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Lymphatic System and Diseases / Cancer, Hypoxia, and Metabolism / Angiogenesis and VEGF in Cancer · Journal article
Biology · August 11, 2026
Raises a question worth testing. It does not answer one.
This narrative review synthesizes mechanistic literature on tumor vasculogenesis—the de novo formation of blood vessels from endothelial progenitor cells—across multiple signaling pathways including VEGF, HIF-1α, Notch, Wnt, PI3K/AKT, and TGF-β. The authors propose that targeting vasculogenesis pathways may complement anti-angiogenic therapy and overcome treatment resistance, but present this as a conceptual framework rather than a tested clinical hypothesis.
Narrative review. Human cancer literature across malignancies; no specific enrolled patient cohort.
Vasculogenesis is recognized as a critical contributor to tumor vascularization, complementing classical angiogenesis and promoting cancer progression, metastasis, therapeutic resistance, and disease recurrence Complex interplay identified between developmental signaling pathways, endothelial plasticity, mechanical cues, inflammatory mediators, and non-coding RNAs in regulating tumor vasculogenesis Targeting vasculogenesis-related pathways proposed as a promising strategy for improving precision oncology and overcoming treatment resistance
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
This review provides a mechanistic framework for understanding how endothelial progenitor cell-derived vessel formation contributes to tumor progression and resistance. Clinicians and researchers should recognize vasculogenesis as a complementary vascularization mechanism alongside angiogenesis when considering antivascular therapy strategies, though the therapeutic recommendations remain exploratory.
This is a narrative mechanistic review synthesizing literature on tumor vasculogenesis pathways; it raises questions about therapeutic targeting rather than testing a specific hypothesis through empirical study.
As stated by the source record.
This review provides a mechanistic framework for understanding how endothelial progenitor cell-derived vessel formation contributes to tumor progression and resistance. Clinicians and researchers should recognize vasculogenesis as a complementary vascularization mechanism alongside angiogenesis when considering antivascular therapy strategies, though the therapeutic recommendations remain exploratory.
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.
What is missing. This record has no reported figures. That is a gap in the analysis, not a judgement about the study.
Vasculogenesis, the de novo formation of blood vessels from endothelial progenitor cells, is increasingly recognized as a critical contributor to tumor vascularization, complementing classical angiogenesis and promoting cancer progression, metastasis, therapeutic resistance, and disease recurrence. This narrative review aims to provide a comprehensive overview of the molecular mechanisms governing vasculogenesis across human malignancies and to discuss their translational relevance for targeted cancer therapy. This is a narrative, mechanistically oriented review rather than a systematic review or meta-analysis. The literature was searched in PubMed, Scopus, and Google Scholar, with the primary search covering publications from January 2010 to February 2026, while seminal earlier studies were included when they established fundamental concepts in vascular biology. Search terms included combinations of “vasculogenesis”, “tumor vasculogenesis”, “angiogenesis”, “endothelial progenitor cells”, “vascular remodeling”, “VEGF”, “HIF-1α”, “Notch”, “Wnt”, “PI3K/AKT”, “TGF-β”, “EndMT”, “mechanotransduction”, “non-coding RNAs”, “tumor microenvironment”, and “cancer”. Evidence was qualitatively appraised and synthesized according to mechanistic relevance and consistency across experimental and clinical studies. The reviewed literature highlights the complex interplay between developmental signaling pathways, endothelial plasticity, mechanical cues, inflammatory mediators, and non-coding RNAs in regulating tumor vasculogenesis. Collectively, these findings suggest that targeting vasculogenesis-related pathways may complement existing anti-angiogenic therapies and represent a promising strategy for improving precision oncology and overcoming treatment resistance.
Taken from the source record, never inferred. Follow any of these and new work involving them reaches your briefing.