Prostate cancer: PET with 18F-FDG, 18F- or 11C-acetate, and 18F- or 11C-choline

Abstract

Prostate cancer is biologically and clinically a heterogeneous disease that makes imaging evaluation challenging. The role of imaging in prostate cancer should include diagnosis, localization, and characterization (indolent vs. lethal) of the primary tumor, determination of extracapsular spread, guidance and evaluation of local therapy in organ-confined disease, staging of locoregional lymph nodes, detection of locally recurrent and metastatic disease in biochemical relapse, planning of radiation treatment, prediction and assessment of tumor response to salvage and systemic therapy, monitoring of active surveillance and definition of a trigger for definitive therapy, and prognostication of time to hormone refractoriness in castrate disease and overall survival. To address these tasks effectively, imaging needs to be tailored to the specific phases of the disease in a patient-specific, risk-adjusted manner. In this article, I review the preclinical and clinical evidence on the potential and emerging role of PET with the 3 most commonly studied radiotracers in prostate cancer, namely 18F-FDG, 18F- or 11C-acetate, and 18F- or 11C-choline.

Figures

FIGURE 1

A 67-y-old man with biopsy-confirmed prostate cancer (Gleason score, 8; PSA level, 14.6 ng/mL). 18F-FDG PET/CT shows intense hypermetabolism (maximum SUV, 7.7) in right prostate lobe.

FIGURE 2

Serial 18F-FDG PET/CT and bone scans of 63-y-old man with castrate-resistant metastatic prostate cancer with original primary cancer Gleason score of 9. Rows from top to bottom are scans at baseline (before chemotherapy) and at 4, 8, and 12 mo after initiation of chemotherapy. Columns from left to right are axial CT scans (bone window level), 18F-FDG PET scan, fused PET/CT scans, mid sagittal CT scan (bone window level), PET maximum-intensity-projection images, and 99mTc-methylene diphosphonate bone scans. Concordant decline in overall metabolic activity of metastatic lesions and PSA level is seen with treatment. Sclerosis of osseous lesions increases as corresponding metabolic activity declines with treatment.

FIGURE 3

A 67-y-old man with history of prostate cancer who had undergone resection and had rising PSA level. 11C-acetate–avid right eighth rib metastasis is seen on maximum-intensity projection (A, long arrow) and selected axial fused (B, arrow) and CT (C, arrow) images, with sclerotic changes seen on CT. Additional L4 vertebral metastasis is seen on maximum-intensity-projection image (A, short arrow). (Courtesy of Martin Allen-Auerbach and Johannes Czernin, University of California, Los Angeles.)

FIGURE 4

A 60-y-old man with history of prostate cancer who had undergone resection and had rising PSA level. Right column from top to bottom shows 18F-fluorocholine PET, pelvis CT, and fused PET/CT images demonstrating abnormal accumulation of radiotracer in normal-sized right internal iliac lymph node (arrows). Maximum-intensity-projection image on left shows normal biodistribution of 18F-fluorocholine and no other suggestive lesions. (Courtesy of Mohsen Beheshti, St. Vincent's Hospital, Linz, Austria.)