Loading
Immune Cells in Cancer / Angiogenesis and VEGF in Cancer · Journal article
Biomedicine & Pharmacotherapy · September 4, 2026
Encouraging direction, but not yet definitive.
This preclinical investigation in triple-negative breast cancer xenografts shows that Poloxamer 188, a membrane-stabilizing polymer, restores endothelial barrier integrity in vitro and enhances tumor vascular perfusion in vivo, resulting in improved efficacy of doxorubicin chemotherapy and adoptively transferred human PBMCs without direct cytotoxic effects on cancer cells. The work is mechanistically sound but remains at the preclinical stage; translation to human TNBC and comparison to established vascular normalization strategies requires clinical evaluation.
Preclinical in vitro and in vivo study. Triple-negative breast cancer (TNBC) cell lines and xenograft tumors in mice; cultured endothelial cells; human peripheral blood mononuclear cells (PBMCs).. Intervention: Poloxamer 188 (P188), a membrane-stabilizing triblock copolymer, combined with doxorubicin chemotherapy and/or adoptively transferred human PBMCs.. Compared with: P188 alone, doxorubicin alone, control (no treatment or vehicle); PBMCs alone versus P188 plus PBMCs..
P188 restored endothelial barrier integrity in vitro, increasing Zonula occludens-1 (ZO-1) expression and sealing endothelial morphology Fluorescently labeled P188 accumulated in TNBC tumors and significantly enhanced Dextran delivery, indicating improved vascular function and tumor perfusion P188 combined with doxorubicin significantly suppressed tumor progression in vivo and reduced treatment-associated weight loss
No human data; clinical endpoints (survival, response rate, toxicity) not addressed
These findings suggest vascular restoration via P188 as a potential adjunctive strategy to enhance both chemotherapy and immunotherapy delivery in TNBC. However, this remains preclinical; clinical translation requires Phase 1 safety and Phase 2 efficacy studies in human TNBC patients to validate vascular normalization, drug delivery, and immune activation.
A sound preclinical study combining in vitro and in vivo work in a mouse TNBC model, demonstrating mechanistic plausibility and efficacy enhancement, but lacking human data, clinical endpoints, or direct comparison to standard anti-angiogenic therapy.
As stated by the source record.
Quoted from the source exactly as published.
These findings suggest vascular restoration via P188 as a potential adjunctive strategy to enhance both chemotherapy and immunotherapy delivery in TNBC. However, this remains preclinical; clinical translation requires Phase 1 safety and Phase 2 efficacy studies in human TNBC patients to validate vascular normalization, drug delivery, and immune activation.
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.
Tumor-associated vascular dysfunction is a major barrier limiting the efficacy of cancer therapies by impairing drug delivery, restricting immune-cell infiltration, and promoting hypoxia within the tumor microenvironment (TME). While anti-angiogenic therapies aim to suppress abnormal vessel formation, excessive vascular inhibition may further worsen hypoxia and therapeutic resistance. Here, we investigated whether restoration of endothelial integrity using Poloxamer 188 (P188), a membrane-stabilizing triblock copolymer, could improve vascular function and enhance therapeutic efficacy in triple-negative breast cancer (TNBC). In vitro, P188 prevented and reversed endothelial leakiness, restoring endothelial barrier integrity and enhancing tight junction formation, as demonstrated by increased Zonula occludens-1 (ZO-1) expression, a tight-junction protein, and sealed endothelial morphology. In vivo, fluorescently labeled P188 accumulated in TNBC tumors and significantly enhanced Dextran delivery, indicating improved vascular function and tumor perfusion. Although P188 showed no direct cytotoxic effect on TNBC cells and did not enhance Doxorubicin activity in vitro, combination treatment significantly suppressed tumor progression in vivo, while simultaneously reducing treatment-associated weight loss. Importantly, P188 also enhanced antitumor immunity. While P188 did not directly activate T cells or increase their cytotoxicity in vitro, it significantly increased T-cell infiltration into tumors in vivo and enhanced the therapeutic efficacy of adoptively transferred human normal peripheral blood mononuclear cell (PBMCs). Collectively, these findings demonstrate that restoration of tumor vascular integrity using P188 improves both chemotherapy and immunotherapy efficacy by enhancing therapeutic delivery and immune-cell infiltration. This study highlights vascular restoration as a promising therapeutic strategy for overcoming TME-mediated resistance in solid tumors.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.