Data for: Loss of TET2 affects proliferation and drug sensitivity through altered dynamics of cell-state transitions

Data accompanying the paper "Loss of TET2 affects proliferation and drug sensitivity through altered dynamics of cell-state transitions". The dataset includes:
* DNA methylation beta values and log2FC (Illumina Infinium)
* RNA transcript counts and log2FC (Lexogen Quantseq)
* Flow cytometry (Aria IIu)
* qPCR
* fit parameter values
* code to generate figures

Please refer to the manuscript for more detailed methods on how the data were generated.

A persistent puzzle in cancer biology is how mutations, which neither alter growth signaling pathways nor directly interfere with drug mechanism, can still recur and persist in tumors. One example is the mutation of the DNA demethylase TET2 in acute myeloid leukemias (AMLs) that frequently persists from diagnosis through remission and relapse, but whose fitness advantage in chemotherapy is unclear. Here we use isogenic human AML cell lines to show that TET2 loss-of-function alters the dynamics of transitions between differentiated and stem-like states. A conceptual mathematical model and experimental validation suggest these altered cell-state dynamics can benefit the cell population by slowing population decay during drug treatment and lowering the number of survivor cells needed to re-establish the initial population. These studies shed light on the functional and phenotypic effects of a TET2 mutation in AML and illustrate how a single gene mutation can alter a cells’ phenotypic plasticity.

随同论文《TET2基因的缺失通过改变细胞状态转换的动态影响增殖和药物敏感性》一同提供的配套数据集包括：
* DNA甲基化β值和log2FC（Illumina Infinium）
* RNA转录计数和log2FC（Lexogen Quantseq）
* 流式细胞术（Aria IIu）
* 定量PCR
* 适配参数值
* 生成图形的代码

请参阅手稿以获取有关数据生成方法的更详细信息。

癌症生物学中的一个持续之谜是，为何那些既未改变生长信号通路，也未直接干扰药物机制的突变，仍然能够在肿瘤中反复出现并持续存在。一个例子是急性髓系白血病（AML）中DNA去甲基化酶TET2的突变，这种突变通常从诊断持续至缓解期和复发期，但其化疗的适应性优势尚不明确。在本研究中，我们利用同源人类AML细胞系展示了TET2功能缺失如何改变分化状态和干样状态之间的转换动态。一个概念性的数学模型和实验验证表明，这些改变的细胞状态动态可以通过减缓药物治疗期间的种群衰减以及降低重建初始种群所需的幸存细胞数量，从而为细胞种群带来益处。这些研究揭示了AML中TET2突变的功能和表型效应，并阐述了单个基因突变如何改变细胞的表型可塑性。