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Radionuclide-fluorescence Reporter Gene Imaging to Track Tumor Progression in Rodent Tumor Models

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The RXR Agonist MSU-42011 Reduces Tumor Burden in a Murine Preclinical NF1-Deficient Model.

Pei-Yu Hung¹, Jessica A Moerland^2,3, Ana S Leal⁴

¹Department of Physiology, Michigan State University, East Lansing, MI 48824, USA.

|June 26, 2025

Summary

Retinoid X receptor (RXR) agonists like MSU-42011 combined with MEK inhibitors show promise for treating neurofibromatosis type 1 (NF1) associated tumors, reducing tumor growth and enhancing anti-tumor immunity.

Keywords:

malignant peripheral nerve sheath tumors (MPNSTs)neurofibromatosis type 1 plexiform neurofibromas (PNFs)retinoid X receptor (RXR) agonist selumetinib

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Area of Science:

Oncology
Immunology
Genetics

Background:

Neurofibromatosis type 1 (NF1) is a genetic disorder predisposing to plexiform neurofibromas (PNFs) and malignant peripheral nerve sheath tumors (MPNSTs).
Current treatments like selumetinib have limited efficacy and dose-limiting toxicities in MPNSTs.
NF1 deficiency drives tumorigenesis and alters immune responses, with macrophages playing a key role in NF1 lesion progression.

Purpose of the Study:

To investigate the therapeutic potential of targeting tumor-promoting immune cells using a retinoid X receptor (RXR) agonist, MSU-42011, in NF1-associated tumors.
To evaluate the efficacy of MSU-42011 alone and in combination with selumetinib in preclinical NF1 models.

Main Methods:

Assessed the effects of MSU-42011 and selumetinib, individually and combined, on NF1-deficient cells and a syngeneic MPNST model.
Analyzed tumor growth, pERK levels, immune cell infiltration (macrophages, CD8+ T cells), and cytokine/chemokine expression in vitro and in vivo.

Main Results:

Combination therapy significantly reduced tumor growth, pERK levels, and tumor-promoting macrophages, while increasing activated CD8+ T cells in vivo.
Both agents reduced pERK levels in NF1-deficient cells, with combination treatment yielding greater reductions.
Treatment partially reversed the pro-inflammatory cytokine and chemokine induction caused by NF1-deficient cell conditioned media.

Conclusions:

RXR agonists, such as MSU-42011, demonstrate therapeutic potential for NF1-associated tumors.
Combining RXR agonists with MEK inhibitors (like selumetinib) presents a promising strategy for treating NF1-related malignancies.
Further research is warranted to confirm these findings and assess clinical applicability.