Total Body Metabolic Tumor Response in ALK Positive Non-Small Cell Lung Cancer Patients Treated with ALK InhibitionKerner, G. S. M. A., Koole, M. J. B., Bongaerts, A. H. H., Pruim, J., Groen, H. J. M. & CTMM Air Force Consortium, 3-May-2016, In : PLoS ONE. 11, 5, 10 p., e0149955.
Research output: Contribution to journal › Article › Academic › peer-review
In ALK-positive advanced NSCLC, crizotinib has a high response rate and effectively increases quality of life and survival. CT measurement of the tumor may insufficiently reflect the actual tumor load changes during targeted therapy with crizotinib. We explored whether F-18-FDG PET measured metabolic changes are different from CT based changes and studied the impact of these changes on disease progression.
F-18-FDG PET/CT was performed prior to and after 6 weeks of crizotinib treatment. Tumor response on CT was classified with RECIST 1.1, while F-18-FDG PET response was assessed according to the 1999 EORTC recommendations and PERCIST criteria. Agreement was assessed using McNemars test. During follow-up, patients received additional PET/CT during crizotinib treatment and second generation ALK inhibition. We assessed whether PET was able to detect progression earlier then CT.
In this exploratory study 15 patients were analyzed who were treated with crizotinib. There was a good agreement in the applicability of CT and F-18-FDG PET/CT using the EORTC recommendations. During first line crizotinib and subsequent second line ALK inhibitors, PET was able to detect progression earlier then CT in 10/22 (45%) events of progression and in the others disease progression was detected simultaneously.
In advanced ALK positive NSCLC PET was able to detect progressive disease earlier than with CT in nearly half of the assessments while both imaging tests performed similar in the others.
|Number of pages||10|
|Publication status||Published - 3-May-2016|
- POSITRON-EMISSION-TOMOGRAPHY, FUSION ONCOGENE, FDG-PET, ADENOCARCINOMA, CRIZOTINIB, EML4-ALK, RECOMMENDATIONS
Dataset: Total Body Metabolic Tumor Response in ALK Positive Non-Small Cell Lung Cancer Patients Treated with ALK Inhibition