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Related Experiment Video

Updated: May 6, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

Effects of Radiotherapy, Immune Checkpoint Inhibitors, and PIM Kinase Inhibition in Castration-Resistant Prostate

Vignesh Chennupati¹, Matthew Eximond², Anita Nwiloh³

¹Vanderbilt University, Nashville, 37235, TN, USA.

Current Cancer Drug Targets

|May 5, 2026

Summary

Radiation therapy combined with immune checkpoint inhibitors and PIM kinase inhibition significantly improves survival in a prostate cancer mouse model. This triple therapy approach activates anti-tumor immunity, offering a promising strategy for treating castration-resistant prostate cancer.

Keywords:

PIM kinase inhibitor STING pathway cytoplasmic double-stranded DNA immune checkpoint inhibitor immunotherapy prostate cancer radiotherapy

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Last Updated: May 6, 2026

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Generation of Prostate Cancer Cell Models of Resistance to the Anti-mitotic Agent Docetaxel

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Published on: September 8, 2017

Area of Science:

Oncology
Immunotherapy
Radiation Oncology

Background:

Prostate cancer exhibits limited response to immune checkpoint inhibitors (ICIs).
Radiation therapy (RT) may enhance anti-tumor immune activity when combined with ICIs and PI3K inhibition.

Purpose of the Study:

To investigate the efficacy of triple therapy combining RT, ICIs, and PIM kinase inhibition in a mouse model of castration-resistant prostate cancer (CRPC).
To assess RT-induced immune activation via cytosolic double-stranded DNA (dsDNA) as a marker for cGAS-STING pathway engagement.

Main Methods:

RT-induced cytosolic dsDNA was measured in prostate cancer cell lines.
Triple therapies were evaluated in a Myc-CaP syngeneic mouse model: (1) anti-CTLA-4, anti-PD-1, and RT; (2) PIM447, anti-PD-1, and RT.
Tumor-immune profiles were analyzed using mass cytometry (CyTOF).

Main Results:

Peak cytosolic dsDNA induction occurred at 13 Gy RT.
Triple therapy with anti-CTLA-4, anti-PD-1, and RT doubled median survival compared to monotherapy (32 vs. 11-22 days).
Triple therapy with PIM447, anti-PD-1, and RT nearly tripled median survival (82 vs. 29 days) and reduced immunosuppressive cells while enhancing CD8+ T-cell infiltration.

Conclusions:

RT can activate immune responses in prostate cancer, potentially via the cGAS-STING pathway.
Combination therapy of RT, ICIs, and PIM kinase inhibition shows significant survival benefits in a CRPC mouse model.
This approach warrants further investigation for optimizing CRPC treatment strategies.