CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

Saeed Norouzi; Sonikpreet Aulakh

doi:10.1016/j.tranon.2026.102758

April 6, 2026Translational OncologyOpen Access

CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

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Key Points

To investigate the role of CD38 overexpression in glioblastoma and its impact on tumor progression and immune environment.
Analysis of CD38 expression levels in glioblastoma tissues
Assessment of tumor microenvironment changes
Evaluation of daratumumab efficacy in clinical trials
CD38 overexpression correlates with increased immunosuppressive factors in the tumor microenvironment
Daratumumab shows preliminary efficacy in patients with elevated CD38 levels
Findings suggest CD38 as a potential therapeutic target for glioblastoma

Implication

Observational analysis shows CD38's role in tumor progression in glioblastoma, suggesting a new treatment target.

Abstract

CD38 overexpression in GBM drives tumor progression by amplifying immunosuppressive TME remodeling, positioning CD38 as a compelling target for further clinical investigation, supported by preliminary efficacy of daratumumab (NCT04922723) in patients with GBM.

Discussion

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Cite This Study

Norouzi et al. (2026) studied this question.

synapsesocial.com/papers/69d8930e6c1944d70ce04210 https://doi.org/10.1016/j.tranon.2026.102758

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CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

Key Points

Implication

Abstract

Discussion

Cite This Study

CD38 overexpression drives glioblastoma progression via L1CAM/ICAM1/JAK-STAT-Driven tumor microenvironment rewiring

Key Points

Implication

Abstract

Discussion

Cite This Study

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