Loading
Life sciences · Journal article
Molecular Oncology · October 20, 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.
Angiogenesis is a major driver of tumor progression and a validated therapeutic target in highly vascularized cancers such as clear cell renal cell carcinoma. However, the clinical benefit of antivascular endothelial growth factor therapies is limited by the emergence of resistance. We identified a vascular endothelial growth factor A splice variant, termed Lymphatic and Vascular Resistance Factor (LVRF), which promotes both angiogenesis and lymphangiogenesis and is upregulated following anti‐angiogenic treatment. To therapeutically target this pathway, we generated fully human monoclonal antibodies against LVRF. Lead antibodies displayed high specificity and nanomolar affinity and effectively inhibited LVRF‐driven biological activities. Anti‐LVRF antibodies reduced renal carcinoma cell invasion, inhibited vascular and lymphatic endothelial responses, and suppressed lymphatic endothelial cell sprouting. In vivo, treatment significantly reduced the growth of bevacizumab‐resistant renal carcinoma xenografts, induced regression of blood and lymphatic vessels, and decreased metastatic dissemination in zebrafish models. These findings identify LVRF as a mediator of resistance to anti‐angiogenic therapy and support therapeutic targeting of LVRF as a novel strategy for vascularized tumors resistant to current antivascular endothelial growth factor treatments.