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本文引用的文献

1
Increase of plasma VEGF after intravenous administration of bevacizumab is predicted by a pharmacokinetic model.贝伐珠单抗静脉给药后血浆 VEGF 的增加可以通过药代动力学模型预测。
Cancer Res. 2010 Dec 1;70(23):9886-94. doi: 10.1158/0008-5472.CAN-10-1419. Epub 2010 Nov 30.
2
Dissecting cancer through mathematics: from the cell to the animal model.通过数学方法解析癌症:从细胞到动物模型。
Nat Rev Cancer. 2010 Mar;10(3):221-30. doi: 10.1038/nrc2808.
3
Harnessing systems biology approaches to engineer functional microvascular networks.利用系统生物学方法构建功能性微血管网络。
Tissue Eng Part B Rev. 2010 Jun;16(3):361-70. doi: 10.1089/ten.TEB.2009.0611.
4
The presence of VEGF receptors on the luminal surface of endothelial cells affects VEGF distribution and VEGF signaling.血管内皮生长因子受体(VEGF receptors)在上皮细胞的管腔表面的存在会影响血管内皮生长因子(VEGF)的分布和 VEGF 信号转导。
PLoS Comput Biol. 2009 Dec;5(12):e1000622. doi: 10.1371/journal.pcbi.1000622. Epub 2009 Dec 24.
5
Tipping the balance: robustness of tip cell selection, migration and fusion in angiogenesis.打破平衡:血管生成中尖端细胞选择、迁移和融合的稳健性。
PLoS Comput Biol. 2009 Oct;5(10):e1000549. doi: 10.1371/journal.pcbi.1000549. Epub 2009 Oct 30.
6
A pharmacologically based multiscale mathematical model of angiogenesis and its use in investigating the efficacy of a new cancer treatment strategy.一种基于药理学的血管生成多尺度数学模型及其在新癌症治疗策略疗效研究中的应用。
J Theor Biol. 2009 Oct 21;260(4):545-62. doi: 10.1016/j.jtbi.2009.06.026. Epub 2009 Jul 15.
7
Targeting tumor angiogenesis.靶向肿瘤血管生成。
Semin Oncol. 2009 Apr;36(2 Suppl 1):S12-9. doi: 10.1053/j.seminoncol.2009.02.002.
8
Multiparameter computational modeling of tumor invasion.肿瘤侵袭的多参数计算建模
Cancer Res. 2009 May 15;69(10):4493-501. doi: 10.1158/0008-5472.CAN-08-3834. Epub 2009 Apr 14.
9
A compartment model of VEGF distribution in humans in the presence of soluble VEGF receptor-1 acting as a ligand trap.在可溶性血管内皮生长因子受体-1作为配体陷阱存在的情况下,人类血管内皮生长因子分布的房室模型
PLoS One. 2009;4(4):e5108. doi: 10.1371/journal.pone.0005108. Epub 2009 Apr 8.
10
Multiscale models of angiogenesis.血管生成的多尺度模型。
IEEE Eng Med Biol Mag. 2009 Mar-Apr;28(2):14-31. doi: 10.1109/MEMB.2009.931791.

癌症中与血管内皮生长因子相关的血管生成过程的计算模型。

Computational models of VEGF-associated angiogenic processes in cancer.

作者信息

Stefanini Marianne O, Qutub Amina A, Mac Gabhann Feilim, Popel Aleksander S

机构信息

Department of Biomedical Engineering, School of Medicine, Johns Hopkins University, Baltimore, MD 21205, USA.

出版信息

Math Med Biol. 2012 Mar;29(1):85-94. doi: 10.1093/imammb/dqq025. Epub 2011 Jan 25.

DOI:10.1093/imammb/dqq025
PMID:21266494
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4104688/
Abstract

Tumour angiogenesis allows a growing mass of cancer cells to overcome oxygen diffusion limitation and to increase cell survival. The growth of capillaries from pre-existing blood vessels is the result of numerous signalling cascades involving different molecules and of cellular events involving multiple cell and tissue types. Computational models offer insight into the mechanisms governing angiogenesis and provide quantitative information on parameters difficult to assess by experiments alone. In this article, we summarize results from computational models of tumour angiogenic processes with a focus on the molecular-detailed vascular endothelial growth factor-associated models that have been developed in our laboratory, spanning multiple scales from the molecular to whole body.

摘要

肿瘤血管生成使不断增长的癌细胞团能够克服氧扩散限制并提高细胞存活率。从已有的血管中生长出毛细血管是众多涉及不同分子的信号级联反应以及涉及多种细胞和组织类型的细胞事件的结果。计算模型有助于深入了解血管生成的调控机制,并提供仅凭实验难以评估的参数的定量信息。在本文中,我们总结了肿瘤血管生成过程计算模型的结果,重点关注我们实验室开发的与血管内皮生长因子相关的分子细节模型,这些模型跨越了从分子到全身的多个尺度。