Table 1.

Immunotherapies for cancer treatment.

Cancer Type	Immunotherapy Approach	Targets/Mechanism	Study Type	Cell Lines Used	Animals Used	Technologies Used/Assays Performed	Results	Reference
Bladder cancer	Monoclonal antibodies
	(i) KMP1 mAb	KMP1 binds to CD44 and blocks its function	In vivo and in vitro	Human bladder cancer cell lines EJ, BIU-87, and T24; normal human bladder cell line HCV29; human liver cancer cell line HepG; human cervical cancer cell lines HeLa	BALB/c normal mice and nude mice	Mass spectrometry and antigen affinity to determine KMP1 mechanism; RNA interference technology to knockdown CD44 expression	Bladder cancer clinical severity and prognosis were consistent with the expression of KMP1 epitope	[130]
	(ii) R3 mAb/ vofatamab	Inhibits proliferation and FGFR3 signaling by binding to wild-type FGFR3 and FGFR3 mutants	In vivo and in vitro	RT112, RT4, OPM2, Ba/F3, and UMUC-14	Female nu/nu mice or CB17 SCID mice	Cell proliferation assay, FACS assay, clonal growth assay, and FACS assay	Bladder cancer development was reduced in vivo by induced shRNA knockdown of FGFR3.	[131]
	Immune checkpoint inhibitors
	(i) Atezolizumab	Blocks immune checkpoint PD-L1/PD-1; reduces immunosuppressive signals; increases T-cell-mediated immunity against tumors	In vivo In vivo and in vitro	Human bladder cancer cell line pumc-91			In comparison to historical controls treated with conventional second-line regimens, individuals with advanced bladder cancer treated with atezolizumab exhibited a significantly improved response rate and survival	[132]
	Bispecific antibody anti-CD3 x anti-CD155	CD155Bi-Ab-armed ATCs secrete more IFN-γ and TNF-α, which increases cytokines and activates endogenous immune cells in vivo, inducing an immune response against tumor cells		MBT-2 cell line		Flow cytometry and ELISA	For CD155-positive bladder cancer, CD155 is a useful target. Additionally, CD155Bi-Ab-armed ATCs show promise concerning developing a novel approach to the present treatment of CD155-positive bladder cancer.	[133]
	BCG vaccines	Prominent infiltration of the bladder wall by immunocompetent cells and the release of cytokines into the urine	In vivo		Female C3H/HeN mice		Vaccine increased NK cell activity	[134,135]
Breast cancer	Monoclonal antibodies
	Trastuzumab	Inhibits intracellular signaling by binding to the extracellular domain of the receptor	In vitro	SK-BR-3 cell line			NK cells killed trastuzumab-coated erbB2-overexpressing cells through an ADCC mechanism mediated by the FcRIII receptor (CD16)	[136]
Lung cancer	Monoclonal antibodies
	Cetuximab	Binds to the extracellular domain of EGFR and blocks EGFR-mediated signal transduction	In vitro	LK-1, EBC-1, A549, LK87, Lu99, N417, Ms1, and LU65; epidermoid carcinoma cell line (A431)		Flow cytometry and immunohistochemistry	A correlation was observed between EGFR molecules on the cell, exerting cytotoxicity against lung cancer cell lines.	[137]
	Monoclonal antibodies
Prostate cancer	BLCA-38	In patients with prostate cancer, the BLCA-38 antibody binds primarily to prostate cancer cells but not to normal cells and may be useful in targeting novel therapies	In vivo and In vitro	PZ-HPV-7 prostate cells; LNCaP, DU145, and PC-3; LNCaP-C4 and LNCaP-C4–2; LNCaP-LN3, PC3-M, and PC3-M-MM2; MDA PCa 2a and MDA PCa 2b; LAPC4 cells.	Male 6–8-week-old athymic nude mice, BALB/c (nu/ nu)	Flow cytometry	Prostate cancer lines PC-3, PC-3 M, PC-3 M-MM2, and DU-145 all expressed cell surface BLCA-38 antigen, whereas LNCaP, MDA PCa 2a, and MDA PCa 2b did not.	[138]