PMID- 20824044
OWN - NLM
STAT- MEDLINE
DCOM- 20110112
LR  - 20220316
IS  - 1476-5586 (Electronic)
IS  - 1522-8002 (Print)
IS  - 1476-5586 (Linking)
VI  - 12
IP  - 9
DP  - 2010 Sep
TI  - Epidermal growth factor receptor in glioma: signal transduction, neuropathology, 
      imaging, and radioresistance.
PG  - 675-84
AB  - Aberrant epidermal growth factor receptor (EGFR) signaling is common in cancer. 
      Increased expression of wild type and mutant EGFR is a widespread feature of 
      diverse types of cancer. EGFR signaling in cancer has been the focus of intense 
      investigation for decades primarily for two reasons. First, aberrant EGFR 
      signaling is likely to play an important role in the pathogenesis of cancer, and 
      therefore, the mechanisms of EGFR-mediated oncogenic signaling are of interest. 
      Second, the EGFR signaling system is an attractive target for therapeutic 
      intervention. EGFR gene amplification and overexpression are a particularly 
      striking feature of glioblastoma (GBM), observed in approximately 40% of tumors. 
      GBM is the most common primary malignant tumor of the central nervous system in 
      adults. In approximately 50% of tumors with EGFR amplification, a specific EGFR 
      mutant (EGFRvIII, also known as EGFR type III, de2-7, Delta EGFR) can be 
      detected. This mutant is highly oncogenic and is generated from a deletion of 
      exons 2 to 7 of the EGFR gene, which results in an in-frame deletion of 267 amino 
      acids from the extracellular domain of the receptor. EGFRvIII is unable to bind 
      ligand, and it signals constitutively. Although EGFRvIII has the same signaling 
      domain as the wild type receptor, it seems to generate a distinct set of 
      downstream signals that may contribute to an increased tumorigenicity. In this 
      review, we discuss recent progress in key aspects of EGFR signaling in GBM, 
      focusing on neuropathology, signal transduction, imaging of the EGFR, and the 
      role of the EGFR in mediating resistance to radiation therapy in GBM.
FAU - Hatanpaa, Kimmo J
AU  - Hatanpaa KJ
AD  - Department of Pathology, University of Texas Southwestern Medical Center, Dallas, 
      TX, USA.
FAU - Burma, Sandeep
AU  - Burma S
FAU - Zhao, Dawen
AU  - Zhao D
FAU - Habib, Amyn A
AU  - Habib AA
LA  - eng
GR  - R01 NS062080/NS/NINDS NIH HHS/United States
GR  - R21 CA141348/CA/NCI NIH HHS/United States
GR  - 1R21 CA141348-01A1/CA/NCI NIH HHS/United States
GR  - R01NS062080-01A2/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Review
PL  - United States
TA  - Neoplasia
JT  - Neoplasia (New York, N.Y.)
JID - 100886622
RN  - 0 (Mutant Proteins)
RN  - 0 (Radiopharmaceuticals)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Adult
MH  - *Brain Neoplasms/diagnosis/etiology/genetics/radiotherapy
MH  - Diagnostic Imaging/*methods
MH  - ErbB Receptors/antagonists & inhibitors/genetics/*physiology
MH  - *Glioma/diagnosis/etiology/genetics/radiotherapy
MH  - Humans
MH  - Models, Biological
MH  - Molecular Targeted Therapy/methods
MH  - Mutant Proteins/genetics/physiology
MH  - Radiation Tolerance/*genetics/physiology
MH  - Radiopharmaceuticals/therapeutic use
MH  - Signal Transduction/genetics/physiology
PMC - PMC2933688
EDAT- 2010/09/09 06:00
MHDA- 2011/01/13 06:00
PMCR- 2010/09/01
CRDT- 2010/09/09 06:00
PHST- 2010/05/17 00:00 [received]
PHST- 2010/06/07 00:00 [revised]
PHST- 2010/06/08 00:00 [accepted]
PHST- 2010/09/09 06:00 [entrez]
PHST- 2010/09/09 06:00 [pubmed]
PHST- 2011/01/13 06:00 [medline]
PHST- 2010/09/01 00:00 [pmc-release]
AID - 10688 [pii]
AID - 10.1593/neo.10688 [doi]
PST - ppublish
SO  - Neoplasia. 2010 Sep;12(9):675-84. doi: 10.1593/neo.10688.