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Article: Topographic association of gastric epithelial expression of Ki-67, Bax, and Bcl-2 with antralization in the gastric incisura, body, and fundus

TitleTopographic association of gastric epithelial expression of Ki-67, Bax, and Bcl-2 with antralization in the gastric incisura, body, and fundus
Authors
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ajg/index.html
Citation
American Journal Of Gastroenterology, 2002, v. 97 n. 12, p. 3023-3031 How to Cite?
AbstractOBJECTIVES: Helicobacter pylori (H. pylori) infection seems to induce antralization (i.e., gastric mucosal transformation from transitional or body type to antral type), which is strongly associated with gastric atrophy and intestinal metaplasia. The aim of this study was to determine the topographic associations of Ki-67 (a protein expressed in proliferative cells), Bax (a pro-apoptotic protein), and Bcl-2 (an antiapoptotic protein) expression with antralization. METHODS: In each of 104 patients, eight biopsy specimens were taken from the gastric antrum, incisura, body, and fundus for the determination of H. pylori infection, histological changes, and epithelial expression of Ki-67, Bax, and Bcl-2. A labeling index (LI), i.e., the rate of positive cells over total cells counted, was used for Ki-67 and Bax expression. Bcl-2 overexpression was considered to be present if the rate of Bcl-2 positive cells over total cells counted was ≥5%. RESULTS: H. pylori infection was present at the gastric antrum, incisura, body, and fundus in 50, 48, 51, and 49 patients, respectively. Ki-67 LI was greater in the presence (vs absence) of H. pylori infection at the antrum (51 vs 40), incisura (47 vs 36), body (43 vs 30), and fundus (41 vs 31) (all p < 0.001). At the incisura, Ki-67 LI was greater (47 vs 32, p < 0.001), Bax LI was lower (22 vs 30, p < 0.05), and prevalence of Bcl-2 overexpression was higher (44% vs 18%, p < 0.001) in the presence (vs absence) of antralization. Compared with normal mucosa, gastric atrophy/intestinal metaplasia were associated with an increased Ki-67 LI and decreased Bax LI at the antrum (49 vs 32 and 15 vs 23, respectively), incisura (47 vs 32 and 15 vs 26, respectively) (all p < 0.001). Bcl-2 overexpression was more frequent in gastric atrophy/intestinal metaplasia at the antrum (56% vs 11%, p < 0.001) and incisura (63% vs 19%, p < 0.001) compared with normal mucosa. CONCLUSIONS: Antralization at the incisura is topographically associated with increased cell proliferation, reduced Bax expression, and Bcl-2 overexpression, which implies that antralization may be an important histological marker for future cancer risk. © 2002 by Am. Coll. of Gastroenterology.
Persistent Identifierhttp://hdl.handle.net/10722/76914
ISSN
2015 Impact Factor: 10.383
2015 SCImago Journal Rankings: 3.946
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorZhang, GSen_HK
dc.contributor.authorTalley, NJen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorYang, Yen_HK
dc.contributor.authorHenwood, Cen_HK
dc.contributor.authorWyatt, JMen_HK
dc.contributor.authorAdams, Sen_HK
dc.contributor.authorCheung, Ken_HK
dc.contributor.authorXia, Ben_HK
dc.contributor.authorZhu, YQen_HK
dc.contributor.authorLam, SKen_HK
dc.date.accessioned2010-09-06T07:26:17Z-
dc.date.available2010-09-06T07:26:17Z-
dc.date.issued2002en_HK
dc.identifier.citationAmerican Journal Of Gastroenterology, 2002, v. 97 n. 12, p. 3023-3031en_HK
dc.identifier.issn0002-9270en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76914-
dc.description.abstractOBJECTIVES: Helicobacter pylori (H. pylori) infection seems to induce antralization (i.e., gastric mucosal transformation from transitional or body type to antral type), which is strongly associated with gastric atrophy and intestinal metaplasia. The aim of this study was to determine the topographic associations of Ki-67 (a protein expressed in proliferative cells), Bax (a pro-apoptotic protein), and Bcl-2 (an antiapoptotic protein) expression with antralization. METHODS: In each of 104 patients, eight biopsy specimens were taken from the gastric antrum, incisura, body, and fundus for the determination of H. pylori infection, histological changes, and epithelial expression of Ki-67, Bax, and Bcl-2. A labeling index (LI), i.e., the rate of positive cells over total cells counted, was used for Ki-67 and Bax expression. Bcl-2 overexpression was considered to be present if the rate of Bcl-2 positive cells over total cells counted was ≥5%. RESULTS: H. pylori infection was present at the gastric antrum, incisura, body, and fundus in 50, 48, 51, and 49 patients, respectively. Ki-67 LI was greater in the presence (vs absence) of H. pylori infection at the antrum (51 vs 40), incisura (47 vs 36), body (43 vs 30), and fundus (41 vs 31) (all p < 0.001). At the incisura, Ki-67 LI was greater (47 vs 32, p < 0.001), Bax LI was lower (22 vs 30, p < 0.05), and prevalence of Bcl-2 overexpression was higher (44% vs 18%, p < 0.001) in the presence (vs absence) of antralization. Compared with normal mucosa, gastric atrophy/intestinal metaplasia were associated with an increased Ki-67 LI and decreased Bax LI at the antrum (49 vs 32 and 15 vs 23, respectively), incisura (47 vs 32 and 15 vs 26, respectively) (all p < 0.001). Bcl-2 overexpression was more frequent in gastric atrophy/intestinal metaplasia at the antrum (56% vs 11%, p < 0.001) and incisura (63% vs 19%, p < 0.001) compared with normal mucosa. CONCLUSIONS: Antralization at the incisura is topographically associated with increased cell proliferation, reduced Bax expression, and Bcl-2 overexpression, which implies that antralization may be an important histological marker for future cancer risk. © 2002 by Am. Coll. of Gastroenterology.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/ajg/index.htmlen_HK
dc.relation.ispartofAmerican Journal of Gastroenterologyen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshBiopsyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGastric Fundus - pathologyen_HK
dc.subject.meshGastric Mucosa - metabolism - pathologyen_HK
dc.subject.meshHelicobacter Infections - metabolism - pathologyen_HK
dc.subject.meshHelicobacter pylorien_HK
dc.subject.meshHumansen_HK
dc.subject.meshKi-67 Antigen - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshProto-Oncogene Proteins - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshPyloric Antrum - pathologyen_HK
dc.subject.meshStomach - pathologyen_HK
dc.subject.meshbcl-2-Associated X Proteinen_HK
dc.titleTopographic association of gastric epithelial expression of Ki-67, Bax, and Bcl-2 with antralization in the gastric incisura, body, and fundusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0002-9270&volume=97&issue=12&spage=3023&epage=31&date=2002&atitle=Topographic+Association+of+Gastric+Epithelial+Expression+of+Ki-67,+Bax,+and+Bcl-2+with+Antralization+in+the+Gastric+Incisura,+Body,+and+Fundusen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0002-9270(02)05537-5en_HK
dc.identifier.pmid12492185-
dc.identifier.scopuseid_2-s2.0-0036897484en_HK
dc.identifier.hkuros82152en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036897484&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue12en_HK
dc.identifier.spage3023en_HK
dc.identifier.epage3031en_HK
dc.identifier.isiWOS:000179696000018-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridZhang, GS=7405267915en_HK
dc.identifier.scopusauthoridTalley, NJ=36045241200en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridYang, Y=8675011000en_HK
dc.identifier.scopusauthoridHenwood, C=6603783147en_HK
dc.identifier.scopusauthoridWyatt, JM=7202561816en_HK
dc.identifier.scopusauthoridAdams, S=7402058282en_HK
dc.identifier.scopusauthoridCheung, K=7402406545en_HK
dc.identifier.scopusauthoridXia, B=7102762263en_HK
dc.identifier.scopusauthoridZhu, YQ=7406071743en_HK
dc.identifier.scopusauthoridLam, SK=55041331600en_HK

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