Using Psoriasis-Genes to readout Overlap Pathways from TCGA

Abstract One major challenge in studying the psoriasis is the lack of multi-omics and sufficient measurement datasets for psoriasis, which only provides limited insights into the pathogenesis of psoriasis. As the psoriasis is associated with the dysfunction of pathways, the pathogenesis of psoriasis can be investigated with the aids of big omics data from tumors in The Cancer Genome Atlas (TCGA), a data set that is in fact the records of random pathway perturbation experiments performed by nature. We first collect psoriasis related genes found by previous researches of psoriasis. We then utilize the gene expression and genomic alteration data from thousands of tumors in TCGA cohort to identify genomic alterations that potentially perturb pathways regulating expressions of these psoriasis related genes. We have found that genomic alterations of some genes are associated with the expression changes of psoriasis related genes in tumors, which implies that the genomic alteration of these genes may perturb pathways involved in the development of the psoriasis. For example, we found that SGAs of certain genes (E.g., TNFAIP8L3, IL-23, ANGPT2, IFIH1) are highly likely to be involved in the pathogenesis of psoriasis. Enrichment analysis showed that SGAs of these genes perturb signaling pathways regulating cell proliferation and/or angiogenesis-relevant activities of cells, which are well-known to be biologically related to the development of both psoriasis and cancers. The approach of using big genomic data of tumors to search for pathways involved in the psoriasis development gains insights into the mechanism of psoriasis.