Toward a systems-level probing of tumor clonality

Emanuelle I. Grody; Ajay Abraham; Vipul Shukla; Yogesh Goyal

doi:10.1016/j.isci.2023.106574

Toward a systems-level probing of tumor clonality

Emanuelle I. Grody, Ajay Abraham, Vipul Shukla^*, Yogesh Goyal^*

^*Corresponding author for this work

Cell & Developmental Biology

Research output: Contribution to journal › Review article › peer-review

3 Scopus citations

Abstract

Cancer has been described as a genetic disease that clonally evolves in the face of selective pressures imposed by cell-intrinsic and extrinsic factors. Although classical models based on genetic data predominantly propose Darwinian mechanisms of cancer evolution, recent single-cell profiling of cancers has described unprecedented heterogeneity in tumors providing support for alternative models of branched and neutral evolution through both genetic and non-genetic mechanisms. Emerging evidence points to a complex interplay between genetic, non-genetic, and extrinsic environmental factors in shaping the evolution of tumors. In this perspective, we briefly discuss the role of cell-intrinsic and extrinsic factors that shape clonal behaviors during tumor progression, metastasis, and drug resistance. Taking examples of pre-malignant states associated with hematological malignancies and esophageal cancer, we discuss recent paradigms of tumor evolution and prospective approaches to further enhance our understanding of this spatiotemporally regulated process.

Original language	English (US)
Article number	106574
Journal	iScience
Volume	26
Issue number	5
DOIs	https://doi.org/10.1016/j.isci.2023.106574
State	Published - May 19 2023

Funding

We thank Karun Kiani and the members of the Goyal and Shukla labs for helpful discussions and comments. Y.G. and E.I.G. acknowledge support from the Career Award at the Scientific Interface from BWF (1020614.01), startup funds from Northwestern University, and the NSF NRT 2021900-Synthesizing Biology Across Scales. V.S. and A.A. are supported by the R00 award from National Cancer Institute (CA248835), startup funds from Northwestern University and developmental funds from the Lurie Comprehensive Cancer Center at Northwestern University (P30CA060553). \u201CTumor microenvironment\u201D depiction in Figure 1 was created with BioRender.com. V.S. and Y.G. conceived the project and E.I.G. A.A. V.S. and Y.G. wrote the manuscript. Y.G. received consultancy fees from the Schmidt Science Fellows and the Rhodes Trust. All other authors declare no conflict of interest. We thank Karun Kiani and the members of the Goyal and Shukla labs for helpful discussions and comments. Y.G. and E.I.G. acknowledge support from the Career Award at the Scientific Interface from BWF ( 1020614.01 ), startup funds from Northwestern University , and the NSF NRT 2021900 -Synthesizing Biology Across Scales. V.S. and A.A. are supported by the R00 award from National Cancer Institute ( CA248835 ), startup funds from Northwestern University and developmental funds from the Lurie Comprehensive Cancer Center at Northwestern University ( P30CA060553 ). \u201CTumor microenvironment\u201D depiction in Figure 1 was created with BioRender.com .

Keywords

Cancer
Cancer systems biology
Immunology

ASJC Scopus subject areas

General

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/j.isci.2023.106574

Cite this

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title = "Toward a systems-level probing of tumor clonality",

abstract = "Cancer has been described as a genetic disease that clonally evolves in the face of selective pressures imposed by cell-intrinsic and extrinsic factors. Although classical models based on genetic data predominantly propose Darwinian mechanisms of cancer evolution, recent single-cell profiling of cancers has described unprecedented heterogeneity in tumors providing support for alternative models of branched and neutral evolution through both genetic and non-genetic mechanisms. Emerging evidence points to a complex interplay between genetic, non-genetic, and extrinsic environmental factors in shaping the evolution of tumors. In this perspective, we briefly discuss the role of cell-intrinsic and extrinsic factors that shape clonal behaviors during tumor progression, metastasis, and drug resistance. Taking examples of pre-malignant states associated with hematological malignancies and esophageal cancer, we discuss recent paradigms of tumor evolution and prospective approaches to further enhance our understanding of this spatiotemporally regulated process.",

keywords = "Cancer, Cancer systems biology, Immunology",

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AU - Grody, Emanuelle I.

AU - Abraham, Ajay

AU - Shukla, Vipul

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Y1 - 2023/5/19

N2 - Cancer has been described as a genetic disease that clonally evolves in the face of selective pressures imposed by cell-intrinsic and extrinsic factors. Although classical models based on genetic data predominantly propose Darwinian mechanisms of cancer evolution, recent single-cell profiling of cancers has described unprecedented heterogeneity in tumors providing support for alternative models of branched and neutral evolution through both genetic and non-genetic mechanisms. Emerging evidence points to a complex interplay between genetic, non-genetic, and extrinsic environmental factors in shaping the evolution of tumors. In this perspective, we briefly discuss the role of cell-intrinsic and extrinsic factors that shape clonal behaviors during tumor progression, metastasis, and drug resistance. Taking examples of pre-malignant states associated with hematological malignancies and esophageal cancer, we discuss recent paradigms of tumor evolution and prospective approaches to further enhance our understanding of this spatiotemporally regulated process.

AB - Cancer has been described as a genetic disease that clonally evolves in the face of selective pressures imposed by cell-intrinsic and extrinsic factors. Although classical models based on genetic data predominantly propose Darwinian mechanisms of cancer evolution, recent single-cell profiling of cancers has described unprecedented heterogeneity in tumors providing support for alternative models of branched and neutral evolution through both genetic and non-genetic mechanisms. Emerging evidence points to a complex interplay between genetic, non-genetic, and extrinsic environmental factors in shaping the evolution of tumors. In this perspective, we briefly discuss the role of cell-intrinsic and extrinsic factors that shape clonal behaviors during tumor progression, metastasis, and drug resistance. Taking examples of pre-malignant states associated with hematological malignancies and esophageal cancer, we discuss recent paradigms of tumor evolution and prospective approaches to further enhance our understanding of this spatiotemporally regulated process.

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KW - Immunology

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Toward a systems-level probing of tumor clonality

Abstract

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

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