Recent applications of chemosensitivity tests for colorectal cancer treatment

Table 2 Protein and gene-based chemosensitivity tests in colorectal cancer

Marker	Target chemotherapy drug	Function	Change	Consequence
TS[34,35]	5-FU	Essential enzyme for DNA synthesis	TS expression ↓	1Chemotherapy response ↑
DPD[33,35]	5-FU	Degradation of 5-FU	DPD expression ↓	1Chemotherapy response ↑
TP[39]	5-FU	Activation of 5-FU (from 5’-DFUR to 5-FU)	Stromal TP expression ↑	1Chemotherapy response ↑
UGT1A1[49]	Irinotecan	Degradation of the active metabolite of irinotecan (SN-38)	Polymorphism of UGT1A (UGT1A1*28)	Irinotecan toxicity↑
ERCC1[54]	Oxaliplatin	Excision nuclease that repairs platinum-induced DNA adducts	ERCC1 expression ↓	1Chemotherapy response ↑
KRAS[65-69]	Anti-EGFR	Proto-oncogene in the EGFR signaling pathway	Mutation of the KRAS gene	Chemotherapy response↓
NRAS[72]	Anti-EGFR	Proto-oncogene in the EGFR signaling pathway	Mutation of the NRAS gene	Chemotherapy response↓
BRAF[74-77]	Anti-EGFR	Signaling gene acting downstream of KRAS	Mutation of the BRAF gene (V600E)	Chemotherapy response↓

¹Chemotherapy responses of these markers are generally inconsistent without strong evidences. TS: Thymidylate synthase; 5-FU: 5-fluoropyrimidine; DPD: Dihydropyrimidine dehydrogenase; TP: Thymidine phosphorylase; 5’-DFUR: 5’-Deoxy-5-fluorouridine; UGT1A1: Uridine diphosphate glucuronosyltransferase 1A1; ERCC1: Excision repair cross-complementation group 1; anti-EGFR: Anti-epidermal growth factor receptor (cetuximab or panitumumab).