Open AccessMedulloblastoma recurrence and metastatic spread are independent of colony-stimulating factor 1 receptor signaling and macrophage survival
Author(s) -
Erin E. Crotty,
Sally J. Smith,
Kenneth Brasel,
Fiona Pakiam,
Emily J. Girard,
Yamicia Connor,
Frédérique Zindy,
Andrew J. Mhyre,
Martine F. Roussel,
James M. Olson
Publication year - 2021
Publication title -
journal of neuro-oncology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.256
H-Index - 114
eISSN - 1573-7373
pISSN - 0167-594X
DOI - 10.1007/s11060-021-03767-x
Subject(s) - medulloblastoma , medicine , foxp3 , sonic hedgehog , microglia , tumor microenvironment , tumor progression , immunophenotyping , cancer research , metastasis , pathology , immunology , biology , immune system , cancer , signal transduction , inflammation , biochemistry , flow cytometry
Tumor infiltration by immunosuppressive myeloid cells or tumor-associated macrophages (TAMs) contributes to tumor progression and metastasis. In contrast to their adult counterparts, higher TAM signatures do not correlate with aggressive tumor behavior in pediatric brain tumors. While prominent TAM infiltrates exist before and after radiation, the degree to which irradiated macrophages and microglia support progression or leptomeningeal metastasis remains unclear. Patients with medulloblastoma often present with distant metastases and tumor recurrence is largely incurable, making them prime candidates for the study of novel approaches to prevent neuroaxis dissemination and recurrence.