"Additionally, we show that soluble MD2 (sMD2) may serve as a non-invasive biomarker of metastatic burden and help predict resistance to poly ADP-ribose polymerase (PARP) inhibitor therapy."
BUFFALO, NY — April 1, 2026 — A new research perspective was published in Volume 13 of Oncoscience on March 11, 2026, titled " Targeting MD2 in prostate cancer bone metastasis: Mechanistic insights and therapeutic potential ."
Led by co-first authors Melina A. Dattilo from Universidad de Buenos Aires and CONICET–Universidad de Buenos Aires , and Marina G. Ferrari from Rush University Medical Center , with corresponding author Adrian P. Mansini from Rush University Medical Center , the perspective builds on prior work identifying MD2/LY96 as a biomarker associated with poor prognosis and metastatic potential in prostate cancer. The authors also present new preclinical data showing that pharmacological MD2 inhibition reduces tumor growth in a mouse model of prostate cancer bone metastasis.
In patient tumor tissues, high MD2 expression was associated not only with metastasis but also with increased infiltration of T regulatory cells and myeloid-derived suppressor cells, consistent with an immunosuppressive tumor microenvironment. The study also reports that soluble MD2 may help predict metastatic burden and resistance to PARP inhibitor therapy, supporting MD2 as both a therapeutic target and a potential biomarker in metastatic prostate cancer.
"These findings support MD2 as a novel therapeutic target and identify soluble MD2 as a promising predictive and prognostic biomarker in metastatic PCa, with mechanistic links to immune evasion and inflammatory signaling."
The authors note that these findings remain preclinical and require further validation in additional models and clinical cohorts. Next steps include testing MD2 inhibition in broader prostate cancer systems, clarifying how MD2 shapes immune evasion and bone colonization, and evaluating whether soluble MD2 can serve as a practical biomarker for treatment response and metastatic burden.
DOI: https://doi.org/10.18632/oncoscience.647
