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Can cancer GWAS variants modulate immune cells in the tumor microenvironment?

Yi Zhang, Mohith Manjunath, Jialu Yan, Brittany A. Baur, Shilu Zhang, Sushmita Roy, Jun S. Song
doi: https://doi.org/10.1101/493171
Yi Zhang
1Department of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
2Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
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Mohith Manjunath
2Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
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Jialu Yan
2Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
3Department of Physics, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
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Brittany A. Baur
4Wisconsin Institute for Discovery, University of Wisconsin–Madison, Madison, WI 53792, USA.
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Shilu Zhang
4Wisconsin Institute for Discovery, University of Wisconsin–Madison, Madison, WI 53792, USA.
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Sushmita Roy
4Wisconsin Institute for Discovery, University of Wisconsin–Madison, Madison, WI 53792, USA.
5Department of Biostatistics and Medical Informatics, University of Wisconsin–Madison, Madison, WI 53792, USA.
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Jun S. Song
2Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
3Department of Physics, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
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  • For correspondence: songj@illinois.edu
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Abstract

Genome-wide association studies (GWAS) have hitherto identified several genetic variants associated with cancer susceptibility, but the molecular functions of these risk modulators remain largely uncharacterized. Recent studies have begun to uncover the regulatory potential of non-coding GWAS SNPs by using epigenetic information in corresponding cancer cell types and matched normal tissues. However, this approach does not explore the potential effect of risk germline variants on other important cell types that constitute the microenvironment of tumor or its precursor. This paper presents evidence that the breast cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor infiltrating lymphocytes. CTSW is a candidate tumor-suppressor gene, with expression highly specific to immune cells and also positively correlated with breast cancer patient survival. Integrative analyses suggest a putative causative variant in a GWAS-linked enhancer in lymphocytes that loops to the 3’ end of CTSW through three-dimensional chromatin interaction. Our work thus poses the possibility that a cancer-associated genetic variant might regulate a gene not only in the cell of cancer origin, but also in immune cells in the microenvironment, thereby modulating the immune surveillance by T lymphocytes and natural killer cells and affecting the clearing of early cancer initiating cells.

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Posted December 13, 2018.
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Can cancer GWAS variants modulate immune cells in the tumor microenvironment?
Yi Zhang, Mohith Manjunath, Jialu Yan, Brittany A. Baur, Shilu Zhang, Sushmita Roy, Jun S. Song
bioRxiv 493171; doi: https://doi.org/10.1101/493171
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Can cancer GWAS variants modulate immune cells in the tumor microenvironment?
Yi Zhang, Mohith Manjunath, Jialu Yan, Brittany A. Baur, Shilu Zhang, Sushmita Roy, Jun S. Song
bioRxiv 493171; doi: https://doi.org/10.1101/493171

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