Abstract
Angiogenesis, an essential component of tumor growth and survival, is regulated by complex interactions between several cell types and soluble mediators. Heterogeneous tumor vasculature originates from the collective effect of the nature of carcinoma and the complexity of the angiogenic network. Although the application of angiogenesis inhibitors in some types of cancers has shown clinical benefits, predictive markers to assess treatment effects have yet to be established. In this review, we focus on tumor vessel maturity as a potential marker for evaluating treatment response.
Highlights
Like normal tissues, malignant tissues are dependent on an adequate blood supply
This result is in agreement with a xenograft model in a human ductal carcinoma in situ (DCIS) study that observed that COX2 upregulation in DCIS xenografts increased Vascular endothelial growth factor platelet-derived growth factor (PDGF) (VEGF) and MMP14 expression [46]
Another animal study has shown that tumor-derived PDGF-BB upregulates the transcription of stromal derived factor-1α (SDF-1α) in Endothelial cell PC (EC) [73]
Summary
Malignant tissues are dependent on an adequate blood supply. Unlike normal tissues, angiogenesis is reactivated under pathological conditions, such as wound healing and malignancies [1]. The “demand” for nutrients and oxygen necessitates new “supply” routes, that is, new blood vessels. Studies in this field have revealed that a tumor mass cannot exceed 1 mm without angiogenesis [3]. Endothelial cells (ECs) are typically quiescent in humans [4], they can proliferate once the angiogenic switch turns on. This switch is off or differentially regulated in normal tissues based on the equilibrium between positive and negative angiogenic regulators. Endothelial precursor cells (EPCs) from bone marrow integrate with these growing vessels [6]
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