Review to better understand the macroscopic subtypes and histogenesis of intrahepatic cholangiocarcinoma

Table 5 Pathobiological studies of intrahepatic cholangiocarcinoma 2

Ref.	n	Method	Target	Conclusion
Shi et al[46]	138	IHC	DKK-1	(+)poor prognosis
				elevated sMMP9 and VEGF-C
		Cell	DKK-1	(-)decrease in cell migration and invasiveness
				(+)LN, Por, advanced stage, V
Yao et al[47]	96	IHC	Vimentin	poor prognosis
			and
			N-cadherin	(+)MF-type
Zhou et al[48]	54	IHC	HBx-protein	well differentiated tumor
				(+)well differentiated tumor, IG-type
Choi et al[49]	46	IHC	CK20	(+)favorable prognosis
			MUC6	(+)Size, LN, V, advanced stage
Jeong et al[50]	43	IHC	FABP-5	(-)decrease in cell proliferation and
		Cell	FABP-5	invasion
				(+)elevated serum CEA and CA
Tsai et al[51]	112	IHC	S100P	19-9 value, MUC2 positive
				poor prognosis
				(+)perineural invasion
	86	Sequencing	K-ras mutation	poor prognosis
			miR-200c	(+)reduction of EMT
Oishi et al[53]	-	Microarray		reduction of NCAM1 expression
			HCV core	(+)enhanced NFAT expression
Liao et al[54]	-	Cell	protein	(+)enhanced Angiotensin II receptor expression and fibrogenesis of
			Angiotensin	cancerous stroma, metastasis
Okamoto et al[55]	-	Cell	II and SDF1

DKK1: Dickkopf-related protein1; MMP: Matrix metalloproteinase; FABP-5: Fatty acid-binding protein 5; SDF1: Stromal cell derived factor 1; NCAM1: Neural cell adhesion molecule1; EMT: Epithelial mesenchymal transition; NFAT1: Nuclear factor of activated T-cells.