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About ImmunEscpMap

Immune escape plays a critical role in tumorigenesis, enabling cancer cells to evade immune surveillance. Despite advances in immunotherapy treatments, the effectiveness is often limited by tumor heterogeneity. A detailed characterization of immune escape mechanisms will be helpful to improve the efficacy of cancer immunotherapy. To achieve this, we build ImmunEscpMap, a Knowledgebase of Cancer Immune Escape Mechanisms, which encompasses 8 key strategies: (1) Chemokine, (2) Endothelial Cell Anergy, (3) Inducing Apoptosis of Cytotoxic T Cells, (4) Inhibiting Recruitment of Dendritic Cells, (5) Inhibiting Target Recognition, (6) Matrix Barrier, (7) Metabolic Barrier, (8) T Cell Dysfunction and Exhaustion. Through literature mining, we curated 517 genes contribute to cancer immune evasion, and conducted functional analyses using large-scale genomic data, primarily sourced from The Cancer Genome Atlas (TCGA) along with additional datasets.

For each gene, ImmunEscpMap provides 7 categories of knowledge, including differential gene expression and methylation analysis, pathway enrichment analysis, immunotherapy response, limmune infiltration, immune subtypes and immune selection status, gene associated drugs and diseases, and the survival analysis. ImmunEscpMap supports researchers to interrogate specific genes within the context of tumor immune escape, and formulate reasonable hypotheses. We hope the application of ImmunEscpMap could enhance the understanding of immune evasion and improve immunotherapeutic strategies.

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Examples: Gene symbol: IFNG, ERBB2; Entrez gene ID: 3458, 2064
bullet pointBrowse by cancer type

Bladder cancer (14)

Bone cancer (11)

Brain cancer (52)

Breast cancer (93)

Colon cancer (14)

Gastrointestinal cancer (43)

Head and neck cancer (23)

Leukemia (93)

Liver cancer (69)

Lung cancer (97)

Lymphoma (31)

Melanoma (92)

Myeloma (11)

Oral cancer (18)

Ovarian cancer (52)

Pancreatic cancer (66)

Prostate cancer (39)

Renal cancer (26)

Other cancers (24)

Pan-cancer (123)
bullet pointBrowse by cancer immune escape mechanisms
Chemokine: The chemokine ((C-X-C motif) participates in the generation and recruitment of immune cells that contribute to a pro-tumorigenic microenvironment.

Chemokine (104)

 Endothelial cell anergy: During angiogensis, the lack of endothelial adhesion molecules suppress the immune infiltration. In addition, the endothelial cells express immunosuppressive molecules that induce the apoptosis of immune cells.

Endothelial cell anergy (93)

 Inducing apoptosis of CTLs: The cancer cell upregulates FasL, which can bind to Fas expressed by activated T cells, leading to T cell apoptosis.

Inducing apoptosis of CTLs (14)
Inhibiting recruitment of dendritic cells: Tumor cell derived PGE2 can inhibit the function of natural killer cells and the recruitment of dendritic cells.

Inhibiting recruitment of dendritic cells (58)

 Inhibiting target recognition: The T cell responses can be inhibited by the involvement of inhibitory ligand, the lack of MHC class I molecules and the loss of neoantigens.

Inhibiting target recognition (135)

 Matrix barrier: The extracellular matrix and surrounding cancer associated fibroblasts can create a physical barrier that suppresses immune cell infiltration.

Matrix barrier (126)
Metabolic barrier: The dysregulated vasculature reduces oxygen and nutrient levels in the tumor core and prevents metabolites that suppress T cells from being transported out of the tumor.

Metabolic barrier (124)

 T cell dysfunction and exhaustion: The activation of mTOR leads to the expression of downstream transcriptional factors, which regulates PD-1 expression and causes T cell exhaustion and dysfunction.

T cell dysfunction and exhaustion (89)