Details

Autor(en) / Beteiligte

• Ott, Katja
• Weber, Wolfgang A.
• Fink, Ulrich
• Helmberger, Hermann
• Becker, Karen
• Stein, Hubert J.
• Müller, James
• Schwaiger, Markus
• Siewert, Jörg Rüdiger

Titel

Fluorodeoxyglucose‐Positron Emission Tomography in Adenocarcinomas of the Distal Esophagus and Cardia

Ist Teil von

• World journal of surgery, 2003-09, Vol.27 (9), p.1035-1039

Ort / Verlag

New York: Springer‐Verlag

Erscheinungsjahr

2003

Link zum Volltext

Quelle

Wiley Online Library Journals Frontfile Complete

Beschreibungen/Notizen

• Adenocarcinomas of the esophagogastric junction (AEG) are now recognized as a separate tumor entity with increasing incidence. The aim of the present study was to evaluate whether positron emission tomography (PET) using the glucose analog F‐18‐fluorodeoxyglucose (FDG) can be used for metabolic characterization of this tumor type. Fifty‐two patients with histologically proven, locally advanced AEG (distal esophagus, type I: n = 31; cardia, type II: n = 21) were studied by FDG‐PET. None of the tumors had been previously treated. Findings of endoscopy (growth type), endoluminal ultrasound (uT, uN), computed tomography (cN, cranio‐caudal extent, tumor thickness), histological evaluation (Lauren classification, tumor grade), anatomical classification, and survival were correlated with the results of FDG‐PET. There was no correlation between FDG uptake and clinical stage, grade, Lauren classification, or survival. All AEG I tumors were visualized by FDG‐PET with high contrast, whereas FDG uptake by five AEG II tumors (24%) did not differ from background activity. In a quantitative analysis, mean FDG uptake of AEG I tumors was 1.6 times higher than that of AEG II tumors (p = 0.0005). PET can be used to visualize type I adenocarcinomas of the esophagogastric junction (AEG I). In AEG II tumors, however, the use of FDG‐PET appears to be limited. The significantly higher FDG uptake of AEG I tumors compared to AEG II tumors suggests that these two tumor types differ in glucose utilization. This finding strengthens the hypothesis that AEG I and AEG II are two different tumor entities.