Loading
Life sciences · Journal article
Cell Death Discovery · October 31, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Abstract Metastatic hormone-naive prostate cancer (mHNPC) refers to a small subset of diagnosed prostate tumors and presents very high mortality and poor response to available therapies. Despite its clinical relevance, we lack immunocompetent models that are both androgen-dependent and reliably metastatic, limiting the implementation of translational research strategies. Here we develop and characterize PL051, a syngeneic, bioluminescence tractable prostate carcinoma cell line derived from a Pten / Lkb1 double knockout genetic mouse model that reproducibly engrafts orthotopically in C57BL/6 mice, maintains androgen-receptor (AR) signaling, and consistently disseminates to soft tissues and bone. PL051 preserves Pten / Lkb1 loss and PI3K–AKT activation, shows intact AR responsiveness in vitro, and responds to AR-pathway intensification in vivo. We provide two complementary proof-of-concept evidence for the preclinical potential of this model. On one hand, we show the therapeutic benefit of combining androgen signaling inhibition and anti-PD1 treatment. On the other hand, we provide evidence showing that co-targeting myeloid cells with a CSF1R inhibitor further enhances therapeutic activity of checkpoint blockade by depleting suppressive macrophages and boosting T-cell recruitment. Together, this preclinical model fills a critical gap for studying mHNPC biology and provides a scalable, immune-competent model for testing rational combinatorial treatments.