[Vasculogenic mimicry--potential target for tumor therapy]

Area of Science:

• Oncology
• Vascular Biology
• Cancer Research

Context:

• Tumor microcirculation is crucial for cancer progression.
• Traditional understanding focused on angiogenesis for tumor vascularization.
• Vasculogenic mimicry (VM) represents an alternative pathway for tumor blood supply.

Purpose:

• To describe the phenomenon of vasculogenic mimicry (VM) in aggressive cancers.
• To differentiate VM from conventional angiogenesis.
• To identify molecular components involved in VM.

Summary:

• Aggressive melanomas and other cancers exhibit VM, a process where tumor cells form extracellular matrix-lined channels.
• These VM networks are distinct from angiogenesis and are not a host stromal response.
• Morphological patterns of VM, like tubular and patterned matrix types, have been identified in uveal melanomas.
• VM has been observed in various cancers including breast, prostate, lung, and glioblastoma, as well as in placenta formation.
• Key molecular players in VM include VE-cadherin, EphA2, laminin5 gamma2, MMPs, VEGF-C, LYVE1, TF, and NOTCH.
• The gene expression profile of aggressive melanoma cells resembles embryonic-like cells, suggesting an undifferentiated state.

Impact:

• Understanding VM heterogeneity and its molecular regulation provides novel therapeutic opportunities.
• Targeting VM could offer new strategies against cancers that rely on this alternative vascularization.
• This research expands the understanding of tumor vascularization beyond angiogenesis.