Multi-omic signatures identify pan-cancer classes of tumors beyond tissue of origin

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作者
Agustín González-Reymúndez
Ana I. Vázquez
机构
[1] Michigan State University,Department of Epidemiology and Biostatistics
[2] Michigan State University,Institute for Quantitative Health Science and Engineering (IQ)
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Scientific Reports | / 10卷
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Despite recent advances in treatment, cancer continues to be one of the most lethal human maladies. One of the challenges of cancer treatment is the diversity among similar tumors that exhibit different clinical outcomes. Most of this variability comes from wide-spread molecular alterations that can be summarized by omic integration. Here, we have identified eight novel tumor groups (C1-8) via omic integration, characterized by unique cancer signatures and clinical characteristics. C3 had the best clinical outcomes, while C2 and C5 had poorest. C1, C7, and C8 were upregulated for cellular and mitochondrial translation, and relatively low proliferation. C6 and C4 were also downregulated for cellular and mitochondrial translation, and had high proliferation rates. C4 was represented by copy losses on chromosome 6, and had the highest number of metastatic samples. C8 was characterized by copy losses on chromosome 11, having also the lowest lymphocytic infiltration rate. C6 had the lowest natural killer infiltration rate and was represented by copy gains of genes in chromosome 11. C7 was represented by copy gains on chromosome 6, and had the highest upregulation in mitochondrial translation. We believe that, since molecularly alike tumors could respond similarly to treatment, our results could inform therapeutic action.
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[21]  
Chang K(2011)Hallmarks of Cancer: The Next Generation Cell 144 14620-775
[22]  
Behring M(2011)Massive Genomic Rearrangement Acquired in a Single Catastrophic Event during Cancer Development Cell 144 757-81
[23]  
Taskesen E(2015)STRING v10: protein-protein interaction networks, integrated over the tree of life Nucleic Acids Res. 43 89-67128
[24]  
Hoadley KA(2016)Association of a Chromosomal Rearrangement Event with Mouse Posterior Polymorphous Corneal Dystrophy and Alterations in Csrp2bp, Dzank1, and Ovol2 Gene Expression PLoS One 11 29-550
[25]  
Yau C(2017)Genomic characteristics of pancreatic squamous cell carcinoma, an investigation by using high throughput sequencing after in-solution hybrid capture Oncotarget 8 20130096-782
[26]  
Stuart JM(2017)Genomic variants at 20p11 associated with body fat mass in the European population Obesity 25 715-176
[27]  
Benz CC(2007)Large-scale mapping of human protein-protein interactions by mass spectrometry Mol. Syst. Biol. 3 775-16
[28]  
Correspondence PWL(2014)A global assessment of cancer genomic alterations in epigenetic mechanisms Epigenetics Chromatin 7 67-1112
[29]  
Hoadley KA(2014)Role of anoctamins in cancer and apoptosis Philos. Trans. R. Soc. B Biol. Sci. 369 67117-600
[30]  
Thorsson V(2010)ANO1 amplification and expression in HNSCC with a high propensity for future distant metastasis and its functions in HNSCC cell lines Br. J. Cancer 103 543-490