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Tumors: wounds that do not heal-redux
1The Center for Vascular Biology Research and the Departments of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts. hdvorak@bidmc.harvard.edu.
Cancer Immunology Research
|January 9, 2015
Summary
Tumors mimic the wound healing process, co-opting vascular permeability factor (VPF)/VEGF to develop their stroma. This involves inflammation, angiogenesis, and matrix deposition, similar to wound repair mechanisms.
Area of Science:
- Oncology
- Inflammation Biology
- Vascular Biology
Background:
- The parallels between tumor stroma formation and wound healing have been observed for over 150 years.
- Vascular permeability factor (VPF)/VEGF, a key mediator, was identified as a potential link.
- The hypothesis posits that tumors hijack wound-healing pathways for stromal development.
Purpose of the Study:
- To explore the hypothesis that tumors act as non-healing wounds.
- To elucidate the molecular mechanisms by which tumors co-opt wound-healing responses.
- To detail the sequence of events initiated by VPF/VEGF in both tumor and wound contexts.
Main Methods:
- Review and synthesis of existing research on tumor stroma and wound healing.
- Focus on the molecular cascade initiated by VPF/VEGF.
- Comparative analysis of cellular and molecular events in tumors, wounds, and inflammatory diseases.
Main Results:
- VPF/VEGF triggers a conserved sequence: increased vascular permeability, plasma extravasation, and clotting.
- This leads to fibrin deposition, angiogenesis, and granulation tissue formation.
- The process culminates in scar tissue (desmoplasia) in cancer, mirroring wound healing.
Conclusions:
- Tumors utilize and manipulate the wound-healing cascade for their own growth and maintenance.
- This shared pathway highlights VPF/VEGF's central role in cancer and inflammation.
- Understanding this connection offers insights into potential therapeutic strategies targeting tumor stroma.