EGFR and EGFRvIII in Glioblastoma: Partners in Crime

Gelareh Zadeh; Krishna P.L. Bhat; Kenneth Aldape

doi:10.1016/j.ccr.2013.09.017

EGFR and EGFRvIII in Glioblastoma: Partners in Crime

Gelareh Zadeh, Krishna P.L. Bhat, Kenneth Aldape

Research output: Contribution to journal › Short survey › peer-review

49 Scopus citations

Abstract

EGFRvIII, a mutated form of EGFR, plays a prominent role in tumorigenesis, but the underlying mechanisms have remained elusive. In this issue of Cancer Cell, Weiss and colleagues implicate phosphorylation of EGFRvIII by EGFR and the consequent phosphorylation of STAT3 as a signaling axis that drives transformation in glioblastoma.

Original language	English (US)
Pages (from-to)	403-404
Number of pages	2
Journal	Cancer cell
Volume	24
Issue number	4
DOIs	https://doi.org/10.1016/j.ccr.2013.09.017
State	Published - Oct 14 2013

ASJC Scopus subject areas

Oncology
Cell Biology
Cancer Research

Access to Document

10.1016/j.ccr.2013.09.017

Cite this

@article{f4d2ca36120b49baa98939da2aef5bde,

title = "EGFR and EGFRvIII in Glioblastoma: Partners in Crime",

abstract = "EGFRvIII, a mutated form of EGFR, plays a prominent role in tumorigenesis, but the underlying mechanisms have remained elusive. In this issue of Cancer Cell, Weiss and colleagues implicate phosphorylation of EGFRvIII by EGFR and the consequent phosphorylation of STAT3 as a signaling axis that drives transformation in glioblastoma.",

author = "Gelareh Zadeh and Bhat, {Krishna P.L.} and Kenneth Aldape",

year = "2013",

month = oct,

day = "14",

doi = "10.1016/j.ccr.2013.09.017",

language = "English (US)",

volume = "24",

pages = "403--404",

journal = "Cancer cell",

issn = "1535-6108",

publisher = "Cell Press",

number = "4",

}

TY - JOUR

T1 - EGFR and EGFRvIII in Glioblastoma

T2 - Partners in Crime

AU - Zadeh, Gelareh

AU - Bhat, Krishna P.L.

AU - Aldape, Kenneth

PY - 2013/10/14

Y1 - 2013/10/14

N2 - EGFRvIII, a mutated form of EGFR, plays a prominent role in tumorigenesis, but the underlying mechanisms have remained elusive. In this issue of Cancer Cell, Weiss and colleagues implicate phosphorylation of EGFRvIII by EGFR and the consequent phosphorylation of STAT3 as a signaling axis that drives transformation in glioblastoma.

AB - EGFRvIII, a mutated form of EGFR, plays a prominent role in tumorigenesis, but the underlying mechanisms have remained elusive. In this issue of Cancer Cell, Weiss and colleagues implicate phosphorylation of EGFRvIII by EGFR and the consequent phosphorylation of STAT3 as a signaling axis that drives transformation in glioblastoma.

UR - http://www.scopus.com/inward/record.url?scp=84885347725&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84885347725&partnerID=8YFLogxK

U2 - 10.1016/j.ccr.2013.09.017

DO - 10.1016/j.ccr.2013.09.017

M3 - Short survey

C2 - 24135276

AN - SCOPUS:84885347725

SN - 1535-6108

VL - 24

SP - 403

EP - 404

JO - Cancer cell

JF - Cancer cell

IS - 4

ER -

EGFR and EGFRvIII in Glioblastoma: Partners in Crime

Abstract

ASJC Scopus subject areas

Access to Document

Other files and links

Fingerprint

Cite this