Makoto Sakane1, Mitsuaki Tatsumi2, Masatoshi Hori3, Hiromitsu Onishi4, Takahiro Tsuboyama5, Atsushi Nakamoto6, Takashi Ota7, Hidetoshi Eguchi8, Kenichi Wakasa9, Jun Hatazawa10, Noriyuki Tomiyama11. 1. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: m-sakane@radiol.osaka-u.ac.jp. 2. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan; Department of Nuclear Medicine and Tracer Kinetics, Osaka University Graduate School of Medicine, Japan. Electronic address: m-tatsumi@radiol.med.osaka-u.ac.jp. 3. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: mhori@radiol.med.osaka-u.ac.jp. 4. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: h-onishi@radiol.med.osaka-u.ac.jp. 5. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: ttsuboyama@gmail.com. 6. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: rad117@osaka-med.ac.jp. 7. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: t-ota@radiol.med.osaka-u.ac.jp. 8. Department of Gastroenterological Surgery, Osaka University Graduate School of Medicine, Japan. Electronic address: heguchi@gesurg.med.osaka-u.ac.jp. 9. Department of Diagnostic Pathology, Ishikiriseiki Hospital, Japan. 10. Department of Nuclear Medicine and Tracer Kinetics, Osaka University Graduate School of Medicine, Japan. Electronic address: hatazawa@tracer.med.osaka-u.ac.jp. 11. Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita-shi, Osaka, 565-0871, Japan. Electronic address: tomiyama@radiol.med.osaka-u.ac.jp.
Abstract
PURPOSE: The purpose of this study was to investigate the clinical potential of 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography/computed tomography (FDG PET/CT) to evaluate histopathologic effects of preoperative chemoradiotherapy (CRT) in pancreatic adenocarcinoma, with particular focus on volumetric PET/CT parameters. MATERIAL AND METHODS: This study included 25 patients with pancreatic adenocarcinoma who underwent radical surgery after gemcitabine- and S-1-based preoperative-CRT. The extent of residual tumor was graded using the Evans grading systems, and patients with more than 50% destruction of tumor cells were defined as responder. Peak SUV corrected for lean body mass (SULpeak), metabolic tumor volume (MTV) with a threshold of SUV=2.0, total lesion glycolysis (TLG) of pre- and post-CRT, and reduction rates of SULpeak in those parameters were assessed by PET/CT. These parameters were compared using the student's t-test between responder and non-responder. The treatment effect was also assessed by contingency table analysis divided with median value of each parameter using chi-square tests. RESULTS: Eight patients (32%) showed histopathologic poor response (Evans grade I), 11 cases (44%) had mild response (Evans grade IIa), and six cases (24%) had moderate response (Evans grade IIb); therefore, six cases (24%) were assigned to responders and others 19 cases (76%) were non-responders. With regards to volumetric PET parameters, post-CRT SULpeak of responders was significantly lower than that of non-responders (p=0.013). Post-CRT MTV and TLG were negative for all six cases of responders. There were significant differences between responder and non-responder on the contingency table analysis of post-CRT MTV and TLG status (p=0.014 for both). CONCLUSIONS: This study demonstrated that the volumetric PET/CT parameters, higher post-treatment SULpeak and positive MTV/TLG could predict the unfavorable histopathological effects of CRT in patients with pancreatic adenocarcinoma.
PURPOSE: The purpose of this study was to investigate the clinical potential of 2-deoxy-2-[18F]fluoro-d-glucose positron emission tomography/computed tomography (FDG PET/CT) to evaluate histopathologic effects of preoperative chemoradiotherapy (CRT) in pancreatic adenocarcinoma, with particular focus on volumetric PET/CT parameters. MATERIAL AND METHODS: This study included 25 patients with pancreatic adenocarcinoma who underwent radical surgery after gemcitabine- and S-1-based preoperative-CRT. The extent of residual tumor was graded using the Evans grading systems, and patients with more than 50% destruction of tumor cells were defined as responder. Peak SUV corrected for lean body mass (SULpeak), metabolic tumor volume (MTV) with a threshold of SUV=2.0, total lesion glycolysis (TLG) of pre- and post-CRT, and reduction rates of SULpeak in those parameters were assessed by PET/CT. These parameters were compared using the student's t-test between responder and non-responder. The treatment effect was also assessed by contingency table analysis divided with median value of each parameter using chi-square tests. RESULTS: Eight patients (32%) showed histopathologic poor response (Evans grade I), 11 cases (44%) had mild response (Evans grade IIa), and six cases (24%) had moderate response (Evans grade IIb); therefore, six cases (24%) were assigned to responders and others 19 cases (76%) were non-responders. With regards to volumetric PET parameters, post-CRT SULpeak of responders was significantly lower than that of non-responders (p=0.013). Post-CRT MTV and TLG were negative for all six cases of responders. There were significant differences between responder and non-responder on the contingency table analysis of post-CRT MTV and TLG status (p=0.014 for both). CONCLUSIONS: This study demonstrated that the volumetric PET/CT parameters, higher post-treatment SULpeak and positive MTV/TLG could predict the unfavorable histopathological effects of CRT in patients with pancreatic adenocarcinoma.