Epidermal growth factor receptor as a therapeutic target in head and neck cancer

被引:40
作者
Bonner, JA
De los Santos, J
Waksal, HW
Needle, MN
Trummel, HQ
Raisch, KP
机构
[1] Univ Alabama, Dept Radiat Oncol, Wallace Tumor Inst 105, Birmingham, AL 35294 USA
[2] ImClone Syst Inc, New York, NY USA
关键词
D O I
10.1053/srao.2002.34864
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Epidermal growth factor receptor (EGFR) is a cell membrane protein that is overexpressed in almost all head and neck squamous cell carcinomas. Overexpression of EGFR has been associated with a poor prognosis in head and neck tumors as well as many other malignancies. This cell membrane protein has been considered an excellent choice as an antitumor therapeutic target. Preclinical and clinical investigations are currently underway to determine the most appropriate use of anti-EGFR therapies. IMC-C225 is a monoclonal antibody that blocks EGFR function and has shown promising radiosensitizing and chemosensitizing properties in preclinical studies. Additionally, initial phase 1/11 clinical studies of IMC-C225 in combination with radiotherapy or chemotherapy have suggested that the preclinical findings may translate into promising clinical results in squamous cell carcinoma of the head and neck. Therefore, patients with head and neck carcinomas are being evaluated in phase III studies exploring the combination of IMC-C225 and radiation as well as the combination of IMC-C225 and cisplatin in locally advanced and recurrent disease. Copyright 2002, Elsevier Science (USA). All rights reserved.
引用
收藏
页码:11 / 20
页数:10
相关论文
共 56 条
[1]  
Akimoto T, 1999, CLIN CANCER RES, V5, P2884
[2]   The effect of ionizing radiation on signal transduction: Antibodies to EGF receptor sensitize A431 cells to radiation [J].
Balaban, N ;
Moni, J ;
Shannon, M ;
Dang, LO ;
Murphy, E ;
Goldkorn, T .
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH, 1996, 1314 (1-2) :147-156
[3]   Phase I studies of anti-epidermal growth factor receptor chimeric antibody C225 alone and in combination with cisplatin [J].
Baselga, J ;
Pfister, D ;
Cooper, MR ;
Cohen, R ;
Burtness, B ;
Bos, M ;
D'Andrea, G ;
Seidman, A ;
Norton, L ;
Gunnett, K ;
Falcey, J ;
Anderson, V ;
Waksal, H ;
Mendelsohn, J .
JOURNAL OF CLINICAL ONCOLOGY, 2000, 18 (04) :904-914
[4]   EPIDERMAL GROWTH-FACTOR RECEPTOR EXPRESSION IN GYNECOLOGICAL MALIGNANCIES [J].
BATTAGLIA, F ;
SCAMBIA, G ;
PANICI, PB ;
BAIOCCHI, G ;
PERRONE, L ;
IACOBELLI, S ;
MANCUSO, S .
GYNECOLOGIC AND OBSTETRIC INVESTIGATION, 1989, 27 (01) :42-44
[5]   Ionizing radiation-induced MEK and Erk activation does not enhance survival of irradiated human squamous carcinoma cells [J].
Bonner, JA ;
Vroman, BT ;
Christianson, TJH ;
Karnitz, LM .
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, 1998, 42 (04) :921-925
[6]   THE INTERACTION OF EPIDERMAL GROWTH-FACTOR AND RADIATION IN HUMAN HEAD AND NECK SQUAMOUS-CELL CARCINOMA CELL-LINES WITH VASTLY DIFFERENT RADIOSENSITIVITIES [J].
BONNER, JA ;
MAIHLE, NJ ;
FOLVEN, BR ;
CHRISTIANSON, TJH ;
SPAIN, K .
INTERNATIONAL JOURNAL OF RADIATION ONCOLOGY BIOLOGY PHYSICS, 1994, 29 (02) :243-247
[7]  
Bonner JA, 2000, J CLIN ONCOL, V18, p47S
[8]  
BONNER JA, 2000, P AN M AM SOC CLIN, V19, pA4
[9]   Reversible G1 arrest induced by inhibition of the epidermal growth factor receptor tyrosine kinase requires up-regulation of p27KIP1 independent of MAPK activity [J].
Busse, D ;
Doughty, RS ;
Ramsey, TT ;
Russell, WE ;
Price, JO ;
Flanagan, WM ;
Shawver, LK ;
Arteaga, CL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (10) :6987-6995
[10]  
Colton T, 1974, STAT MED