Helicobacter pylori plays a key role in gastric adenocarcinoma induced by spasmolytic polypeptide-expressing metaplasia

Table 1 Characteristics of various spasmolytic polypeptide-expressing metaplasia inducers

Inducers of SPEM	Pharmacological action	Inflammatory response	Dosage and usage	Time to onset of SPEM	Notes
DMP-777	It may cause backwash of acid into the cell leading to parietal cell death	No significant inflammatory response in reaction the acute parietal cell loss	> 200 mg/kg/d, oral gavage	7–10 d	(1) SPEM induced by these drugs may completely revert to normal mucosal cell lineages after a withdrawal period, despite the profound oxyntic atrophy and SPEM; and (2) L-635 and tamoxifen elicit parietal cell loss and induce SPEM faster than DMP-777, because of the inflammation cause by L-635 and tamoxifen
L-635	Same as DMP-777	A prominent submucosal and intramucosal inflammatory infiltrate is observed	350 mg/kg/d, oral gavage	3 d
Tamoxifen	Same as DMP-777	Inflammatory is scant than L-635	≥ 3 mg/20 g body weight dose, oral or intra-peritoneal	3 d

SPEM: Spasmolytic polypeptide-expressing metaplasia.

Table 2 The influence of the absence of additional signals and epidermal growth factor

Genotype	SPEM	IM	Neoplasia
AR-null mouse	Yes	Yes	Yes
TGF-α-null mouse	No	No	No
IL33 KO mouse + L635	No	No	No
ST2 KO mouse + L635	No	No	No
IL13 KO mouse + L635	No	No	No
IFN-γ overexpression mouse	Yes	No	No

SPEM: Spasmolytic polypeptide-expressing metaplasia; AR: Amphiregulin; TGF: Transforming growth factor; IL: Interleukin; IFN: Interferon; IM: Intestinal metaplasia; KO: Knockout.