Different Pathways of Macromolecule Extravasation from Hyperpermeable Tumor Vessels

To characterize tumor vessels more precisely and to elucidate the pathways by which macromolecules extravasated from them, we studied two well-defined, VPF/VEGF-secreting murine carcinomas, MOT and TA3/St

Dian Feng; Janice A. Nagy; Ann M. Dvorak; Harold F. Dvorak

2002

Scholarcy highlights

  • Tumor microvessels are hyperpermeable to plasma proteins, a consequence of tumor cell-secreted vascular permeability factor/vascular endothelial growth factor
  • The pathways by which macromolecules extravasate from tumor vessels have been little investigated
  • To characterize tumor vessels more precisely and to elucidate the pathways by which macromolecules extravasated from them, we studied two well-defined, VPF/VEGF-secreting murine carcinomas, MOT and TA3/St
  • Fenestrae developed in parallel with markedly reduced endothelial cell vesiculo-vacuolar organelles
  • VVOs provide an internal store of membrane that can be transferred to the endothelial cell surface to provide the substantial increase in plasma membrane necessary for mother vessel formation in MOT tumors
  • Such transfer was apparently unnecessary in TA3/St tumors in which extensive early endothelial cell division provided the increased plasma membrane necessary for forming mother vessels

Need more features? Save interactive summary cards to your Scholarcy Library.