TY - JOUR
T1 - Inhibitors of HER2/neu (erbB-2) signal transduction
AU - Arteaga, Carlos L.
AU - Chinratanalab, Wichai
AU - Carter, Mary Beth
N1 - Funding Information:
From the Departments of Medicine and Cell Biolog)l , Vanderbilt University School of Medicine, Nashville; Department of Veterans Affairs Medical Center, Nashville; and Vanderbilt-Ingram Cancer Center, Nashville, TN. Supported by National Institutes of Health Grunt no. R01 CA80195, a Clinical Investigator Award from the Department of Veterans Affairs, and Vanderbilt-Ingram Cancer Center support Grant no. CA68545. Dr Arteaga has received research pant support from Bristol- Myers Squibb and Genentech. He has served on the speakers bureau for AstraZeneca and Genentech and has served as a paid consultant to Genentech. Address reprint requests to Carlos L. Arteugu, MD, Division of Hematology/Oncology, Vanderbilt University School of Medicine, 22nd Awe S, 1956 TVC, Nashville, TN 37232-5536. Copyright 0 2001 by W.B. Saunders Company 0093-7754/01/2806-1805$35,00/O doi:lO.I053/sonc.2001.29722
PY - 2001
Y1 - 2001
N2 - Signaling by the HER2 proto-oncogene product results in the activation of several biochemical pathways that in turn modulate the expression and function of molecules involved in cell proliferation and survival. It is well established that forced overexpression of HER2 results in transformation of nontumor cells, and that high levels of HER2 in tumors are associated with a more aggressive biological behavior. It is also clear that a subset of HER2-overexpressing tumors is dependent on HER2 function for proliferation and/or survival. Over the last few years, several elegant studies have dissected the biochemical mechanisms of HER2 signaling. This research has provided information about critical functional domains in HER2 that can be targeted with rational molecular approaches, some of which are already being implemented at the bedside. This report will focus on one of these anti-HER2 signaling strategies.
AB - Signaling by the HER2 proto-oncogene product results in the activation of several biochemical pathways that in turn modulate the expression and function of molecules involved in cell proliferation and survival. It is well established that forced overexpression of HER2 results in transformation of nontumor cells, and that high levels of HER2 in tumors are associated with a more aggressive biological behavior. It is also clear that a subset of HER2-overexpressing tumors is dependent on HER2 function for proliferation and/or survival. Over the last few years, several elegant studies have dissected the biochemical mechanisms of HER2 signaling. This research has provided information about critical functional domains in HER2 that can be targeted with rational molecular approaches, some of which are already being implemented at the bedside. This report will focus on one of these anti-HER2 signaling strategies.
UR - http://www.scopus.com/inward/record.url?scp=0035687013&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035687013&partnerID=8YFLogxK
U2 - 10.1016/S0093-7754(01)90106-X
DO - 10.1016/S0093-7754(01)90106-X
M3 - Article
C2 - 11774203
AN - SCOPUS:0035687013
SN - 0093-7754
VL - 28
SP - 30
EP - 35
JO - Seminars in oncology
JF - Seminars in oncology
IS - 6 SUPPL. 18
ER -