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PMID: 286118 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

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 regression.

Journal of the National Cancer Institute ·Vol. 62 ·No. 6 ·1979-06-00 ·Pages 1459-72

Dvorak HF, Dvorak AM, Manseau EJ, Wiberg L, Churchill WH

Abstract

Line 1 and line 10 tumors became invested in a fibrin-gel cocoon within hours after transplantation to the subcutaneous spaces of unsensitized syngeneic inbred Sewall Wright strain 2 guinea pigs. The fibrin gel comprised more than 80% of the line 1 tumor mass and, after day 3, became organized and was subsequently replaced by fibrous connective tissue, which gave the tumor the appearance of a scirrhous carcinoma. A cellular infiltrate of lymphocytes and basophils developed at the periphery of line 1 tumors after day 8, and tumors regressed by day 13. The fibrin gel investing the highly malignant line 10 tumors accounted for less than 10% of the tumor mass and persisted without fibrous organization as a tumor grew progressively and invaded adjacent tissues. These data provide new and potentially important insights into the biology of solid tumor growth and the mechanisms of immunologic tumor rejection. Envelopment of tumors in a fibrin gel created an anatomic barrier separating the tumors from the host. Neovascularization mimicking that about line 1 and line 10 tumors was induced by sc fibrin implants; these data suggest that activation of the clotting and/or fibrinolytic systems by tumor cells may itself provide sufficient stimulus for induction of tumor angiogenesis without requiring a separate tumor angiogenesis factor. The scirrhous pattern of growth characteristic of line 1 tumors apparently was achieved by organization of an abundant fibrin gel. Line 1 tumor regression did not for the most part involve direct contacts between tumor cells and any type of inflammatory cell, including macrophages; rather, tumor destruction was effected by ischemic necrosis secondary to widespread microvascular injury. The mechanisms of such injury are uncertain, but tumor rejection was correlated with evidence of developing cellular immunity and anatomic associations between lymphocytes and myofibroblasts. Further experiments will be necessary before these findings can be generalized to other tumor systems.

MeSH Terms
Animals Female Fibrin/physiology Fibrinogen/administration & dosage Fibroblasts/immunology Graft Rejection Granulation Tissue/immunology Guinea Pigs Immunity, Cellular Infarction/immunology Liver Neoplasms, Experimental/blood supply,immunology,pathology Male Soft Tissue Neoplasms/immunology Thrombin/administration & dosage Time Factors
Chemicals
Fibrin Fibrinogen Thrombin
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Dvorak H F
Dvorak A M
Manseau E J
Wiberg L
Churchill W H
Article Info
Journal
Journal of the National Cancer Institute
Abbr.
J Natl Cancer Inst
ISSN
0027-8874
Published
1979-06-00
Pages
1459-72
Language
English
Region
United States
NLM ID
7503089
Subset
IM
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