Role of gastrin-peptides in Barrett's and colorectal carcinogenesis

Table 1 Studies assessing expression levels and/or biological effects of gastrin through its interaction with cholecystokinin-B receptor

Ref.	Specimen	CCKBR expression	G17 expression	G17 effects
Haigh et al[4]	Esophageal biopsies from healthy, esophagitis, BE and EAC patients; Ex vivo culture of BE cells; OE33(E)GR cells	CCKBR is expressed in 3/9 of healthy, 5/7 esophagitis, 10/10 BE and 7/12 EAC samples	Not assessed	G17 stimulates cell proliferation through CCKBR
Konturek et al[46]	Tumor and plasma samples from CRC patients; Plasma and normal colonic mucosa biopsies from healthy subjects	All the tumor samples showed CCKBR expression	CRC patients showed normal G17 plasma levels, and higher progastrin levels than healthy subjects; Celecoxib diminished plasma gastrin and progastrin levels	Not assessed
Smith et al[49]	Healthy colonic mucosa and colonic polyps biopsies	Normal colonic mucosa didn’t show CCKBR expression; Most of the polyps analyzed showed CCKBR expression	Most of the polyps showed higher expression of the gastrin precursors than amidated forms	Not assessed
Harris et al[70]	Healthy esophagus and BE biopsies; OE19 and OE33 cell culture; OE21 cell culture	All three esophageal cancer cell lines express CCKBR; BE biopsies show higher CCKBR expression levels than normal esophageal biopsies	BE samples express higher gastrin levels than healthy esophageal biopsies	G17 increases activation of the antiapoptotic factor PKB/Akt, through CCKBR

BE: Barrett’s esophagus; EAC: Esophageal adenocarcinoma; CCKBR: Cholecystokinin-B receptor; G17: Amidated gastrin-17; CRC: Colorectal carcinoma; OE19 and OE33 cells: Esophageal adenocarcinoma cell lines; OE21 cells: Esophageal squamous carcinoma cell line; OE33(E)GR cells: Esophageal adenocarcinoma cells permanently transfected with the human CCKB receptor.