IL11在腫瘤微環境上的影響

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”異質性是怎樣出現的以及它對癌癥病情發展的后果是什么仍然比較模糊。

現在，Kornelia Polyak及同事利用一個小鼠模型發現，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基 lonza 04-418Q無血清培養基  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基 lonza 12-725F無血清培養基 網址鏈接http://bitebo.com/a/gb2312/gongsixinxi/shichanghuodong/2014/0514/5157.html

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