Lymph node metastasis is of major prognostic significance for
breast cancer.
Lymph node metastasis arises at a very early stage in some patients. Using the data downloaded from the TCGA database, we studied the differences between primary
tumors with and without
lymph node metastasis at the multi-omics level using bioinformatics approaches. Our study found that low mutation and neoantigen burdens correlated with lymph node metastazation of
breast cancer. All three conserved domains in TP53 were mutated in lymph node-negative breast
cancers, whereas only one domain was mutated in lymph node-positive samples. Mutations in microtubule-related
proteins appear to help immune cells recognize
tumors and inhibit their
lymph node metastasis. Destroying microtubule-related
proteins is a potential therapeutic strategy to inhibit
lymph node metastasis of
breast cancer. As the neoantigens specifically present in lymph node-positive breast
cancers, MAPK10, BC9L, TRIM65, CD93, KITLG, CNPPD1, CPED1, CCDC146, TMEM185A, INO80D, and PSMD11 are potential targets for
vaccine design. In the tumor microenvironment, reduced numbers of effector immune cells, especially activated memory CD4+ T cells and activated mast cells, facilitate
breast cancer metastasis to the lymph nodes. According to transcriptome data,
lymph node metastasis was mostly driven by gene mutation rather than by gene expression. Although differential gene expression analysis was based on
lymph node metastasis status, many genes were shown to be differentially expressed based on
estrogen receptor status.