Sustained focal antitumor activity of bevacizumab in recurrent glioblastoma

Oliver Bähr*, Patrick N. Harter, Lutz M. Weise, Se Jong You, Michel Mittelbronn, Michael W. Ronellenfitsch, Johannes Rieger, Joachim P. Steinbach, Elke Hattingen

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

26 Citations (Scopus)


Objectives: To investigate the relevance of bevacizumab (BEV)-induced diffusion-restricted lesions and T1-hyperintense lesions in patients with recurrent glioblastoma. Methods: We prospectively screened 74 BEV-treated patients with recurrent glioblastoma for (1) diffusion-restricted lesions and/or, (2) lesions with a hyperintense signal on precontrast T1-weighted images. We further evaluated overall survival (OS), histopathology of the lesions, and patterns of progression. Results: Twenty-five of 74 patients (34%) developed T1-hyperintense lesions, whereas diffusionrestricted lesions could be detected in 35 of 74 patients (47%). In 21 of 74 patients (28%), the lesions displayed both features ("double-positive"). OS for patients with double-positive lesions was 13.0 months; patients with neither of these lesions had an OS of 6.6 months (p < 0.005). Histologic evaluation of double-positive lesions revealed extensive calcified necrosis in 4 of 4 patients. Notably, these double-positive lesions were rarely involved in further tumor progression. However, they were associated with an increase in distant recurrences at BEV failure. Conclusions: BEV-induced double-positive MRI lesions are a predictive imaging marker associated with a substantial survival benefit and with improved local control in patients with recurrent glioblastoma. Our data suggest that these lesions are the result of a sustained focal antitumor activity of BEV.

Original languageEnglish
Pages (from-to)227-234
Number of pages8
Issue number3
Publication statusPublished - 15 Jul 2014
Externally publishedYes


Dive into the research topics of 'Sustained focal antitumor activity of bevacizumab in recurrent glioblastoma'. Together they form a unique fingerprint.

Cite this