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摘要翻译：
我们研究了表皮生长因子受体(EGFR)密度对肿瘤生长动力学的影响，在亚细胞和多细胞水平上使用我们先前开发的模型。该算法采用基于多尺度二维Agent的方法，结合转化生长因子α（TGFalpha）诱导的EGFR-基因-蛋白相互作用网络，模拟脑肿瘤的生长。结果证实，细胞受体密度的增加与肿瘤系统时空扩展动力学的加速有关。这种多细胞行为不能仅仅根据空间亚细胞动力学来解释，这在Silico中研究的三种胶质瘤细胞系中保持定性相似。相反，我们发现EGFR密度较高的细胞在增殖和迁移特性之间的表型转换活性早期增加，这与PLCgamma介导的TGFalpha-EGFR自分泌网络所产生的较高水平的初始自刺激有关。这表明在这些趋化作用的肿瘤系统中有更活跃的蛋白质水平的相互作用，并支持EGFR通路翻译后调节的作用。讨论了这些结果对实验性癌症研究的影响。
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英文标题：
《The Effects of EGF-Receptor Density on Multiscale Tumor Growth Patterns》
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作者：
Chaitanya A. Athale and Thomas S. Deisboeck
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最新提交年份：
2005
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分类信息：
一级分类：Quantitative Biology 数量生物学
二级分类：Cell Behavior 细胞行为
分类描述：Cell-cell signaling and interaction; morphogenesis and development; apoptosis; bacterial conjugation; viral-host interaction; immunology
细胞-细胞信号传导及相互作用；形态发生和发育；细胞凋亡；细菌接合；病毒-宿主相互作用；免疫学
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一级分类：Quantitative Biology 数量生物学
二级分类：Molecular Networks 分子网络
分类描述：Gene regulation, signal transduction, proteomics, metabolomics, gene and enzymatic networks
基因调控、信号转导、蛋白质组学、代谢组学、基因和酶网络
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一级分类：Quantitative Biology 数量生物学
二级分类：Other Quantitative Biology 其他定量生物学
分类描述：Work in quantitative biology that does not fit into the other q-bio classifications
不适合其他q-bio分类的定量生物学工作
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英文摘要：
We studied the effects of epidermal growth factor receptor (EGFR) density on tumor growth dynamics, both on the sub- and the multi-cellular level using our previously developed model. This algorithm simulates the growth of a brain tumor using a multi-scale two-dimensional agent-based approach with an integrated transforming growth factor alpha (TGFalpha) induced EGFR-gene-protein interaction network. The results confirm that increasing cell receptor density correlates with an acceleration of the tumor system's spatio-temporal expansion dynamics. This multicellular behavior cannot be explained solely on the basis of spatial sub-cellular dynamics, which remain qualitatively similar amongst the three glioma cell lines investigated here in silico. Rather, we find that cells with higher EGFR density show an early increase in the phenotypic switching activity between proliferative and migratory traits, linked to a higher level of initial auto-stimulation by the PLCgamma-mediated TGFalpha-EGFR autocrine network. This indicates a more active protein level interaction in these chemotactically acting tumor systems and supports the role of post-translational regulation for the implemented EGFR pathway. Implications of these results for experimental cancer research are discussed.
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PDF链接：
https://arxiv.org/pdf/q-bio/0502002
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