Continuing Medical Education Article
18F-FDG Uptake in Lung, Breast, and Colon Cancers: Molecular Biology Correlates
and Disease Characterization
JNM, November 2009, Volume 50, Number 11
Hossein Jadvar1, Abass Alavi2, and Sanjiv S. Gambhir3
1Department of Radiology, Keck School of Medicine, University of Southern California,
Los Angeles, California; 2Department of Radiology, School of Medicine, University of
Pennsylvania, Philadelphia, Pennsylvania; and 3Molecular Imaging Program at Stanford,
Division of Nuclear Medicine, Department of Radiology, Stanford University, Stanford,
In accordance with ACCME Revised Standards for Commercial Support and SNM
Conflict-of-Interest Policy, the authors have indicated no relevant relationships that could
be perceived as a real or apparent conflict of interest. Disclosure of a relationship is not
intended to suggest or to condone bias but is made to provide participants with
information that might be of potential importance to their evaluation of the activity.
This article will be of interest to nuclear medicine professionals, including physicians and
technologists, radiologists, scientists, physicians in training, and students.
On successful completion of this activity, participants should be able to:
1. Describe the primary biologic factors underlying 18F-FDG accumulation in tumors.
2. Reflect on the current evidence on the correlation of 18F-FDG accumulation in lung,
breast, and colon cancer to the underlying major biologic factors in these cancers.
1. Enhanced tumor glucose metabolism is associated with deregulated overexpression of
glucose transporters (GLUTs) (primarily GLUT1 or GLUT3).
2. Increased hexokinase enzymatic activity (primarily hexokinase type II) has also been
implicated in many cancers.
3. The following factors may contribute to the discrepant findings in relation to 18F-FDG
accumulation in lung cancer: