SNM Annual Meeting Abstracts
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     




J Nucl Med. 2008; 49 (Supplement 1):346P
This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Strauss, L.
Right arrow Articles by Dimitrakopoulou-Strauss, A.
PubMed
Right arrow Articles by Strauss, L.
Right arrow Articles by Dimitrakopoulou-Strauss, A.

Oncology-Clinical Diagnosis: Solid Tumors

Clinical Diagnosis-Solid Tumors Posters

Correlation of hypoxia associated genes with FDG uptake and kinetics

Ludwig Strauss1, Sven Klippel2, Dirk Koczan3, Caixia Cheng1, Leyun Pan1, Uwe Haberkorn1 and Antonia Dimitrakopoulou-Strauss1

1 Clinical Cooperation Unit Nuclear Medicine, German Cancer Research Center, Heidelberg, Germany; 2 Surgical Clinic, Klinikum Ludwigshafen, Ludwigshafen, Germany; 3 Institute of Immunology, Univ. of Rostock, Ludwigshafen, Germany

1462

Objectives: The kinetics of F-18-Deoxyglucose (FDG) in tumors is determined by transporters and hexokinases, but modulated by other factors. Some studies gave evidence, that hypoxia may have an impact on FDG kinetics.

Methods: The evaluation comprises dynamic PET FDG studies performed in 24 patients with primary colorectal malignancies. Volumes-of-Interest were used to obtain tracer concentrations. A 2-tissue-compartment model was fitted to the data and k1-k4 as well as the fractional blood volume (vessel density, VB) were calculated. Tissue specimen from the tumor region evaluated by PET as well as specimen from a reference area (normal colon) were obtained by surgery. Quantitative gene expression data were obtained by gene array analysis using the U133A gene chip (Affymetrix Inc., Santa Clara,CA,USA). PET and gene array data were evaluated with the GenePET module of PMOD (PMOD Technologies Ltd.).

Results: The tumor-to-normal ratio was highest for the The hypoxia-inducible protein 2 (6.28), followed by a ratio of 1.58 for the hypoxia-inducible factor 1 alpha (HIF-1a). Correlation analysis demonstrated a significant correlation of HIF-1a and SUV (r=0.5344), influx (r=0.5958), fractal dimension (r=0.5521), and k3 (r==.5246). HIF-1, hypoxia-inducible protein 2, and hypoxia inducible factor 3 alpha revealed a correlation of r=0.65 with the FDG influx.

Conclusions: Enhanced expression of HIF-1a was primarily associated with an enhanced influx of FDG. Therefore, the quantitative analysis of the FDG kinetics can help to predict the expression of HIF-1a in primary colorectal tumors.





This Article
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Google Scholar
Right arrow Articles by Strauss, L.
Right arrow Articles by Dimitrakopoulou-Strauss, A.
PubMed
Right arrow Articles by Strauss, L.
Right arrow Articles by Dimitrakopoulou-Strauss, A.