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回复 marrowstem 的帖子
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你的回答让我学到了很多,由于对这个领域了解很少,所以关于clonal evolution等问题我在网上搜了些答案,然后加上我自己的理解写一下个人看法,不足之处请指正。; C5 J* O* N# n* ]8 q: S
维基百科上是这样说csc假说和clonal evolution假说的:“The cancer stem-cell hypothesis relies on the fact that a lot of tumors are heterogeneous – the cells in the tumor vary by phenotype and functions[71][72][73]. Current research shows that in many cancers there is apparent hierarchy among cells[71][72][73]. in general, there is a small population of cells in the tumor – about 0.2%-1% [72] – that exhibits stem cell-like properties. These cells have the ability to give rise to a variety of cells in tumor tissue, self-renew indefinitely, and upon transfer can form new tumors. According to the hypothesis, cancer stem cells are the only cells capable of tumorigenesis – initiation of a new tumor[71]. Cancer stem cell hypothesis might explain such phenomena as metastasis and remission.* f8 h x. R$ |. }% q4 c- W# k
& ~/ c& ^- n! p( u# rThe monoclonal model of cancer and the cancer stem-cell model are not mutually exclusive[71]. Cancer stem cell arises by clonal evolution as a result of selection for the cell with the highest fitness in the neoplasm. This way, the heterogeneous nature of neoplasm can be explained by two processes – clonal evolution, or the hierarchical differentiation of cells, regulated by cancer stem cells[71]. All cancers arise as a result of somatic evolution, but only some of them fit the cancer stem cell hypothesis[71]. The evolutionary processes do not cease when a population of cancer stem cells arises in a tumor. Cancer treatment drugs pose a strong selective force on all types of cells in tumors, including cancer stem cells, which would be forced to evolve resistance to the treatment. It is interesting to note that cancer stem cells do not always have to have the highest resistance among the cells in the tumor to survive chemotherapy and re-emerge afterwards. The surviving cells might be in a special microenvironment, which protects them from adverse effects of treatment[71].- i% i) q0 L0 P' Z
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It is currently unclear as to whether cancer stem cells arise from adult stem cell transformation, a maturation arrest of progenitor cells, or as a result of dedifferentiation of mature cells ”& D o" F' m5 W% Q! B$ ~, l7 b
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另外有人关于这两个假说的讨论:http://www.fightaging.org/archiv ... ncer-stem-cells.php
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我个人认为,你前面说的clonal evolution假说和csc假说并不矛盾,9 s, q9 M. {$ [1 M5 s: |$ r. d
1 我们可以认为这些异质性的细胞都是来源于一个细胞的,这个细胞可能是失控的干细胞,它通过有丝分裂产生大量子代细胞,这些后代有一定的分裂和分化能力,但能力强弱可能不同,这些细胞可能就是肿瘤细胞,而产生这些肿瘤细胞的那个源头细胞可能就是csc
' G1 O8 u% @' @1 B/ R0 s5 G' r2 你说的那些增殖力强的细胞在肿瘤发生中起了主要作用,但它们不能被称为csc。这个观点我是同意的,很有可能csc只是负责产生这些细胞,但这些细胞才是在肿瘤发生的过程中发挥高效力的细胞,而且它们也不能被称为csc,我个人认为可以称它们为肿瘤组织的progenitors,它们是csc的后代,能够大快速增殖并有一定的分化能力,它们也有clonal evolution的能力,但它们都是来源于csc的。csc或许只能在特定的时候产生一些这样类型的progenitors,由这些progenitors去形成肿瘤组织。 |
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