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Nat Commun. 2017 Oct 20;8(1):1077. doi: 10.1038/s41467-017-01027-z.

Comprehensive analysis of normal adjacent to tumor transcriptomes.

Author information

1
Institute for Computational Health Sciences, University of California, San Francisco, CA, 94158, USA. dvir.aran@ucsf.edu.
2
Department of Cell and Tissue Biology, University of California, San Francisco, CA, 94143, USA.
3
Biomedical Sciences Graduate Program, University of California, San Francisco, CA, 94143, USA.
4
Department of Pathology, Stanford University Medical Center, Stanford, CA, 94305, USA.
5
Institute for Computational Health Sciences, University of California, San Francisco, CA, 94158, USA.
6
Korea Institute of Science and Technology Information, Biomedical HPC Research Center, 245 Daehak-ro, Yuseong-gu, Daejeon, Korea.
7
Department of Pathology, University of California, San Francisco, CA, 94143, USA.
8
Department of Medicine, University of California, San Francisco, CA, 94143, USA.
9
Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, CA, 94115, USA.
10
Institute for Computational Health Sciences, University of California, San Francisco, CA, 94158, USA. atul.butte@ucsf.edu.

Abstract

Histologically normal tissue adjacent to the tumor (NAT) is commonly used as a control in cancer studies. However, little is known about the transcriptomic profile of NAT, how it is influenced by the tumor, and how the profile compares with non-tumor-bearing tissues. Here, we integrate data from the Genotype-Tissue Expression project and The Cancer Genome Atlas to comprehensively analyze the transcriptomes of healthy, NAT, and tumor tissues in 6506 samples across eight tissues and corresponding tumor types. Our analysis shows that NAT presents a unique intermediate state between healthy and tumor. Differential gene expression and protein-protein interaction analyses reveal altered pathways shared among NATs across tissue types. We characterize a set of 18 genes that are specifically activated in NATs. By applying pathway and tissue composition analyses, we suggest a pan-cancer mechanism of pro-inflammatory signals from the tumor stimulates an inflammatory response in the adjacent endothelium.

PMID:
29057876
PMCID:
PMC5651823
DOI:
10.1038/s41467-017-01027-z
[Indexed for MEDLINE]
Free PMC Article

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