Moran Artzi1, Felix Bokstein2, Deborah T Blumenthal3, Orna Aizenstein4, Gilad Liberman5, Benjamin W Corn6, Dafna Ben Bashat7. 1. Functional Brain Center, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel. Electronic address: artzimy@gmail.com. 2. Neuro-Oncology Service, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Electronic address: felixb@tlvmc.gov.il. 3. Neuro-Oncology Service, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Electronic address: deborahblumenthal@gmail.com. 4. Functional Brain Center, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Electronic address: Ornaaizenstein@gmail.com. 5. Functional Brain Center, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Gonda Multidisciplinary Brain Research Center, Bar Ilan University, Ramat Gan, Israel. Electronic address: giladliberman@gmail.com. 6. Functional Brain Center, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Institute of Radiotherapy, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel. Electronic address: bencorn@tlvmc.gov.il. 7. Functional Brain Center, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel; Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel Aviv, Israel. Electronic address: dafnab@tlvmc.gov.il.
Abstract
BACKGROUND: Treatment with bevacizumab is associated with substantial radiologic response in patients with glioblastoma (GB). However, following this initial response, changes in T2-weighted MRI signal may develop, suggesting an infiltrative pattern of tumor progression. The aim of this study was to differentiate between vasogenic-edema versus tumor-infiltrative area in GB patients. METHODS AND MATERIALS: Fourteen patients with GB were longitudinally scanned, before and during intravenous bevacizumab therapy (5/10mg/kg every 2-weeks). A total of 40 MR scans including conventional, diffusion, dynamic susceptibility contrast, dynamic contrast enhancement imaging, and MR-spectroscopy (MRS) were analyzed. Classification of non-enhancing fluid-attenuation-inversion-recovery (FLAIR) area was performed based on mean diffusivity, cerebral blood volume and flow maps, and further characterized using multiple MRI parameters. RESULTS: The non-enhancing FLAIR lesion area was classified into: vasogenic-edema, characterized by reduced perfusion and increased FLAIR values; or tumor-infiltrative area, characterized by increased perfusion. Tumor-infiltrative area demonstrated a higher malignant pattern on MRS compared to areas of vasogenic-edema. Substantial reductions of the enhanced T1-weighted (58 ± 10%) and hyperintense FLAIR (53 ± 9%) lesion volumes were detected mainly during the first weeks of therapy, with a shift to an infiltrative pattern of tumor progression thereafter, as detected by an increase in tumor-infiltrative area in the majority of patients, which correlated with progression-free survival (week 8: r=-0.86, p=0.003, week 16: r=-0.99, p=0.001). CONCLUSION: Characterization of non-enhancing hyperintense FLAIR lesion area in GB patients can provide an MR-based biomarker, indicating a shift to an infiltrative progression pattern, and may improve therapy response assessment in patients following bevacizumab therapy.
BACKGROUND: Treatment with bevacizumab is associated with substantial radiologic response in patients with glioblastoma (GB). However, following this initial response, changes in T2-weighted MRI signal may develop, suggesting an infiltrative pattern of tumor progression. The aim of this study was to differentiate between vasogenic-edema versus tumor-infiltrative area in GB patients. METHODS AND MATERIALS: Fourteen patients with GB were longitudinally scanned, before and during intravenous bevacizumab therapy (5/10mg/kg every 2-weeks). A total of 40 MR scans including conventional, diffusion, dynamic susceptibility contrast, dynamic contrast enhancement imaging, and MR-spectroscopy (MRS) were analyzed. Classification of non-enhancing fluid-attenuation-inversion-recovery (FLAIR) area was performed based on mean diffusivity, cerebral blood volume and flow maps, and further characterized using multiple MRI parameters. RESULTS: The non-enhancing FLAIR lesion area was classified into: vasogenic-edema, characterized by reduced perfusion and increased FLAIR values; or tumor-infiltrative area, characterized by increased perfusion. Tumor-infiltrative area demonstrated a higher malignant pattern on MRS compared to areas of vasogenic-edema. Substantial reductions of the enhanced T1-weighted (58 ± 10%) and hyperintense FLAIR (53 ± 9%) lesion volumes were detected mainly during the first weeks of therapy, with a shift to an infiltrative pattern of tumor progression thereafter, as detected by an increase in tumor-infiltrative area in the majority of patients, which correlated with progression-free survival (week 8: r=-0.86, p=0.003, week 16: r=-0.99, p=0.001). CONCLUSION: Characterization of non-enhancing hyperintense FLAIR lesion area in GB patients can provide an MR-based biomarker, indicating a shift to an infiltrative progression pattern, and may improve therapy response assessment in patients following bevacizumab therapy.
Authors: N Bahrami; D Piccioni; R Karunamuni; Y-H Chang; N White; R Delfanti; T M Seibert; J A Hattangadi-Gluth; A Dale; N Farid; C R McDonald Journal: AJNR Am J Neuroradiol Date: 2018-04-05 Impact factor: 3.825
Authors: I Hwang; S H Choi; C-K Park; T M Kim; S-H Park; J K Won; I H Kim; S-T Lee; R-E Yoo; K M Kang; T J Yun; J-H Kim; C-H Sohn Journal: AJNR Am J Neuroradiol Date: 2019-12-05 Impact factor: 3.825
Authors: Markus Hutterer; Elke Hattingen; Christoph Palm; Martin Andreas Proescholdt; Peter Hau Journal: Neuro Oncol Date: 2014-12-27 Impact factor: 12.300