JNM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

First published online July 17, 2009, 10.2967/jnumed.109.062117
This Article
Right arrow Figures Only
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
jnumed.109.062117v1
50/8/1199    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Related articles in JNM
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Mishani, E.
Right arrow Articles by Hagooly, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Mishani, E.
Right arrow Articles by Hagooly, A.
Journal of Nuclear Medicine Vol. 50 No. 8 1199-1202
© 2009 by Society of Nuclear Medicine
doi: 10.2967/jnumed.109.062117

Focus on Molecular Imaging

Strategies for Molecular Imaging of Epidermal Growth Factor Receptor Tyrosine Kinase in Cancer

Eyal Mishani and Aviv Hagooly

Cyclotron Unit, Department of Nuclear Medicine, Hadassah Hebrew University Hospital, Jerusalem, Israel

Correspondence: For correspondence or reprints contact: Eyal Mishani, Department of Nuclear Medicine, Hadassah University Hospital, P.O. Box 12000, Jerusalem, Israel 91120. E-mail: eyalmi{at}ekmd.huji.ac.il

ABSTRACT

A wealth of research has focused on developing targeted cancer therapies by specifically inhibiting epidermal growth factor receptor tyrosine kinase (EGFR-TK). However, the outcome of most EGFR-TK–targeted drugs that were approved by the Food and Drug Administration or entered clinical trials has been only moderate. Enhancement of EGFR-targeted therapy hinges on a reliable in vivo quantitative molecular imaging method. Such a method would enable monitoring of receptor drug binding and receptor occupancy in vivo; determination of the duration of EGFR inhibition in vivo; and, potentially, identification of a primary or secondary mutation in EGFR leading to drug interaction or loss of EGFR recognition by the drug. This review analyzes the most recent strategies to visualize and quantify EGFR-TK in cancer by nuclear medicine imaging and describes future directions.

Key Words: EGFR • PET • cancer • imaging • tyrosine kinase • cetuximab • gefitinib

FOOTNOTES

Guest Editor: Caius Radu, UCLA Crump Institute

COPYRIGHT © 2009 by the Society of Nuclear Medicine, Inc.


Related articles in JNM:

This Month in JNM

JNM 2009 50: 11A-12A. [Full Text]  





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH RSS TABLE OF CONTENTS
JOURNAL OF NUCLEAR MEDICINE TECHNOLOGY THE JOURNAL OF NUCLEAR MEDICINE
Copyright © 2009 by the Society of Nuclear Medicine.