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| 購買進口儀器、試劑和耗材——就在始于2001年的畢特博生物 www.gducity.com |
 IL11在腫瘤微環(huán)境上的影響 腫瘤經常由在基因損傷和生物性質上都不同的細胞群組成，但這種“亞克隆”異質性是怎樣出現(xiàn)的以及它對癌癥病情發(fā)展的后果是什么仍然比較模糊。 現(xiàn)在，Kornelia Polyak及同事利用一個小鼠模型發(fā)現(xiàn)，腫瘤生長可以由一個小的細胞子類群通過一個非細胞自主機制(non-cell-autonomous mechanism)來驅動。然而，這一小的細胞子類群也可被更快的增殖競爭對手超越，導致腫瘤瓦解。這些結果顯示了異質腫瘤中亞克隆相互作用和克隆干涉的復雜性，對于治療也有潛在的意義。 原文摘要： Non-cell-autonomous driving of tumour growth supports sub-clonal heterogeneity Andriy Marusyk, Doris P. Tabassum, Philipp M. Altrock, Vanessa Almendro, Franziska Michor & Kornelia Polyak Cancers arise through a process of somatic evolution that can result in substantial sub-clonal heterogeneity within tumours. The mechanisms responsible for the coexistence of distinct sub-clones and the biological consequences of this coexistence remain poorly understood. Here we used a mouse xenograft model to investigate the impact of sub-clonal heterogeneity on tumour phenotypes and the competitive expansion of individual clones. We found that tumour growth can be driven by a minor cell subpopulation, which enhances the proliferation of all cells within a tumour by overcoming environmental constraints and yet can be outcompeted by faster proliferating competitors, resulting in tumour collapse. We developed a mathematical modelling framework to identify the rules underlying the generation of intra-tumour clonal heterogeneity. We found that non-cell-autonomous driving of tumour growth, together with clonal interference, stabilizes sub-clonal heterogeneity, thereby enabling inter-clonal interactions that can lead to new phenotypic traits.
細胞治療所用的無血清培養(yǎng)基 lonza 04-418Q無血清培養(yǎng)基 網址鏈接http://www.gducity.com/a/gb2312/info/2013/0413/5029.html 干細胞治療所用的無血清培養(yǎng)基 lonza 12-725F無血清培養(yǎng)基 網址鏈接http://bitebo.com/a/gb2312/gongsixinxi/shichanghuodong/2014/0514/5157.html
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購買進口儀器、試劑和耗材——就在始于2001年的畢特博生物
www.gducity.com |
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