Faculty of Science and Engineering, Waseda University, 3-4-1 Okubo, Shinjuku-ku, Tokyo, 169-8555, Japan.
Research and Development Centre for Minimally Invasive Therapies, Medical Research Institute, Tokyo Medical University, 6-1-1, Shinjuku, Tokyo, 160-0022, Japan.
Sci Rep. 2021 Jan 11;11(1):419. doi: 10.1038/s41598-020-79824-8.
Excessive tumour growth results in a hypoxic environment around cancer cells, thus inducing tumour angiogenesis, which refers to the generation of new blood vessels from pre-existing vessels. This mechanism is biologically and physically complex, with various mathematical simulation models proposing to reproduce its formation. However, although temporary vessel regression is clinically known, few models succeed in reproducing this phenomenon. Here, we developed a three-dimensional simulation model encompassing both angiogenesis and tumour growth, specifically including angiopoietin. Angiopoietin regulates both adhesion and migration between vascular endothelial cells and wall cells, thus inhibiting the cell-to-cell adhesion required for angiogenesis initiation. Simulation results showed a regression, i.e. transient decrease, in the overall length of new vessels during vascular network formation. Using our model, we also evaluated the efficacy of administering the drug bevacizumab. The results highlighted differences in treatment efficacy: (1) earlier administration showed higher efficacy in inhibiting tumour growth, and (2) efficacy depended on the treatment interval even with the administration of the same dose. After thorough validation in the future, these results will contribute to the design of angiogenesis treatment protocols.
肿瘤过度生长会导致癌细胞周围缺氧,从而诱导肿瘤血管生成,即从预先存在的血管生成新的血管。该机制在生物学和物理学上都很复杂,各种数学模拟模型都提出了复制其形成的方法。然而,尽管临床上已知血管会暂时退化,但很少有模型能够重现这一现象。在这里,我们开发了一个包含血管生成和肿瘤生长的三维模拟模型,特别纳入了血管生成素。血管生成素调节血管内皮细胞和壁细胞之间的黏附和迁移,从而抑制了血管生成起始所需的细胞间黏附。模拟结果显示,在血管网络形成过程中,新血管的总长度会出现退化,即暂时减少。我们还使用该模型评估了给予贝伐单抗药物的疗效。结果突出了治疗效果的差异:(1)早期给药在抑制肿瘤生长方面显示出更高的疗效,(2)即使给予相同剂量,治疗间隔也会影响疗效。在未来进行彻底验证后,这些结果将有助于设计血管生成治疗方案。