Hehlgans, Thomas and Stoelcker, Benjamin and Stopfer, Peter and Mueller, Peter and Cernaianu, Grigore and Guba, Markus and Steinbauer, Markus and Nedospasov, Sergei A. and Pfeffer, Klaus and Maennel, Daniela N. (2002) Lymphotoxin-beta receptor immune interaction promotes tumor growth by inducing angiogenesis. CANCER RESEARCH, 62 (14). pp. 4034-4040. ISSN 0008-5472
Full text not available from this repository. (Request a copy)Abstract
Growth of solid fibrosarcoma tumors in mice was inhibited by the release of a soluble lymphotoxin-beta receptor inhibitor (LTbetaR-immunoglobulin fusion protein) from the tumor cells. Tumor growth arrest in mice deficient in the ligand LTalpha(1)beta(2) demonstrated the requirement for activation of the LTbetaR on the tumor cells by host cell-derived LTalpha(1)beta(2). Activation of the LTbetaR resulted in enhanced release of macrophage inflammatory protein-2. Blocked angiogenesis was revealed in LTbetaR inhibitor-producing tumor nodules by immunohistochemistry and in vivo microscopy. The growth arrest of LTbetaR inhibitor-producing fibrosarcomas was overcome by forced MIP-2 expression in the tumor cells. Thus, LTbetaR activation on tumor cells by activated host lymphocytes can initiate a novel proangiogenic pathway leading to organized tumor tissue development.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | MACROPHAGE INFLAMMATORY PROTEIN-2; NECROSIS-FACTOR RECEPTOR; MELANOMA-CELLS; EXPRESSION; INTERLEUKIN-8; CHEMOKINE; ACTIVATION; MICE; CARCINOMA; CLONING; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Chirurgie Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 12 Oct 2021 10:26 |
| Last Modified: | 12 Oct 2021 10:26 |
| URI: | https://pred.uni-regensburg.de/id/eprint/40079 |
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