Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis

Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG)‐induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach thr...

Full description

Saved in:
Bibliographic Details
Published in:Cancer science 2002-05, Vol.93 (5)
Main Authors: Øvrebø, Kjell K, Svanes, Knut, Aase, Steinar, Grong, Ketil, Sørbye, Halfdan
Format: Article
Language:English
Subjects:
Autoradiography
Carcinogenesis
Cell growth
Cell proliferation
Gastric cancer
Immunohistochemistry
Mucosa
Risk factors
Stomach
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by
cites
container_end_page
container_issue 5
container_start_page
container_title Cancer science
container_volume 93
creator Øvrebø, Kjell K
Svanes, Knut
Aase, Steinar
Grong, Ketil
Sørbye, Halfdan
description Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG)‐induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach through the pylorus (pyloric reflux group) or through a gastrojejunostomy (jejunal reflux group). After twenty‐four weeks, 5‐bromo‐2‐deoxyuridine (BrdU) was injected intravenously and the stomach was exposed to N‐3H‐methyl‐N‐nitro‐N‐nitrosoguanidine (3H‐MNNG). The antral mucosa was examined with immunohistochemistry and autoradiography for identification of proliferating cells (BrdU labelled) and cells at risk of MNNG‐induced carcinogenesis (3H‐MNNG and BrdU‐labelled cells). Duodenogastric reflux increased the number of double‐labelled cells in the antral mucosa from 4.8±0.6 per mm in the control group to 11.3±1.9 in the jejunal reflux group (P
format article
fullrecord <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_journals_2400015918</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2400015918</sourcerecordid><originalsourceid>FETCH-proquest_journals_24000159183</originalsourceid><addsrcrecordid>eNqNT01Lw0AQDaJg_fgPA54Dmya2xluJ1XqohOC9rMmk3bLM6M4u6M2f4G_04t_otgTx6GXeY-bx5r2jZJTlRZlOlZocH_g0LVU-Pk3ORLZK5ZOiLEbJz13gDonXWrwzLTTY2_AOj9Q61IICfoNQI6F32hsm4B6evj-_IIdFhCX6zYeNZL8j4x3_5cLroMl0hhAMeT6YzShaWViGlkXv7Rrt5RZmULOIebEIDcfRsxs0FubRKv4W0NT9RuugQmuhdmxNj0M6Q_AwNKm0a00sFrOLkYvkpNdW8HLA8-Tqfv5cLdJXx28Bxa-2HBzF02pcKKWy6zK7yf-n2gHquX0L</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2400015918</pqid></control><display><type>article</type><title>Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis</title><source>Open Access: PubMed Central</source><source>Publicly Available Content Database</source><creator>Øvrebø, Kjell K ; Svanes, Knut ; Aase, Steinar ; Grong, Ketil ; Sørbye, Halfdan</creator><creatorcontrib>Øvrebø, Kjell K ; Svanes, Knut ; Aase, Steinar ; Grong, Ketil ; Sørbye, Halfdan</creatorcontrib><description>Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG)‐induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach through the pylorus (pyloric reflux group) or through a gastrojejunostomy (jejunal reflux group). After twenty‐four weeks, 5‐bromo‐2‐deoxyuridine (BrdU) was injected intravenously and the stomach was exposed to N‐3H‐methyl‐N‐nitro‐N‐nitrosoguanidine (3H‐MNNG). The antral mucosa was examined with immunohistochemistry and autoradiography for identification of proliferating cells (BrdU labelled) and cells at risk of MNNG‐induced carcinogenesis (3H‐MNNG and BrdU‐labelled cells). Duodenogastric reflux increased the number of double‐labelled cells in the antral mucosa from 4.8±0.6 per mm in the control group to 11.3±1.9 in the jejunal reflux group (P&lt;0.05) and 12.7±0.9 in the pyloric reflux group (P&lt;0.05). Mucosal erosions were observed in 15 of 28 annuals with pyloric reflux and the number of double‐labelled cells in the erosion area (4.3±0.7) was higher than in the same area of animals without erosion (1.4±0.5) (P&lt;0.05). Duodenogastric reflux increased the cell proliferation and significantly changed the distance between the surface epithelial lining and the proliferating cells when compared to the controls. These results indicate that duodenogastric reflux increases the penetration of 3H‐MNNG into the antrum mucosa of rats. Increased cell proliferation and erosions increase the number of cells at risk of an initiation process from a penetrating gastric carcinogen.</description><identifier>ISSN: 1347-9032</identifier><identifier>EISSN: 1349-7006</identifier><language>eng</language><publisher>Tokyo: John Wiley &amp; Sons, Inc</publisher><subject>Autoradiography ; Carcinogenesis ; Cell growth ; Cell proliferation ; Gastric cancer ; Immunohistochemistry ; Mucosa ; Risk factors ; Stomach</subject><ispartof>Cancer science, 2002-05, Vol.93 (5)</ispartof><rights>Copyright John Wiley &amp; Sons, Inc. May 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2400015918/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2400015918?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,25752,37011,44589,74897</link.rule.ids></links><search><creatorcontrib>Øvrebø, Kjell K</creatorcontrib><creatorcontrib>Svanes, Knut</creatorcontrib><creatorcontrib>Aase, Steinar</creatorcontrib><creatorcontrib>Grong, Ketil</creatorcontrib><creatorcontrib>Sørbye, Halfdan</creatorcontrib><title>Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis</title><title>Cancer science</title><description>Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG)‐induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach through the pylorus (pyloric reflux group) or through a gastrojejunostomy (jejunal reflux group). After twenty‐four weeks, 5‐bromo‐2‐deoxyuridine (BrdU) was injected intravenously and the stomach was exposed to N‐3H‐methyl‐N‐nitro‐N‐nitrosoguanidine (3H‐MNNG). The antral mucosa was examined with immunohistochemistry and autoradiography for identification of proliferating cells (BrdU labelled) and cells at risk of MNNG‐induced carcinogenesis (3H‐MNNG and BrdU‐labelled cells). Duodenogastric reflux increased the number of double‐labelled cells in the antral mucosa from 4.8±0.6 per mm in the control group to 11.3±1.9 in the jejunal reflux group (P&lt;0.05) and 12.7±0.9 in the pyloric reflux group (P&lt;0.05). Mucosal erosions were observed in 15 of 28 annuals with pyloric reflux and the number of double‐labelled cells in the erosion area (4.3±0.7) was higher than in the same area of animals without erosion (1.4±0.5) (P&lt;0.05). Duodenogastric reflux increased the cell proliferation and significantly changed the distance between the surface epithelial lining and the proliferating cells when compared to the controls. These results indicate that duodenogastric reflux increases the penetration of 3H‐MNNG into the antrum mucosa of rats. Increased cell proliferation and erosions increase the number of cells at risk of an initiation process from a penetrating gastric carcinogen.</description><subject>Autoradiography</subject><subject>Carcinogenesis</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Gastric cancer</subject><subject>Immunohistochemistry</subject><subject>Mucosa</subject><subject>Risk factors</subject><subject>Stomach</subject><issn>1347-9032</issn><issn>1349-7006</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><recordid>eNqNT01Lw0AQDaJg_fgPA54Dmya2xluJ1XqohOC9rMmk3bLM6M4u6M2f4G_04t_otgTx6GXeY-bx5r2jZJTlRZlOlZocH_g0LVU-Pk3ORLZK5ZOiLEbJz13gDonXWrwzLTTY2_AOj9Q61IICfoNQI6F32hsm4B6evj-_IIdFhCX6zYeNZL8j4x3_5cLroMl0hhAMeT6YzShaWViGlkXv7Rrt5RZmULOIebEIDcfRsxs0FubRKv4W0NT9RuugQmuhdmxNj0M6Q_AwNKm0a00sFrOLkYvkpNdW8HLA8-Tqfv5cLdJXx28Bxa-2HBzF02pcKKWy6zK7yf-n2gHquX0L</recordid><startdate>20020501</startdate><enddate>20020501</enddate><creator>Øvrebø, Kjell K</creator><creator>Svanes, Knut</creator><creator>Aase, Steinar</creator><creator>Grong, Ketil</creator><creator>Sørbye, Halfdan</creator><general>John Wiley &amp; Sons, Inc</general><scope>8FE</scope><scope>8FH</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20020501</creationdate><title>Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis</title><author>Øvrebø, Kjell K ; Svanes, Knut ; Aase, Steinar ; Grong, Ketil ; Sørbye, Halfdan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_journals_24000159183</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Autoradiography</topic><topic>Carcinogenesis</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Gastric cancer</topic><topic>Immunohistochemistry</topic><topic>Mucosa</topic><topic>Risk factors</topic><topic>Stomach</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Øvrebø, Kjell K</creatorcontrib><creatorcontrib>Svanes, Knut</creatorcontrib><creatorcontrib>Aase, Steinar</creatorcontrib><creatorcontrib>Grong, Ketil</creatorcontrib><creatorcontrib>Sørbye, Halfdan</creatorcontrib><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Cancer science</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Øvrebø, Kjell K</au><au>Svanes, Knut</au><au>Aase, Steinar</au><au>Grong, Ketil</au><au>Sørbye, Halfdan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis</atitle><jtitle>Cancer science</jtitle><date>2002-05-01</date><risdate>2002</risdate><volume>93</volume><issue>5</issue><issn>1347-9032</issn><eissn>1349-7006</eissn><abstract>Duodenogastric reflux is a risk factor for gastric carcinogenesis, but the pathogenesis is not fully understood. We studied the risk of N‐methyl‐N‐nitro‐N‐nitrosoguanidine (MNNG)‐induced carcinogenesis in the antrum of rats with duodenogastric reflux. Duodenal fluid was directed into the stomach through the pylorus (pyloric reflux group) or through a gastrojejunostomy (jejunal reflux group). After twenty‐four weeks, 5‐bromo‐2‐deoxyuridine (BrdU) was injected intravenously and the stomach was exposed to N‐3H‐methyl‐N‐nitro‐N‐nitrosoguanidine (3H‐MNNG). The antral mucosa was examined with immunohistochemistry and autoradiography for identification of proliferating cells (BrdU labelled) and cells at risk of MNNG‐induced carcinogenesis (3H‐MNNG and BrdU‐labelled cells). Duodenogastric reflux increased the number of double‐labelled cells in the antral mucosa from 4.8±0.6 per mm in the control group to 11.3±1.9 in the jejunal reflux group (P&lt;0.05) and 12.7±0.9 in the pyloric reflux group (P&lt;0.05). Mucosal erosions were observed in 15 of 28 annuals with pyloric reflux and the number of double‐labelled cells in the erosion area (4.3±0.7) was higher than in the same area of animals without erosion (1.4±0.5) (P&lt;0.05). Duodenogastric reflux increased the cell proliferation and significantly changed the distance between the surface epithelial lining and the proliferating cells when compared to the controls. These results indicate that duodenogastric reflux increases the penetration of 3H‐MNNG into the antrum mucosa of rats. Increased cell proliferation and erosions increase the number of cells at risk of an initiation process from a penetrating gastric carcinogen.</abstract><cop>Tokyo</cop><pub>John Wiley &amp; Sons, Inc</pub><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 1347-9032
ispartof Cancer science, 2002-05, Vol.93 (5)
issn 1347-9032
1349-7006
language eng
recordid cdi_proquest_journals_2400015918
source Open Access: PubMed Central; Publicly Available Content Database
subjects Autoradiography
Carcinogenesis
Cell growth
Cell proliferation
Gastric cancer
Immunohistochemistry
Mucosa
Risk factors
Stomach
title Duodenogastric Reflux Increases the Penetration of N‐ 3 H‐Methyl‐N‐nitro‐N‐nitrosoguanidine into the Antral Mucosa of Rats: A Possible Role for Mucosal Erosions and Increased Cell Proliferation in Gastric Carcinogenesis
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-12T18%3A00%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Duodenogastric%20Reflux%20Increases%20the%20Penetration%20of%20N%E2%80%90%203%20H%E2%80%90Methyl%E2%80%90N%E2%80%90nitro%E2%80%90N%E2%80%90nitrosoguanidine%20into%20the%20Antral%20Mucosa%20of%20Rats:%20A%20Possible%20Role%20for%20Mucosal%20Erosions%20and%20Increased%20Cell%20Proliferation%20in%20Gastric%20Carcinogenesis&rft.jtitle=Cancer%20science&rft.au=%C3%98vreb%C3%B8,%20Kjell%20K&rft.date=2002-05-01&rft.volume=93&rft.issue=5&rft.issn=1347-9032&rft.eissn=1349-7006&rft_id=info:doi/&rft_dat=%3Cproquest%3E2400015918%3C/proquest%3E%3Cgrp_id%3Ecdi_FETCH-proquest_journals_24000159183%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2400015918&rft_id=info:pmid/&rfr_iscdi=true