Introduction. The aim of this study was to determine the frequency of pseudoprogression in a cohort of glioblastoma (GBM) patients following radiotherapy/temozolomide (RT/TMZ) by comparing Macdonald criterial to Response Assessment in Neuro-Oncology (RANO) criteria. The impact on prognosis and survival analysis was also studied. Materials and Methods. All patients receiving RT/TMZ for newly diagnosed GBM from January 2005 to December 2009 were retrospectively evaluated, and demographic, clinical, radiographic, treatment, and survival data were reviewed. Updated RANO criteria were used for the evaluation of the pre-RT and post-RT MRI and compared to classic Macdonald criteria. Survival data was evaluated using the Kaplan-Meier and log-rank analysis. Results and Discussion. 70 patients were available for full radiological response assessment. Early progression was confirmed in 42 patients (60%) according to Macdonald criteria and 15 patients (21%) according to RANO criteria. Pseudoprogression was identified in 10 (23.8%) or 2 (13.3%) patients in Macdonald and RANO groups, respectively. Cumulative survival of pseudoprogression group was higher than that of true progression group and not statistically different from the non-progressive disease group. Conclusion. In this cohort, the frequency of pseudoprogression varied between 13% and 24%, being overdiagnosed by older Macdonald criteria, which emphasizes the importance of RANO criteria and new radiological biomarkers for correct response evaluation. 1. Introduction The current standard of care for newly diagnosed glioblastoma (GBM) remains surgical resection followed by radiotherapy with concurrent temozolomide (RT/TMZ) and then maintenance temozolomide for at least six months [1]. The addition of chemotherapy introduced new questions regarding biological response of the tumor and the surrounding brain. Pseudoprogression is a phenomenon of subacute imaging changes in human glioma subsequent to radiochemotherapy suggestive of progression, with or without associated clinical sequelae, which resolve spontaneously without further therapy [2]. It was first reported by Hoffman et al. [3] in 1979 and fully described by de Wit et al. [4] in 2004. The underlying pathophysiological mechanisms are not fully understood [5]. Some authors suggest that it likely reflects an inflammatory tissue reaction after a local treatment secondary to vascular and oligodendroglial injury, whereas others associate it with an exaggerated response to effective therapy [2, 6, 7]. The incidence of pseudoprogression, time of occurrence, and
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