生物
癌症的体细胞进化
谱系(遗传)
病毒系统动力学
表观遗传学
肿瘤进展
表观基因组
表型
进化生物学
克拉斯
系统发育树
计算生物学
遗传学
癌症
突变
基因
DNA甲基化
基因表达
作者
Dian Yang,Matthew G. Jones,Santiago Naranjo,William M. Rideout,Kyung Hoi Min,Raymond Ho,Wei Wu,Joseph M. Replogle,Jennifer L. Page,Jeffrey J. Quinn,Felix Horns,Xiaojie Qiu,Michael Z. Chen,William A. Freed-Pastor,Christopher S. McGinnis,David M. Patterson,Zev J. Gartner,Eric D. Chow,Trever G. Bivona,Michelle M. Chan,Nir Yosef,Tyler Jacks,Jonathan S. Weissman
出处
期刊:Cell
[Elsevier]
日期:2022-05-01
卷期号:185 (11): 1905-1923.e25
被引量:175
标识
DOI:10.1016/j.cell.2022.04.015
摘要
Tumor evolution is driven by the progressive acquisition of genetic and epigenetic alterations that enable uncontrolled growth and expansion to neighboring and distal tissues. The study of phylogenetic relationships between cancer cells provides key insights into these processes. Here, we introduced an evolving lineage-tracing system with a single-cell RNA-seq readout into a mouse model of Kras;Trp53(KP)-driven lung adenocarcinoma and tracked tumor evolution from single-transformed cells to metastatic tumors at unprecedented resolution. We found that the loss of the initial, stable alveolar-type2-like state was accompanied by a transient increase in plasticity. This was followed by the adoption of distinct transcriptional programs that enable rapid expansion and, ultimately, clonal sweep of stable subclones capable of metastasizing. Finally, tumors develop through stereotypical evolutionary trajectories, and perturbing additional tumor suppressors accelerates progression by creating novel trajectories. Our study elucidates the hierarchical nature of tumor evolution and, more broadly, enables in-depth studies of tumor progression.
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