Tumors larger than about 2 mm cannot rely on diffusion for nutrients and must induce new vessel formation. Under hypoxic conditions, the transcription factor HIF-1 accumulates and drives angiogenesis chiefly by increasing production of:
- A Vascular endothelial growth factor from tumor and stromal cells ✓
- B Angiopoietin-1 from pericytes
- C Basic fibroblast growth factor from fibroblasts
- D Thrombospondin-1 from platelets
Explanation
Hypoxia stabilizes HIF-1 alpha, which induces transcription of vascular endothelial growth factor (VEGF) in tumor and stromal cells. VEGF increases endothelial proliferation, migration, and permeability, forming the basis of anti-VEGF therapy such as bevacizumab. Basic FGF contributes to angiogenesis but is not the principal HIF-1 driven mediator, angiopoietins regulate vessel maturation later, and thrombospondin-1 is an endogenous inhibitor of angiogenesis, not a promoter.
Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.
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