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Background  Differences in genetics and microenvironment of LUAD patients with or without  TP53  mutation were analyzed to illustrate the role of  TP53  mutation within the carcinogenesis of LUAD, which will provide new concepts for the treatment of LUAD.    Methods   In this study, we used genetics and clinical info from the TCGA database, including somatic mutations data, RNA-seq, miRNA-seq, and clinical data. More than one bioinformatics tools were used to analyze the unique genomic pattern of  TP53 -related LUAD.    Results  According to  TP53  gene mutation status, we divided the LUAD patients into two groups, including 265 in the mutant group (MU) and 295 in the wild-type group (WT). 787 significant somatic mutations were detected between the groups, including mutations in  titin (TTN), type 2 ryanodine receptor (RYR2)  and  CUB and Sushi multiple domains 3(CSMD3) , which were up-regulated in the MU. However, no significant survival difference was observed. At the RNA level, we obtained 923 significantly differentially expressed genes; in the MU,  α-defensin 5(DEFA5), pregnancy-specific glycoprotein 5(PSG5)  and  neuropeptide Y(NPY)  were the most up-regulated genes,  glucose-6-phosphatase (G6PC), alpha-fetoprotein (AFP)  and  carry gametocidal (GC)  were the most down-regulated genes. GSVA analysis revealed 30 significant pathways. Compared with the WT, the expression of 12 pathways in the mutant group was up-regulated, most of which pointed to cell division. There were significant differences in tumor immune infiltrating cells, such as Macrophages M1, T cells CD4 memory activated, Mast cells resting, and Dendritic cells resting. In terms of immune genes, a total of 35 immune-related genes were screened, of which  VGF (VGF nerve growth factor inducible)  and  PGC (peroxisome proliferator-activated receptor gamma coactivator)  were the most significant up-regulated and down-regulated genes, respectively. Research on the expression pattern of immunomodulators found that 9 immune checkpoint molecules and 6 immune costimulatory molecules were considerably wholly different between the two groups.    Conclusions  Taking the mutant group as a reference, LUAD patients in the mutant group had significant differences in somatic mutations, mRNA-seq, miRNA-seq, immune infiltration, and immunomodulators, indicating that  TP53  mutation plays a crucial role in the occurrence and development of LUAD.    Supplementary Information  The online version contains supplementary material available at 10.1186/s12890-021-01671-8.

Differences in genetics and microenvironment of lung adenocarcinoma patients with or without TP53 mutation