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Abstract

PURPOSE:

Pseudoprogression (PsP) is characterized by therapy-associated but not tumor growth-associated increases of contrast-enhancing glioblastoma lesions on MRI. Although typically occurring during the first 3 months after radiochemotherapy, PsP may occur later in the course of the disease and may then be particularly difficult to distinguish from true tumor progression. We explored PET using O-(2-[(18)F]fluoroethyl)-L-tyrosine ((18)F-FET-PET) to approach the diagnostic dilemma.

EXPERIMENTAL DESIGN:

Twenty-six patients with glioblastoma that presented with increasing contrast-enhancing lesions later than 3 months after completion of radiochemotherapy underwent (18)F-FET-PET. Maximum and mean tumor/brain ratios (TBRmax and TBRmean) of (18)F-FET uptake as well as time-to-peak (TTP) and patterns of the time-activity curves were determined. The final diagnosis of true progression versus late PsP was based on follow-up MRI using RANO criteria.

RESULTS:

Late PsP occurred in 7 patients with a median time from radiochemotherapy completion of 24 weeks while the remaining patients showed true tumor progression. TBRmax and TBRmean were significantly higher in patients with true progression than in patients with late PsP (TBRmax 2.4 ± 0.1 vs. 1.5 ± 0.2, P = 0.003; TBRmean 2.1 ± 0.1 vs. 1.5 ± 0.2, P = 0.012) whereas TTP was significantly shorter (mean TTP 25 ± 2 vs. 40 ± 2 min, P < 0.001). ROC analysis yielded an optimal cutoff value of 1.9 for TBRmax to differentiate between true progression and late PsP (sensitivity 84%, specificity 86%, accuracy 85%, P = 0.015).

CONCLUSIONS:

O-(2-[(18)F]fluoroethyl)-L-tyrosine PET provides valuable information in assessing the elusive phenomenon of late PsP. 

Author information​

Kebir S1, Fimmers R2, Galldiks N3, Schäfer N4, Mack F5, Schaub C5, Stuplich M5, Niessen M5, Tzaridis T5, Simon M6, Stoffels G7, Langen KJ8, Scheffler B9, Glas M10, Herrlinger U5.

1Division of Clinical Neurooncology, Department of Neurology, University of Bonn Medical Centre, Bonn, Germany. Stem Cell Pathologies, Institute of Reconstructive Neurobiology, University of Bonn, Bonn, Germany. Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany. sied.kebir@ukb.uni-bonn.de.

2Institute for Medical Biometry, Informatics and Epidemiology (IMBIE), University of Bonn Medical Centre, Bonn, Germany.

3Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany. Deptartment of Neurology, University of Cologne, Cologne, Germany. Institute of Neuroscience and Medicine, Forschungszentrum Jülich, Jülich, Germany.

4Division of Clinical Neurooncology, Department of Neurology, University of Bonn Medical Centre, Bonn, Germany. Stem Cell Pathologies, Institute of Reconstructive Neurobiology, University of Bonn, Bonn, Germany. Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany.

5Division of Clinical Neurooncology, Department of Neurology, University of Bonn Medical Centre, Bonn, Germany. Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany.

6Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany. Department of Neurosurgery, Forschungszentrum Jülich, Jülich, Germany.

7Institute of Neuroscience and Medicine, Forschungszentrum Jülich, Jülich, Germany.

8Institute of Neuroscience and Medicine, Forschungszentrum Jülich, Jülich, Germany. Department of Nuclear Medicine, University of Aachen, Aachen, Germany.

9Stem Cell Pathologies, Institute of Reconstructive Neurobiology, University of Bonn, Bonn, Germany.

10Division of Clinical Neurooncology, Department of Neurology, University of Bonn Medical Centre, Bonn, Germany. Stem Cell Pathologies, Institute of Reconstructive Neurobiology, University of Bonn, Bonn, Germany. Center of Integrated Oncology (CIO), Universities of Cologne and Bonn, Bonn, Germany. Clinical Cooperation Unit Neurooncology, MediClin Robert Janker Klinik, Bonn, Germany.