PurposeGallium-68 (Ga-68)-labeled tracers for imaging expression of the prostate-specific membrane antigen (PSMA) such as the [68Ga]Ga-PSMA-HBED-CC have already demonstrated high potential for the detection of recurrent prostate cancer. However, compared to Ga-68, a labeling with fluorine-18 (F-18) would offer advantages with respect to availability, production amount, and image resolution. [18F]DCFPyL is a promising F-18-labeled candidate for PSMA-positron emission tomography (PET) imaging that has been recently introduced. In the current study, we aimed to compare [68Ga]Ga-PSMA-HBED-CC and [18F]DCFPyL for clinical use in biochemically relapsed prostate cancer.ProceduresIn 14 selected patients with PSA relapse of prostate cancer, [18F]DCFPyL PET/X-ray computed tomography (CT) was performed in addition to [68Ga]Ga-PSMA-HBED-CC PET/CT. A systematic comparison was carried out between results obtained with both tracers with regard to the number of detected PSMA-positive lesions, the standardized uptake value (SUV)max and the lesion to background ratios.ResultsAll suspicious lesions identified by [68Ga]Ga-PSMA-HBED-CC were also detected with [18F]DCFPyL. In three patients, additional lesions were observed using [18F]DCFPyL PET/CT. The mean SUVmax in the concordant [18F]DCFPyL PSMA-positive lesions was significantly higher as compared to [68Ga]Ga-PSMA-HBED-CC (14.5 vs. 12.2, p = 0.028, n = 15). The mean tumor to background ratios (n = 15) were significantly higher for [18F]DCFPyL compared to [68Ga]Ga-PSMA-HBED-CC using kidney, spleen, or parotid as reference organs (p = 0.006, p = 0.002, p = 0.008), but no significant differences were found using the liver (p = 0.167) or the mediastinum (p = 0.363) as reference organs.Conclusion[18F]DCFPyL PET/CT provided a high image quality and visualized small prostate lesions with excellent sensitivity. [18F]DCFPyL represents a highly promising alternative to [68Ga]Ga-PSMA-HBED-CC for PSMA-PET/CT imaging in relapsed prostate cancer.

Several studies outlined the sensitivity of Ga-labeled PET tracers against the prostate-specific membrane antigen (PSMA) for localization of relapsed prostate cancer in patients with renewed increase in the prostate-specific antigen (PSA), commonly referred to as biochemical recurrence. Labeling of PSMA tracers withF offers numerous advantages, including improved image resolution, longer half-life, and increased production yields. The aim of this study was to assess the PSA-stratified performance of the F-labeled PSMA tracerF-DCFPyL and the Ga-labeled referenceGa-PSMA-HBED-CC. We examined 191 consecutive patients with biochemical recurrence according to standard acquisition protocols usingF-DCFPyL ( = 62, 269.8 MBq, PET scan at 120 min after injection) or Ga-PSMA-HBED-CC ( = 129, 158.9 MBq, 60 min after injection). We determined PSA-stratified sensitivity rates for both tracers and corrected our calculations for Gleason scores using iterative matched-pair analyses. As an orthogonal validation, we directly compared tracer distribution patterns in a separate cohort of 25 patients, sequentially examined with both tracers. After prostatectomy ( = 106), the sensitivity of both tracers was significantly associated with absolute PSA levels ( = 4.3 × 10). Sensitivity increased abruptly, when PSA values exceeded 0.5 μg/L ( = 2.4 × 10). For a PSA less than 3.5 μg/L, most relapses were diagnosed at a still limited stage ( = 3.4 × 10). For a PSA of 0.5-3.5 μg/L, PSA-stratified sensitivity was 88% (15/17) for F-DCFPyL and 66% (23/35) forGa-PSMA-HBED-CC. This significant difference was preserved in the Gleason-matched-pair analysis. Outside of this range, sensitivity was comparably low (PSA < 0.5 μg/L) or high (PSA > 3.5 μg/L). After radiotherapy ( = 85), tracer sensitivity was largely PSA-independent. In the 25 patients examined with both tracers, distribution patterns of F-DCFPyL andGa-PSMA-HBED-CC were strongly comparable ( = 2.71 × 10). However, in 36% of the PSMA-positive patients we detected additional lesions on the F-DCFPyL scan ( = 3.7 × 10). Our data suggest thatF-DCFPyL is noninferior to Ga-PSMA-HBED-CC, while offering the advantages ofF labeling. Our results indicate that imaging with F-DCFPyL may even exhibit improved sensitivity in localizing relapsed tumors after prostatectomy for moderately increased PSA levels. Although the standard acquisition protocols, used forF-DCFPyL and Ga-PSMA-HBED-CC in this study, stipulate different activity doses and tracer uptake times after injection, our findings provide a promising rationale for validation ofF-DCFPyL in future prospective trials.

Advanced renal cell carcinoma (RCC) has a poor prognosis and is characterized by an unpredictable clinical course. The aim of this study was to assess the systemic phospholipid distribution as a possible marker of tumor stage and tumor spread beyond the kidney. To this end, the effect of renal cell carcinoma (RCC) on phospholipid concentrations in blood plasma using 31P NMR spectroscopy was studied in: (a) 29 patients with RCC prior to nephrectomy; (b) 19 healthy volunteers; (c) three patients with other renal tumors (renal metastases of bronchial carcinoma and of renal pelvic carcinoma, and a benign renal tumor). Furthermore, the phospholipid concentrations of eight patients of group (a) were determined 6 months after nephrectomy, when they were in remission. We found considerable deviations in the concentrations of the lysophosphatidylcholines (LPC1, LPC2) in both male and female patients with RCC compared to healthy volunteers (male--LPC1 0.217+/-0.062 vs 0.297+/-0.049 mmol/l, LPC2 0.036+/-0.014 vs 0.068+/-0.024 mmol/l; female--LPC1 0.195+/-0.071 vs 0.296+/-0.044 mmol/l, LPC2 0.037+/-0.027 vs 0.044+/-0.014 mmol/l). In addition, female patients with RCC showed lower concentrations of phosphatidylcholines (PC; 1.409+/-0.268 vs 1.947+/-0.259 mmol/l). The low phospholipid concentrations normalized for patients in remission. Phospholipid concentrations were found to depend on tumor stage and metastatic spread. The deviations in phospholipid concentrations (LPC1, LPC2, PC) observed may be attributable to systemic effects caused by the tumor as well as changes in enzyme activities.

Tho ma s Sta ud ing er -He rau sge be r 2. Aufl age

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