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J Nucl Med. 2008; 49 (Supplement 1):58P
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Oncology-Clinical Diagnosis: Solid Tumors

GI Cancers - Esophagus, Gastric and Pancreas

Rapamycin induced "stunning" on FDG PET/CT in pancreatic cancer

Heather Jacene1, Oleg Teytelboym1, Wen Wee Ma1, Wells Messersmith1, Antonio Jimeno1, Daniel Laheru1, Manuel Hidalgo1 and Richard Wahl1

1 Johns Hopkins University, Baltimore, Maryland

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Objectives: Rapamycin is an anti-tumor agent which inhibits mTOR, a serine-threonine kinase important for cell cycle regulation and closely linked to glycolysis. We evaluated early FDG PET/CT to predict response of advanced pancreatic cancer to rapamycin in patients.

Methods: 15 patients (13 M, mean age 61±10) with advanced pancreatic cancer were treated with rapamycin (5 mg/day) on a phase II clinical trial. FDG PET/CT scans were obtained at baseline and after 1 cycle of rapamycin (28 days). SUVleanmax (SUL) was determined in up to 10 target lesions per patient. Percent change in SUL was calculated and metabolic response categorized by EORTC PET response criteria (PET) and correlated with tumor response by RECIST criteria. Early PET response was correlated with progression free survival (PFS).

Results: By PET, 8 patients (53%) had a partial metabolic response (PMR), 1 (7%) had stable disease (SD), and 6 (40%) progressed (PD) (5 with new FDG-avid lesions). Percent change of SUL in target lesions was not significantly different between those with PMR and PD (-21±38% vs. 4±38%, p=0.25). By RECIST, 9 patients (60%) had SD and 6 (40%) progressed. All 9 patients with a PMR or SD by PET had SD by RECIST. All 6 patients with PD by RECIST had PD by PET. Early response assessment by PET and RECIST completely agreed ({chi}2 test, p<0.01). PFS was not predicted by early response by PET or RECIST with median time to progression of 52±12 days in patients with PD by PET or RECIST and 59±27 days in patients without PD (Mann-Whitney U, p=0.42).

Conclusions: Early metabolic response of pancreatic cancer to rapamycin is consistent with transiently SD but does not correlate with PFS, despite declines in FDG uptake in 53% of our patients. This suggests that rapamycin may "stun" tumor glycolysis without markedly affecting tumor growth.





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 Jacene, H.
Right arrow Articles by Wahl, R.
PubMed
Right arrow Articles by Jacene, H.
Right arrow Articles by Wahl, R.