肿瘤通过血液供应获取营养
科学家们现在对肿瘤细胞如何吸收营养有了新的发现，也解释了为何使用血管生长抑制剂阻断血液的供应，仅仅只能减慢肿瘤的生长速度。这为未来研发新型抗癌药物提供了新的理论基础。
这项研究的结果发表在了最新一期的《American Journal of Pathology》杂志上。
该论文的主要作者，匈牙利泽梅尔魏斯大学肿瘤研究中心的Sándor Paku博士和维也纳医学院的Balazs Dome博士说道：“肿瘤中的毛细血管芽生对其生长至关重要，因此被认为是一个很好的临床癌症治疗的靶点。但是我们的研究发现阻止这些毛细血管的生成在抑制肿瘤生长上并没有起到很好的作用。”
科学家们将恶性肿瘤细胞转入小鼠体内，并用电子共聚焦显微镜观察肿瘤组织的成长。通过观察研究，他们证实了一个全新的肿瘤脉管系统生长机制：仅仅只抑制肿瘤细胞中血管的生长如使用血管生长抑制剂vatalanib来阻断新血管的生成，会引起肿瘤中原有的血管加速生长，如套叠式血管。（套叠式血管的最典型特征是它们能通过一支血管折叠最终形成二支血管）。
在这之前，肿瘤脉管的形成机制还没有被充分理解。研究显示一系列引起内皮桥接和套叠式血管生长的反应都将引起肿瘤脉管在原来的基础上快速生长。科学家们对这种脉管形成机制提出了一个新的名词“反芽生”。
众所周知的是，肿瘤在没有毛细血管芽生的条件下也能够通过其它的类型的血管来获得充足的血液供应（如套叠式血管）。因此，抗血管生成治疗药物的选择应当基于肿瘤的具体特性，在癌症中靶向那些非芽生性血管似乎是一个合理的选择。该研究提出了一个肿瘤诱导的套叠式血管生成的全新机制，这也许能为未来研发靶向这种血管形成的药物提供理论基础。
英文论文原文摘要：
Alternative Vascularization Mechanisms in Cancer
Although cancer cells are not generally controlled by normal regulatory mechanisms, tumor growth is highly dependent on the supply of oxygen, nutrients, and host-derived regulators. It is now established that tumor vasculature is not necessarily derived from endothelial cell sprouting; instead, cancer tissue can acquire its vasculature by co-option of pre-existing vessels, intussusceptive microvascular growth, postnatal vasculogenesis, glomeruloid angiogenesis, or vasculogenic mimicry. The best-known molecular pathway driving tumor vascularization is the hypoxia-adaptation mechanism. However, a broad and diverse spectrum of genetic aberrations is associated with the development of the “angiogenic phenotype.” Based on this knowledge, novel forms of antivascular modalities have been developed in the past decade. When applying these targeted therapies, the stage of tumor progression, the type of vascularization of the given cancer tissue, and the molecular machinery behind the vascularization process all need to be considered. A further challenge is finding the most appropriate combinations of antivascular therapies and standard radio- and chemotherapies. This review intends to integrate our recent knowledge in this field into a rational strategy that could be the basis for developing effective clinical modalities using antivascular therapy for cancer.
