Table 1.

Summary of angiogenic and oncogenic pathways implicated in immune editing

Gene	Mechanism	References
Angiogenesis	Expression of FasL allows selective killing of effector T cells through tumor-derived VEGF, IL-10, and prostaglandin action.	Motz et al.[20] Carman et al.[21]
	Expression of molecules such as IDO and STING by endothelial cells is associated with response or overcoming resistance to immunotherapy.	Seeber et al.[27] Chevolet et al.[28]; Krähenbühl et al.[29] Meireson et al.[30] Yang et al.[33]
EGFR Mutation/ Overexpression	Aberrant expression leads to decreased PD-L1 expression in NSCLC and is associated with decreased tumor mutational burden and immunogenicity.	Dong et al.[45]; Soo et al.[46]; Zhang et al.[49]; Gainor et al.[52]
	Activating mutations associated with increased PD-L1 and immunosuppressive cytokine expression, and reduced T-cell viability.	Chen et al.[39]; Akbay et al.[40]; Azuma et al.[41]
PTEN Loss	Loss leads to increased PD-L1 expression, increased autologous T-cell apoptosis, and overall decreased tumor immunogenicity.	Parsa et al.[65]; Waldron et al.[66]
	PTEN loss leads to increased immunosuppressive cytokine expression (including VEGF), decreased T-cell trafficking, and inhibition of autophagy and cytolytic activity.	Peng et al.[67]; George et al.[69]
NOTCH Amplification	Promotes an immunosuppressive microenvironment by increasing myeloid-derived suppressor cells, tumor-associated macrophages and regulatory T cells, and decreasing cytotoxic T cells.	Shen et al.[78] Balli et al.[79] Qiu et al.[80]
	Activation of the NOTCH pathway promotes TH1 and inhibits TH2 differentiation.	Tindemans et al.[81]
	Promotes TGFβ signaling-mediated tumor growth through upregulation of proinflammatory IL1B and CCL2 cytokines and recruitment of tumor-associated macrophages.	Shen et al.[78]

FasL: Fas ligand; VEGF: vascular endothelial growth factor; IL-10: interleukin-10; IDO: indoleamine 2,3-dioxygenase; STING: stimulator of interferon genes; PD-L1: programmed death-ligand 1; NSCLC: non-small cell lung cancer; PTEN: phosphatase and tensin homolog; TH1: T helper type 1; TH2: T helper type 2; TGFβ: transforming growth factor beta; IL1β: interleukin 1 beta; CCL2: C-C motif chemokine ligand 2.