Table 2.

Summary of the studies performed with clinical samples reporting the potential clinical use of the determination of complement components.

Component Type	Complement Component(s)	Role in Cancer	Type of Sample	Methodology	Stage(s)	Mechanism	Ref
Complement effectors and receptors	C1q	Diagnosis	Serum	Mass spectrometry	III–IV	Overexpression	[115]
	gC1qR	Prognosis	Tissue	IHC	III–IV	Overexpression associated with shorter overall survival	[116]
	MBL and MASP-2	Diagnosis	Serum	ELISA	I–IV	Overexpression	[117]
	Ficolin-2 and ficolin-3	Diagnosis	Serum	ELISA	I–IV	Overexpression	[118]
	C3 and C4	Prediction of response	Plasma	Mass spectrometry	III–IV	Downregulation (C3) or upregulation (C4) in platinum-resistant patients	[119]
	C3	Diagnosis	Serum	Mass spectrometry	I–IV	Downregulation	[120]
	C3 and C5aR1	Prognosis	Tissue	Real-time PCR	I–II	mRNA levels associated with decreased overall survival	[104]
Complement regulators	CD59, CD46, FH, and FHL-1	Pro-tumor	Ascitic fluid	Immunoblotting, ELISA, IHC	I, III, IV	Complement activation and regulation occurs locally in ascites	[64]
	CD46	Prognosis	Tissue	IHC	I–III	Expression associated with shorter survival	[121]
	CD46 and CD59	Therapy	Tissue	cDNA microarray, IHC	Advanced stage	Neutralization improves CDC mediated by mAb therapy	[112]
	CD46, CD55, and CD59	Pro-tumor	Tissue	IHC	Not specified	Overexpression in malignant tissue	[122]
	FH, FHL-1, and sCD46	Pro-tumor	Ascitic fluid, tissue	ELISA, IHC	III–IV	Overexpression in malignant tissue	[114]

IHC: immunohistochemistry, mAb: monoclonal antibody, CDC: complement-dependent cytotoxicity.