Objective To study the pathogenesis of recurrent venous thromboembolism(VTE)and its correlation with malignant tumors,bioinformatics methods were used to predict susceptibility genes,and their expression in tumor tissue and overall survival(OS)were analyzed.Methods Genes prediction were based on the analysis of GSE19151 chip by GEO2R online analysis tool.Differentially expressed genes(DEGs)were screened for enrichment analysis of Gene Ontology(GO)biological process and Kyoto Encyclopedia of Genes(KEGG)signaling pathway.Network of PPI was constructed to obtain key genes and intersected with disease-related genes to obtain candidate genes.The expression and prognosis of susceptibility genes in tumors were analyzed using GEPIA2 database.Results A total of 211 DEGs were screened,of which 49 were up-regulated and 162 were down-regulated.The GO biological process of up-regulated genes mainly involved the regulation of auxin response factor(ARF)protein signal transduction,B cell receptor signaling pathway,Rho protein signal transduction and positive regulation of cell extravasation,etc.Signaling pathways of KEGG were involved in shigellosis,human T-cell leukemia virus type Ⅰ infection,phospholipase D signaling pathway,Rap1 signaling pathway and phosphatidylinositol signaling system,etc.Nineteen key genes were analyzed by network of PPI which mapped with disease-related genes,and 5 susceptibility genes were obtained,namely TP53,ICAM1,PIK3CD,PLEC and TLN1.Susceptibility genes were widely distributed in malignant tumors by GEPIA2.Compared with other tumors,the OS of high expression group of TP53,ICAM1,PIK3CD and TLN1 in glioma were significantly lower than that of low expression group(P<0.05).The expression of TP53,ICAM1 and TLN1 in malignant tumor tissues of glioma were significantly higher than that in normal tissues(P<0.05).Conclusion TP53,ICAM1,PIK3CD,PLEC and TLN1 maybe potential markers of recurrent VTE through bioinformatics analysis.The high expression of these genes were significantly correlated with poor prognosis,which provided clues and directions for studying the mechanism of tumor-induced recurrent VTE.