Intra-individual comparison of  68 Ga-PSMA-11 and  18 F-DCFPyL normal-organ biodistribution

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Abstract

Purpose

Detailed data comparing the biodistribution of PSMA radioligands is still scarce, raising concerns regarding the comparability of different compounds. We investigated differences in normal-organ biodistribution and uptake variability between the two most commonly PSMA tracers in clinical use, ⁶⁸Ga-PSMA-11 and ¹⁸F-DCFPyL.

Methods

This retrospective analysis included 34 patients with low tumor burden referred for PET/CT imaging with ⁶⁸Ga-PSMA-11 and subsequently ¹⁸F-DCFPyL. Images were acquired with 4 cross-calibrated PET/CT systems. Volumes of interest were placed on major salivary and lacrimal glands, liver, spleen, duodenum, kidneys, bladder, blood-pool and muscle. Normal-organ biodistribution of both tracers was then quantified as SUV _peak and compared using paired tests, linear regression and Bland-Altman analysis. Between-patient variability was also assessed. Clinical and protocol variables were investigated for possible interference.

Results

For both tracers the highest uptake was found in the kidneys and bladder and low background activity was noted across all scans. In the quantitative analysis there was significantly higher uptake of ⁶⁸Ga-PSMA-11 in the kidneys, spleen and major salivary glands ( p < 0.001), while the liver exhibited slightly higher ¹⁸F-DCFPyL uptake ( p = 0.001, mean bias 0.79 ± 1.30). The lowest solid-organ uptake variability was found in the liver (COV 21.9% for ⁶⁸Ga-PSMA-11, 22.5% for ¹⁸F-DCFPyL). There was a weak correlation between ¹⁸F-DCFPyL uptake time and liver SUV _peak (r = 0.488, p = 0.003) and, accordingly, patients scanned at later time-points had a larger mean bias between the two tracers’ liver uptake values (0.05 vs 1.46, p = 0.001).

Conclusion

Normal tissue biodistribution patterns of ⁶⁸Ga-PSMA-11 and ¹⁸F-DCFPyL were similar, despite subtle differences in quantitative values. Liver uptake showed an acceptable intra-patient agreement and low inter-patient variability between the two tracers, allowing its use as a reference organ for thresholding scans in the qualitative comparison of PSMA expression using these different tracers.

Electronic supplementary material

The online version of this article (10.1186/s40644-019-0211-y) contains supplementary material, which is available to authorized users.

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Most cited references 30

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From RECIST to PERCIST: Evolving Considerations for PET response criteria in solid tumors.

Richard L. Wahl, Heather Jacene, Yvette Kasamon … (2009)

The purpose of this article is to review the status and limitations of anatomic tumor response metrics including the World Health Organization (WHO) criteria, the Response Evaluation Criteria in Solid Tumors (RECIST), and RECIST 1.1. This article also reviews qualitative and quantitative approaches to metabolic tumor response assessment with (18)F-FDG PET and proposes a draft framework for PET Response Criteria in Solid Tumors (PERCIST), version 1.0. PubMed searches, including searches for the terms RECIST, positron, WHO, FDG, cancer (including specific types), treatment response, region of interest, and derivative references, were performed. Abstracts and articles judged most relevant to the goals of this report were reviewed with emphasis on limitations and strengths of the anatomic and PET approaches to treatment response assessment. On the basis of these data and the authors' experience, draft criteria were formulated for PET tumor response to treatment. Approximately 3,000 potentially relevant references were screened. Anatomic imaging alone using standard WHO, RECIST, and RECIST 1.1 criteria is widely applied but still has limitations in response assessments. For example, despite effective treatment, changes in tumor size can be minimal in tumors such as lymphomas, sarcoma, hepatomas, mesothelioma, and gastrointestinal stromal tumor. CT tumor density, contrast enhancement, or MRI characteristics appear more informative than size but are not yet routinely applied. RECIST criteria may show progression of tumor more slowly than WHO criteria. RECIST 1.1 criteria (assessing a maximum of 5 tumor foci, vs. 10 in RECIST) result in a higher complete response rate than the original RECIST criteria, at least in lymph nodes. Variability appears greater in assessing progression than in assessing response. Qualitative and quantitative approaches to (18)F-FDG PET response assessment have been applied and require a consistent PET methodology to allow quantitative assessments. Statistically significant changes in tumor standardized uptake value (SUV) occur in careful test-retest studies of high-SUV tumors, with a change of 20% in SUV of a region 1 cm or larger in diameter; however, medically relevant beneficial changes are often associated with a 30% or greater decline. The more extensive the therapy, the greater the decline in SUV with most effective treatments. Important components of the proposed PERCIST criteria include assessing normal reference tissue values in a 3-cm-diameter region of interest in the liver, using a consistent PET protocol, using a fixed small region of interest about 1 cm(3) in volume (1.2-cm diameter) in the most active region of metabolically active tumors to minimize statistical variability, assessing tumor size, treating SUV lean measurements in the 1 (up to 5 optional) most metabolically active tumor focus as a continuous variable, requiring a 30% decline in SUV for "response," and deferring to RECIST 1.1 in cases that do not have (18)F-FDG avidity or are technically unsuitable. Criteria to define progression of tumor-absent new lesions are uncertain but are proposed. Anatomic imaging alone using standard WHO, RECIST, and RECIST 1.1 criteria have limitations, particularly in assessing the activity of newer cancer therapies that stabilize disease, whereas (18)F-FDG PET appears particularly valuable in such cases. The proposed PERCIST 1.0 criteria should serve as a starting point for use in clinical trials and in structured quantitative clinical reporting. Undoubtedly, subsequent revisions and enhancements will be required as validation studies are undertaken in varying diseases and treatments.

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F-18 labelled PSMA-1007: biodistribution, radiation dosimetry and histopathological validation of tumor lesions in prostate cancer patients

Frederik L. Giesel, B Hadaschik, Christopher J Cardinale … (2016)

Purpose The prostate-specific membrane antigen (PSMA) targeted positron-emitting-tomography (PET) tracer 68Ga-PSMA-11 shows great promise in the detection of prostate cancer. However, 68Ga has several shortcomings as a radiolabel including short half-life and non-ideal energies, and this has motivated consideration of 18F-labelled analogs. 18F-PSMA-1007 was selected among several 18F-PSMA-ligand candidate compounds because it demonstrated high labelling yields, outstanding tumor uptake and fast, non-urinary background clearance. Here, we describe the properties of 18F-PSMA-1007 in human volunteers and patients. Methods Radiation dosimetry of 18F-PSMA-1007 was determined in three healthy volunteers who underwent whole-body PET-scans and concomitant blood and urine sampling. Following this, ten patients with high-risk prostate cancer underwent 18F-PSMA-1007 PET/CT (1 h and 3 h p.i.) and normal organ biodistribution and tumor uptakes were examined. Eight patients underwent prostatectomy with extended pelvic lymphadenectomy. Uptake in intra-prostatic lesions and lymph node metastases were correlated with final histopathology, including PSMA immunostaining. Results With an effective dose of approximately 4.4–5.5 mSv per 200–250 MBq examination, 18F-PSMA-1007 behaves similar to other PSMA-PET agents as well as to other 18F-labelled PET-tracers. In comparison to other PSMA-targeting PET-tracers, 18F-PSMA-1007 has reduced urinary clearance enabling excellent assessment of the prostate. Similar to 18F-DCFPyL and with slightly slower clearance kinetics than PSMA-11, favorable tumor-to-background ratios are observed 2–3 h after injection. In eight patients, diagnostic findings were successfully validated by histopathology. 18F-PSMA-1007 PET/CT detected 18 of 19 lymph node metastases in the pelvis, including nodes as small as 1 mm in diameter. Conclusion 18F-PSMA-1007 performs at least comparably to 68Ga-PSMA-11, but its longer half-life combined with its superior energy characteristics and non-urinary excretion overcomes some practical limitations of 68Ga-labelled PSMA-targeted tracers. Electronic supplementary material The online version of this article (doi:10.1007/s00259-016-3573-4) contains supplementary material, which is available to authorized users.

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Initial Evaluation of [(18)F]DCFPyL for Prostate-Specific Membrane Antigen (PSMA)-Targeted PET Imaging of Prostate Cancer.

Zsolt Szabó, Esther Mena, Steven Rowe … (2015)

Prostate-specific membrane antigen (PSMA) is a recognized target for imaging prostate cancer. Here we present initial safety, biodistribution, and radiation dosimetry results with [(18)F]DCFPyL, a second-generation fluorine-18-labeled small-molecule PSMA inhibitor, in patients with prostate cancer.

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Author and article information

Contributors

Gonçalo Ferreira:

ORCID: http://orcid.org/0000-0001-9588-7203

+351 911 131 051 , goncalo.ferreira@ipoporto.min-saude.pt

Amir Iravani: amir.iravani@petermac.og

Michael S. Hofman: michael.hofman@petermac.org

Rodney J. Hicks: rod.hicks@petermac.org

Journal

Journal ID (nlm-ta): Cancer Imaging

Journal ID (iso-abbrev): Cancer Imaging

Title: Cancer Imaging

Publisher: BioMed Central (London )

ISSN (Print): 1740-5025

ISSN (Electronic): 1470-7330

Publication date (Electronic): 15 May 2019

Publication date PMC-release: 15 May 2019

Publication date Collection: 2019

Volume: 19

Electronic Location Identifier: 23

Affiliations

[1 ]ISNI 0000 0004 0631 0608, GRID grid.418711.a, Nuclear Medicine Department, , Instituto Português de Oncologia do Porto, ; Rua Dr. António Bernardino de Almeida, 4200-072 Porto, Portugal

[2 ]ISNI 0000000403978434, GRID grid.1055.1, Centre for Molecular Imaging, Department of Cancer Imaging, , Peter MacCallum Cancer Centre, ; Melbourne, Victoria Australia

[3 ]ISNI 0000 0001 2179 088X, GRID grid.1008.9, Sir Peter MacCallum Department of Oncology, , University of Melbourne, ; Melbourne, Victoria Australia

Author information

Gonçalo Ferreira http://orcid.org/0000-0001-9588-7203

Article

Publisher ID: 211

DOI: 10.1186/s40644-019-0211-y

PMC ID: 6521415

PubMed ID: 31092293

SO-VID: f4f0707b-a7cc-4165-8c93-536871527d9c

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 18 January 2019

Date accepted : 1 May 2019

Custom metadata

Keywords: 18f-dcfpyl,68ga-psma-11,pet/ct,biodistribution,prostate cancer

Data availability:

Keywords: 18f-dcfpyl, 68ga-psma-11, pet/ct, biodistribution, prostate cancer

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