癌症侵袭和微环境:可塑性和互惠性
Peter Friedl1, Stephanie Alexander
1Department of Cell Biology, Radboud University Nijmegen Medical Centre, 6500 HC Nijmegen, The Netherlands. p.friedl@ncmls.ru.nl
Cell
|November 29, 2011
概括
癌症侵袭涉及复杂的细胞和组织相互作用,由控制细胞运动和组织重塑的信号通路驱动. 这一过程产生了多样化的入侵路线,并促进了瘤异质性,导致转移.
科学领域:
- 细胞生物学 细胞生物学
- 癌症研究 癌症研究
- 生物物理学的生物物理.
背景情况:
- 癌症侵袭是一个动态的过程,涉及整个疾病进展过程中的细胞和组织适应.
- 关键机制包括控制细胞骨动力学和细胞/细胞/细胞矩阵结合的信号通路.
- 了解这些过程对于破译转移至关重要.
研究的目的:
- 阐明癌症入侵背后的细胞和组织驱动机制.
- 描述涉及组织入侵的分子系统 (粘附,蛋白酶,细胞因子).
- 解释瘤和组织环境的相互重编程如何塑造入侵路线和传播.
主要方法:
- 对癌症侵袭现有文献的审查和综合.
- 分析控制细胞骨动态和细胞结合的信号通路.
- 检查细胞矩阵和细胞-细胞粘附系统,蛋白酶和细胞因子.
主要成果:
- 癌症侵袭是由影响细胞骨动态和细胞结交周转的信号通路启动的.
- 细胞矩阵和细胞-细胞粘附,蛋白酶和细胞因子系统对于组织入侵至关重要.
- 瘤细胞和周围组织之间的相互重编程产生了多种不同的入侵模式,并增强了瘤异质性.
结论:
- 癌症侵袭是一个多方面的过程,涉及复杂的细胞和组织相互作用.
- 相互重编程产生的可塑性驱动着不同的入侵路线和转移性传播.
- 针对这些入侵机制可能会提供新的治疗策略.
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