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首页> 外文期刊>Endothelium: Journal of endothelial cell research >The contribution of Harold F. Dvorak to the study of tumor angiogenesis and stroma generation mechanisms.
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The contribution of Harold F. Dvorak to the study of tumor angiogenesis and stroma generation mechanisms.

机译：Harold F. Dvorak对肿瘤血管生成和基质生成机制研究的贡献。

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In 1983, Harold Dvorak and his colleagues were the first to show that tumor cells secreted vascular permeability factor (VPF) and that a blocking antibody to VPF could prevent the edema and fluid accumulation that is characteristic of human cancers. In 1986, Dvorak went on to demonstrate that VPF was secreted by a variety of human tumor cell lines and proposed that VPF was in part responsible for the abnormal vasculature seen in human tumors. As a result, he and other investigators demonstrated that VPF was capable of stimulating endothelial cell growth and angiogenesis. These fundamental discoveries led to additional research conducted by Napoleone Ferrara and his laboratory, confirming the cloning of VPF and renaming the protein vascular endothelial growth factor (VEGF). In 1986, Dvorak proposed that by secreting VPF, tumors induce angiogenesis by turning on the wound healing response. He noted that wounds, like tumors, secrete VPF, causing blood vessels to leak plasma fibrinogen, which stimulates blood vessel growth and provides a matrix on which they can spread. Unlike wounds, however, that turn off VPF production after healing, tumors did not turn off their VPF production and instead continued to make large amounts of VPF, allowing malignant cells to continue to induce new blood vessels and so to grow and spread. Thus, tumors behave like wounds that fail to heal. This work is again extremely significant for patients worldwide, as Dvorak's scientific research is leading his colleagues all over the world to examine how to treat a tumor through its blood supply.
机译：1983年，Harold Dvorak和他的同事们第一个证明肿瘤细胞分泌了血管通透性因子（VPF），并且针对VPF的阻断抗体可以预防人类癌症所特有的水肿和积液。 1986年，德沃夏克（Dvorak）继续证明VPF由多种人类肿瘤细胞系分泌，并提出VPF部分负责人类肿瘤中可见的脉管系统异常。结果，他和其他研究人员证明了VPF能够刺激内皮细胞的生长和血管生成。这些基本发现促成拿破仑·费拉拉（Napoleone Ferrara）及其实验室的进一步研究，证实了VPF的克隆并重命名了蛋白血管内皮生长因子（VEGF）。 1986年，德沃夏克（Dvorak）提出，通过分泌VPF，肿瘤可通过打开伤口愈合反应来诱导血管生成。他指出，伤口像肿瘤一样会分泌VPF，导致血管渗漏血浆纤维蛋白原，从而刺激血管生长并提供可以扩散的基质。但是，与伤口在愈合后会关闭VPF产生的伤口不同，肿瘤并未关闭其VPF产生，而是继续产生大量VPF，从而使恶性细胞继续诱导新血管，从而生长并扩散。因此，肿瘤表现得像无法愈合的伤口。由于德沃夏克（Dvorak）的科学研究正带领世界各地的同事研究如何通过血液供应来治疗肿瘤，因此这项工作对全世界的患者再次具有极其重要的意义。

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