M1 macrophage recruitment correlates with worse outcome in SHH Medulloblastomas

Chanhee Lee, Joongyub Lee, Seung Ah Choi, Seung Ki Kim, Kyu Chang Wang, Sung Hye Park, Se Hoon Kim, Ji Yeoun Lee, Ji Hoon Phi

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40 Citations (Scopus)


Background: Recent progress in molecular analysis has advanced the understanding of medulloblastoma (MB) and is anticipated to facilitate management of the disease. MB is composed of 4 molecular subgroups: WNT, SHH, Group 3, and Group 4. Macrophages play a crucial role in the tumor microenvironment; however, the functional role of their activated phenotype (M1/M2) remains controversial. Herein, we investigate the correlation between tumor-associated macrophage (TAM) recruitment within the MB subgroups and prognosis. Methods: Molecular subgrouping was performed by a nanoString-based RNA assay on retrieved snap-frozen tissue samples. Immunohistochemistry (IHC) and immunofluorescence (IF) assays were performed on subgroup identified samples, and the number of polarized macrophages was quantified from IHC. Survival analyses were conducted on collected clinical data and quantified macrophage data. Results: TAM (M1/M2) recruitment in SHH MB was significantly higher compared to that in other subgroups. A Kaplan-Meier survival curve and multivariate Cox regression demonstrated that high M1 expressers showed worse overall survival (OS) and progression-free survival (PFS) than low M1 expressers in SHH MB, with relative risk (RR) values of 11.918 and 6.022, respectively. Conclusion: M1 rather than M2 correlates more strongly with worse outcome in SHH medulloblastoma.

Original languageEnglish
Article number535
JournalBMC cancer
Issue number1
Publication statusPublished - 2018 May 8

Bibliographical note

Funding Information:
The present study was financially supported by a grant from the National R&D Program for Cancer Control, Ministry for Health and Welfare, Republic of Korea (1420020).

Publisher Copyright:
© 2018 The Author(s).

All Science Journal Classification (ASJC) codes

  • Oncology
  • Genetics
  • Cancer Research


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