Article
Assessment of pseudoprogression in primary and secondary GBM using FET PET and molecular genetics
Search Medline for
Authors
-
Hosai Sadat
- Heinrich-Heine-Universität, Universitätsklinikum, Klinik für Neurochirurgie, Düsseldorf, Deutschland
-
Hans-Jakob Steiger
- Heinrich-Heine-Universität, Universitätsklinikum, Klinik für Neurochirurgie, Düsseldorf, Deutschland
-
Marion Rapp
- Heinrich-Heine-Universität, Universitätsklinikum, Klinik für Neurochirurgie, Düsseldorf, Deutschland
-
Michael Sabel
- Heinrich-Heine-Universität, Universitätsklinikum, Klinik für Neurochirurgie, Düsseldorf, Deutschland
-
Marcel Alexander Kamp
- Heinrich-Heine-Universität, Universitätsklinikum, Klinik für Neurochirurgie, Düsseldorf, Deutschland
-
Norbert Galldiks
- Uniklinik Köln, Klinik für Neurologie, Köln, Deutschland
-
Karl-Josef Langen
- Forschungszentrum Jülich, Institut für Neurowissenschaften und Medizin, Jülich, Deutschland
-
Gabriele Stoffels
- Forschungszentrum Jülich, Institut für Neurowissenschaften und Medizin, Jülich, Deutschland
| Published: | June 18, 2018 |
|---|
Outline
Text
Objective: One of the major challenges in GBM treatment is to differentiate between tumor progression (TP) and pseudoprogression (PsP). The aim of this study was to analyze
- 1.
- the incidence of TP and PsP in primary and secondary GBM (pGBM, sGBM),
- 2.
- the role of PET using F-18-fluoroethyltyrosine (FET PET) to differentiate TB and PsP and
- 3.
- the predictive value of clinical and molecular markers to identify PsP.
Methods: Diagnosis of TP vs. PsP in patients with GBM after initial therapy was confirmed either by histopathology or by radiological follow-up according to the RANO criteria. Age, molecular markers (IDH, MGMT), KPS, extent of resection, timing following radiation and number of operations were correlated with occurrence of PsP. Accuracy of FET PET to differentiate TB and PsP was only evaluated in patients with histopathological confirmation.
Results: From 2002 to 2017 initial MRI findings following therapy were suspicious for TP in 220 pGBM and 27 sGBM (f=74 vs. 10, m=146 vs. 17, mean age=59,1 vs. 41,6y, IDH mutated n=5 vs. 15, MGMT methylated n=65 vs. 11).Of these, 70% of pGBM and 63% of sGBM had a previous complete resection. In 101 pGBM (45.9%) and 12 sGBM (44.4%) a PsP was diagnosed histopathologically (26.7 vs. 33.3%) or according to RANO criteria (73.3 vs. 66.7%) (median time 3 vs. 17 months following radiochemotherapy). There was a significant correlation between the occurrence of PsP and methylated MGMT (p < 0.001) in pGBM. In contrast, IDH status, KPS, age, number of previous resections and extent of resection showed no correlation with the occurrence of PsP, neither in pGBM nor in sGBM. FET PET in patients with histopathology (88 pGBM, 4 sGBM, 17 cases of PSP) yielded a sensitivity of 91% and specificity of 44% (PPV=88%, NPV=50%). OAS (p<0.001) as well as PFS (p<0.001) were significantly increased in pGBM with PsP.
Conclusion: PsP was associated with methylated MGMT in pGBM only. Incidence of PsP was similar in sGBM but no predictive factors could be identified. FET PET shows a high sensitivity in assessing PsP but an unusual low specificity probably caused by a selection bias. In contrast to sGBM OAS and PFS were increased in pGBM with confirmed PsP.
