Pseudoprogression in glioblastoma patients: the impact of extent of resection

Hun Ho Park, Tae Hoon Roh, Seok Gu Kang, Eui Hyun Kim, Chang Ki Hong, Se Hoon Kim, Sung Soo Ahn, Seung Koo Lee, Hye Jin Choi, Jaeho Cho, Sun Ho Kim, Kyu Sung Lee, Chang Ok Suh, Jong Hee Chang

Research output: Contribution to journalArticlepeer-review

11 Citations (Scopus)

Abstract

Pseudoprogression (psPD) is a radiation-induced toxicity that has substantial neurological consequence in glioblastoma (GBM) patients. MGMT promoter methylation has been shown to be an important prognostic factor of psPD, but the significance of extent of resection (EOR) remains unclear. We performed a retrospective analysis on newly diagnosed GBM patients with assessable MGMT promoter status who underwent the Stupp protocol. EOR was grouped into gross total resection (GTR), subtotal resection (STR), partial resection (PR) and stereotactic biopsy. Contrast enhancing lesion enlargement was classified as psPD or non-psPD. Among a total of 101 patients, GTR, STR, PR and stereotactic biopsy was performed in 57 (56.4 %), 34 (33.7 %), 9 (8.9 %) and 1 patient (1 %), respectively. Follow-up imaging at the end of Stupp protocol classified 45 patients (44.6 %) as psPD and 56 (55.4 %) as non-psPD. psPD was observed in 24 (61.5 %) of 39 patients with methylated MGMT promoter and 21 (33.9 %) of 62 patients with unmethylated MGMT promoter (p < 0.01). psPD was documented in 17 (29.8 %), 19 (55.9 %), 8 (88.9 %) and 1 (100 %) patient with GTR, STR, PR and stereotactic biopsy (p < 0.01), respectively. On multivariate analysis MGMT promoter status (OR 3.36, 95 % CI 1.36–8.34) and EOR (OR 4.12, 95 % CI 1.71–9.91) were independent predictors of psPD. A Cox proportional hazards model showed that MGMT status (HR 2.51, p < 0.01) and EOR (HR 2.99, p < 0.01) significantly influenced survival. MGMT status and EOR have a significant impact on psPD. GTR can reduce the side effects of psPD and prolong survival.

Original languageEnglish
Pages (from-to)559-566
Number of pages8
JournalJournal of Neuro-Oncology
Volume126
Issue number3
DOIs
Publication statusPublished - 2016 Feb 1

Bibliographical note

Funding Information:
This study was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, Science and Technology (NRF-2014R1A1A2058058).

Publisher Copyright:
© 2015, Springer Science+Business Media New York.

All Science Journal Classification (ASJC) codes

  • Oncology
  • Neurology
  • Clinical Neurology
  • Cancer Research

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