期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 114, 期 26, 页码 E5226-E5235出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1705066114
关键词
angiogenesis; VEGF; tumor growth; cancer therapy; chemotherapy
资金
- European Research Council Advanced Grant ANGIOFAT [250021]
- Swedish Research Council
- Swedish Cancer Foundation
- Children Cancer Foundation
- Diabetes Foundation
- Karolinska Institute Foundation
- Karolinska Institute Distinguished Professor Award
- Torsten Soderbergs Foundation
- Maud and Birger Gustavsson Foundation
- NOVO Nordisk Foundation
- Knut and Alice Wallenberg Foundation
- Fund for High Level University Construction of Medical Discipline, China [2016031638]
- Shenzhen Science and Technology Innovation Committee [JCYJ20150403091443336]
- Novo Nordisk Fonden [NNF14OC0012835] Funding Source: researchfish
Long-term uninterrupted therapy is essential for maximizing clinical benefits of antiangiogenic drugs (AADs) in cancer patients. Unfortunately, nearly all clinically available AADs are delivered to cancer patients using disrupted regimens. We aim to develop lifetime, nontoxic, effective, orally active, and low-cost antiangiogenic and antitumor drugs for treatment of cancer patients. Here we report our findings of long-term maintenance therapy with orally active, nontoxic, low cost antiangiogenic chemotherapeutics for effective cancer treatment. In a sequential treatment regimen, robust antiangiogenic effects in tumors were achieved with an anti-VEGF drug, followed by a low-dose chemotherapy. The nontoxic, low dose of the orally active prodrug capecitabine was able to sustain the anti-VEGF-induced vessel regression for long periods. In another experimental setting, maintenance of low-dose capecitabine produced greater antiangiogenic and antitumor effects after AAD plus chemotherapy. No obvious adverse effects were developed after more than 2-mo of consecutive treatment with a low dose of capecitabine. Together, our findings provide a rationalized concept of effective cancer therapy by long-term maintenance of AAD-triggered antiangiogenic effects with orally active, nontoxic, low-cost, clinically available chemotherapeutics.
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