also been found in low-grade gliomas,
including the nuclear localization of EGFR, expression in the microfoci of anaplastic transformation, and
association with neovascularization in the mesenchyma of the glioma, which suggests that some unknown
EGFR-related mechanisms are possibly responsible for its central role in the initiation and progression of
malignant glioma. Uncovering these mechanisms will have potential value in the development of radiotherapy, chemotherapy, and EGFR-targeted therapy for glioma. |
| 英文摘要: |
| The epidermal growth factor receptor (EGFR) is a member of the ErbB/EGFR family, including EGFR/Her1,
ErbB2/Her2, ErbB-3/Her3, and ErbB-4/Her4. EGFR exerts its effects through the receptor tyrosine kinase
phosphorylation and activation of important downstream signaling pathways in normal and neoplastic cells,
mainly the Ras GTPase/MAP kinase (MAPK), STAT3, and phosphatidylinositide 3 kinase-AKT pathways.
EGFR deregulation is common in malignant glioma, especially primary glioblastoma, and exists in three
forms: gene overexpression (amplification), autocrine effects of EGFR activation, and activating receptor
mutation (EGFRvIII). However, some EGFR abnormalities have also been found in low-grade gliomas,
including the nuclear localization of EGFR, expression in the microfoci of anaplastic transformation, and
association with neovascularization in the mesenchyma of the glioma, which suggests that some unknown
EGFR-related mechanisms are possibly responsible for its central role in the initiation and progression of
malignant glioma. Uncovering these mechanisms will have potential value in the development of radiotherapy, chemotherapy, and EGFR-targeted therapy for glioma. |
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