## Abstract Angiogenesis is critical to the growth and metastasis of solid tumors, and acquired drug resistance is one of the major hindrances to chemotherapy. Thus, we sought a rational strategy using the combination of antiangiogenic biotherapy and chemotherapy for cancer therapy. We explored the
Active immunotherapy of tumors with a recombinant xenogeneic endoglin as a model antigen
✍ Scribed by Guang-Hong Tan; Yu-Quan Wei; Ling Tian; Xia Zhao; Li Yang; Jiong Li; Qiu-Ming He; Yang Wu; Yan-Jun Wen; Tao Yi; Zhen-Yu Ding; Bin Kan; Yong-Qiu Mao; Hong-Xin Deng; Hong-Li Li; Chun-Hua Zhou; Chun-Hua Fu; Fei Xiao; Xiao-Wei Zhang
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 359 KB
- Volume
- 34
- Category
- Article
- ISSN
- 0014-2980
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Angiogenesis play a critical role in tumor growth and metastasis. Increasing evidence suggests that endoglin is a powerful marker of angiogenesis in solid malignancies. Thus, breaking of immune tolerance of self‐endoglin‐associated angiogenesis is an attractive approach to cancer therapy. To test this concept, we recombined the extracellular domains of porcine endoglin, and used it as a xenogeneic vaccine. We found that immunotherapy with porcine endoglin was effective at both protective and therapeutic anti‐tumor immunity in several mouse tumor models. Autoantibodies against mouseendoglin were identified by Western blot and ELISA. IgG1 and IgG2b were substantially increased. Anti‐endoglin antibody‐producing B cells were detectable by ELISPOT assay. There was endothelial deposition of immunoglobulins within tumors. The anti‐tumor activity was also induced by the adoptive transfer of the purified immunoglobulins. Angiogenesis was apparently inhibited within the tumor tissues and on the alginate beads. The increased apoptotic cells were found within the tumor tissues from the mice treated with porcine endoglin. The anti‐tumor activity and production of autoantibodies againstmouse endoglin could be abrogated by depletion of CD4^+^ T lymphocytes. Remarkably, no marked toxicity was found in the immunized mice. These observations may provide an alternative rationalstrategy for active cancer immunotherapy.
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