CSF-1R expression in tumor-associated macrophages is associated with worse prognosis in classical Hodgkin lymphoma

Young Wha Koh1, Chansik Park, Dok Hyun Yoon

  • 1Dept of Pathology, University of Ulsan College of Medicine, Asan Medical Center, 88, Olympic-ro 43-gil, Seoul 138-736, South Korea; jrhuh@amc.seoul.kr.

Insights

High colony-stimulating 1 receptor (CSF-1R) expression in non-Hodgkin/Reed-Sternberg (non-HRS) cells indicates a worse prognosis for classical Hodgkin lymphoma (CHL) patients. This correlates with increased tumor macrophages and poorer survival outcomes.

Area of Science:

  • Oncology
  • Immunology
  • Pathology

Background:

  • Classical Hodgkin lymphoma (CHL) is a malignancy of lymphocytes.
  • The tumor microenvironment, including macrophages, plays a role in lymphoma progression.
  • Colony-stimulating 1 receptor (CSF-1R) is involved in macrophage regulation.

Purpose of the Study:

  • To investigate the prognostic significance of CSF-1R expression in both malignant (HRS) and non-malignant (non-HRS) cells in CHL.
  • To correlate CSF-1R expression with tumor-associated macrophage (TAM) infiltration.
  • To assess the impact of CSF-1R expression on patient survival outcomes.

Main Methods:

  • Retrospective analysis of diagnostic tissues from 112 CHL patients.
  • Immunohistochemical assessment of CSF-1R, CD68, and CD163 expression.
  • Correlation of CSF-1R expression levels with event-free survival (EFS) and overall survival (OS).

Main Results:

  • High CSF-1R expression (≥30%) in non-HRS cells was linked to inferior EFS and OS.
  • Elevated non-HRS cell CSF-1R expression correlated significantly with increased TAMs (CD163+).
  • Coexpression of CSF-1R and CD163 in non-HRS cells predicted the worst survival outcomes.

Conclusions:

  • Increased CSF-1R expression in non-HRS cells is a marker of poor prognosis in CHL.
  • This finding is associated with a higher density of tumor-associated macrophages.
  • CSF-1R expression in the tumor microenvironment warrants further investigation for therapeutic targeting.
Abstract