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肿瘤间和肿瘤内侵袭潜能的异质性。

Between-tumor and within-tumor heterogeneity in invasive potential.

机构信息

Center for Cell Dynamics and Department of Cell Biology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.

High-Throughout Biology Center and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland, United States of America.

出版信息

PLoS Comput Biol. 2020 Jan 21;16(1):e1007464. doi: 10.1371/journal.pcbi.1007464. eCollection 2020 Jan.

Abstract

For women with access to healthcare and early detection, breast cancer deaths are caused primarily by metastasis rather than growth of the primary tumor. Metastasis has been difficult to study because it happens deep in the body, occurs over years, and involves a small fraction of cells from the primary tumor. Furthermore, within-tumor heterogeneity relevant to metastasis can also lead to therapy failures and is obscured by studies of bulk tissue. Here we exploit heterogeneity to identify molecular mechanisms of metastasis. We use "organoids", groups of hundreds of tumor cells taken from a patient and grown in the lab, to probe tumor heterogeneity, with potentially thousands of organoids generated from a single tumor. We show that organoids have the character of biological replicates: within-tumor and between-tumor variation are of similar magnitude. We develop new methods based on population genetics and variance components models to build between-tumor and within-tumor statistical tests, using organoids analogously to large sibships and vastly amplifying the test power. We show great efficiency for tests based on the organoids with the most extreme phenotypes and potential cost savings from pooled tests of the extreme tails, with organoids generated from hundreds of tumors having power predicted to be similar to bulk tests of hundreds of thousands of tumors. We apply these methods to an association test for molecular correlates of invasion, using a novel quantitative invasion phenotype calculated as the spectral power of the organoid boundary. These new approaches combine to show a strong association between invasion and protein expression of Keratin 14, a known biomarker for poor prognosis, with p = 2 × 10-45 for within-tumor tests of individual organoids and p < 10-6 for pooled tests of extreme tails. Future studies using these methods could lead to discoveries of new classes of cancer targets and development of corresponding therapeutics. All data and methods are available under an open source license at https://github.com/baderzone/invasion_2019.

摘要

对于能够获得医疗保健和早期检测的女性来说,乳腺癌死亡主要是由转移而不是原发性肿瘤的生长引起的。转移很难研究,因为它发生在身体深处,需要多年时间,并且涉及原发性肿瘤的一小部分细胞。此外,与转移相关的肿瘤内异质性也可能导致治疗失败,并被对大块组织的研究所掩盖。在这里,我们利用异质性来识别转移的分子机制。我们使用“类器官”,即从患者身上取出的数百个肿瘤细胞群,在实验室中进行培养,以探测肿瘤异质性,从单个肿瘤中可以生成数千个类器官。我们表明,类器官具有生物学复制的特征:肿瘤内和肿瘤间的变异程度相似。我们开发了基于群体遗传学和方差分量模型的新方法,基于类器官建立肿瘤间和肿瘤内的统计检验,使用类器官类似于大的同胞群体,并大大提高了检验能力。我们展示了基于最极端表型的类器官检验的高效率,以及极端尾部的 pooled 检验的潜在成本节约,从数百个肿瘤中生成的类器官具有预测的与数万肿瘤的 bulk 检验相似的检验能力。我们将这些方法应用于侵袭的分子相关性的关联检验,使用作为类器官边界的光谱功率的新的定量侵袭表型。这些新方法结合起来,显示出侵袭与角蛋白 14(一种预后不良的已知生物标志物)的蛋白表达之间存在很强的关联,个体类器官的肿瘤内检验的 p 值为 2×10-45,极端尾部 pooled 检验的 p 值小于 10-6。未来使用这些方法的研究可能会发现新的癌症靶点,并开发相应的治疗方法。所有数据和方法都在一个开源许可证下可用,网址为 https://github.com/baderzone/invasion_2019。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d7da/6994152/8215d9d24e2a/pcbi.1007464.g001.jpg

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