June 1, 1979JNCI Journal of the National Cancer Institute
Fibrin Gel Investment Associated With Line 1 and Line 10 Solid Tumor Growth, Angiogenesis, and Fibroplasia in Guinea Pigs. Role of Cellular Immunity, Myofibroblasts, Microvascular Damage, and Infarction in Line 1 Tumor Regression2
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Discussion
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Implication
Experimental animal study reveals fibrin-induced angiogenesis and immune-mediated vascular infarction in guinea pigs, highlighting clot pathways in tumor rejection.
Key Points
- To examine the development of fibrin gel matrices in solid tumors and determine their roles in angiogenesis, fibroplasia, and immune-mediated tumor regression.
- Transplanted syngeneic Line 1 and Line 10 solid tumors into the subcutaneous spaces of unsensitized Sewall Wright strain 2 guinea pigs.
- Implanted subcutaneous fibrin matrices alone to determine if fibrin independently induces host neovascularization.
- Monitored tumor growth, stromal organization, cellular infiltration, and microvascular changes histologically over a 13-day period.
- Line 1 tumors formed a fibrin gel comprising more than 80% of the tumor mass that organized into fibrous connective tissue, followed by peripheral lymphocyte and basophil infiltration after day 8 and complete regression by day 13.
- Line 10 tumors exhibited an unorganized fibrin gel accounting for less than 10% of the mass, followed by progressive growth and invasion into adjacent tissues.
- Fibrin implants alone stimulated neovascularization, and Line 1 regression was driven by ischemic necrosis from microvascular damage rather than direct immune cell contact with tumor cells.
Cite This Study
Dvorak et al. (1979) studied this question.