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Effect of Helicobacter pylori eradication on oncogenes and cell proliferation
Background Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression...
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| Published in: | European journal of clinical investigation 2008-09, Vol.38 (9), p.628-633 |
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| creator | Zhu, Y. Shu, X. Chen, J. Xie, Y. Xu, P. Huang, D.-Q. Lu, N.-H. |
| description | Background Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression of human telomerase RNA (hTR), human telomerase reverse transcriptase (hTERT), c‐myc and proliferation nuclear cell antigen (PCNA) in H. pylori associated chronic gastritis.
Materials and methods hTR was determined by in situ hybridization, hTERT, c‐myc and PCNA were detected by immunohistochemistry using stomach tissues obtained from 39 H. pylori‐infected and 21 H. pylori‐negative patients with chronic gastritis before and after H. pylori eradication therapy or treatment for symptom relief only.
Results Levels of hTR, hTERT, c‐myc and PCNA were significantly higher in H. pylori‐infected mucosa (51·3%, 53·8%, 53·8% and 16·8 ± 5·8, respectively) when compared to H. pylori‐negative mucosa before therapy (19·0%, 23·8%, 28·6%, 8·8 ± 3·4, respectively; P |
| doi_str_mv | 10.1111/j.1365-2362.2008.01987.x |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_19653761</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19653761</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4667-895bae0f725e74a315bebaed5ed6fa61ccc5b4c22c656b4abef9c6a984d2f2a33</originalsourceid><addsrcrecordid>eNqNkElv2zAQRomgReKm-QsBL-lNChdx0SGHwnCTAEkXoNuNoKhhQEeWHFJG7X9fKjbcawkCJMj3zQweQpiSkuZ1vSwpl6JgXLKSEaJLQmutyu0Jmh0_3qAZIbQqWK3YGXqX0pJkknJ2is6o1lwprmfoceE9uBEPHt9BF9zQWDdCxOtdN8SAIdo2ODuGocev2w1P0EPCtm-xg67D6zh0wWduYt6jt952CS4O5zn68WnxfX5XPHy5vZ9_fChcJaUqdC0aC8QrJkBVllPRQH5oBbTSW0mdc6KpHGNOCtlUtgFfO2lrXbXMM8v5Ofqwr5u7v2wgjWYV0jSO7WHYJENrKbiSNIN6D7o4pBTBm3UMKxt3hhIzqTRLMxkzkzEzqTSvKs02Ry8PPTbNCtp_wYO7DFwdAJuc7Xy0vQvpyDEiiWZiGvZmz_0JHez-ewCzmN9Pt5wv9vmQRtge8zY-G6m4EubX51vzjdKv4vdPYSr-F7Yyn4w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19653761</pqid></control><display><type>article</type><title>Effect of Helicobacter pylori eradication on oncogenes and cell proliferation</title><source>Wiley</source><creator>Zhu, Y. ; Shu, X. ; Chen, J. ; Xie, Y. ; Xu, P. ; Huang, D.-Q. ; Lu, N.-H.</creator><creatorcontrib>Zhu, Y. ; Shu, X. ; Chen, J. ; Xie, Y. ; Xu, P. ; Huang, D.-Q. ; Lu, N.-H.</creatorcontrib><description>Background Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression of human telomerase RNA (hTR), human telomerase reverse transcriptase (hTERT), c‐myc and proliferation nuclear cell antigen (PCNA) in H. pylori associated chronic gastritis.
Materials and methods hTR was determined by in situ hybridization, hTERT, c‐myc and PCNA were detected by immunohistochemistry using stomach tissues obtained from 39 H. pylori‐infected and 21 H. pylori‐negative patients with chronic gastritis before and after H. pylori eradication therapy or treatment for symptom relief only.
Results Levels of hTR, hTERT, c‐myc and PCNA were significantly higher in H. pylori‐infected mucosa (51·3%, 53·8%, 53·8% and 16·8 ± 5·8, respectively) when compared to H. pylori‐negative mucosa before therapy (19·0%, 23·8%, 28·6%, 8·8 ± 3·4, respectively; P < 0·05 in all cases). In patients with successful eradication of H. pylori the levels of hTR, hTERT, c‐myc and PCNA (55·5%, 59·3%, 59·3%, 16·8 ± 5·8, respectively) were significantly reduced after the therapy (22·2%, 22·2%, 14·8%, 7·0 ± 5·0, respectively; P < 0·05 in all cases). In the H. pylori failed eradication and H. pylori‐negative groups, there was no statistical difference in all four measurements.
Conclusions H. pylori infection may induce the overexpression of hTR, hTERT, c‐myc and stimulate cell proliferation. Eradication of H. pylori may reverse the aberrant expression of these oncoproteins and thus correct the abnormal cell proliferation.</description><identifier>ISSN: 0014-2972</identifier><identifier>EISSN: 1365-2362</identifier><identifier>DOI: 10.1111/j.1365-2362.2008.01987.x</identifier><identifier>PMID: 18837738</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>Adult ; Aged ; Bacterial diseases ; Bacterial diseases of the digestive system and abdomen ; Biological and medical sciences ; c-myc ; Cell Proliferation - drug effects ; eradication therapy ; Female ; Gastric Mucosa - pathology ; Gastritis, Atrophic - drug therapy ; Gastritis, Atrophic - genetics ; Gene Expression ; General aspects ; Helicobacter Infections - drug therapy ; Helicobacter Infections - genetics ; Helicobacter Infections - pathology ; Helicobacter pylori ; Human bacterial diseases ; Humans ; Immunohistochemistry ; Infectious diseases ; Male ; Medical sciences ; Middle Aged ; Oncogenes - drug effects ; proliferating cell nuclear antigen ; Proliferating Cell Nuclear Antigen - metabolism ; RNA - metabolism ; Telomerase - metabolism ; telomerase reverse transcriptase ; telomerase RNA ; Treatment Outcome</subject><ispartof>European journal of clinical investigation, 2008-09, Vol.38 (9), p.628-633</ispartof><rights>2008 The Authors. Journal Compilation © 2008 Blackwell Publishing Ltd</rights><rights>2008 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4667-895bae0f725e74a315bebaed5ed6fa61ccc5b4c22c656b4abef9c6a984d2f2a33</citedby><cites>FETCH-LOGICAL-c4667-895bae0f725e74a315bebaed5ed6fa61ccc5b4c22c656b4abef9c6a984d2f2a33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20608253$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/18837738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhu, Y.</creatorcontrib><creatorcontrib>Shu, X.</creatorcontrib><creatorcontrib>Chen, J.</creatorcontrib><creatorcontrib>Xie, Y.</creatorcontrib><creatorcontrib>Xu, P.</creatorcontrib><creatorcontrib>Huang, D.-Q.</creatorcontrib><creatorcontrib>Lu, N.-H.</creatorcontrib><title>Effect of Helicobacter pylori eradication on oncogenes and cell proliferation</title><title>European journal of clinical investigation</title><addtitle>Eur J Clin Invest</addtitle><description>Background Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression of human telomerase RNA (hTR), human telomerase reverse transcriptase (hTERT), c‐myc and proliferation nuclear cell antigen (PCNA) in H. pylori associated chronic gastritis.
Materials and methods hTR was determined by in situ hybridization, hTERT, c‐myc and PCNA were detected by immunohistochemistry using stomach tissues obtained from 39 H. pylori‐infected and 21 H. pylori‐negative patients with chronic gastritis before and after H. pylori eradication therapy or treatment for symptom relief only.
Results Levels of hTR, hTERT, c‐myc and PCNA were significantly higher in H. pylori‐infected mucosa (51·3%, 53·8%, 53·8% and 16·8 ± 5·8, respectively) when compared to H. pylori‐negative mucosa before therapy (19·0%, 23·8%, 28·6%, 8·8 ± 3·4, respectively; P < 0·05 in all cases). In patients with successful eradication of H. pylori the levels of hTR, hTERT, c‐myc and PCNA (55·5%, 59·3%, 59·3%, 16·8 ± 5·8, respectively) were significantly reduced after the therapy (22·2%, 22·2%, 14·8%, 7·0 ± 5·0, respectively; P < 0·05 in all cases). In the H. pylori failed eradication and H. pylori‐negative groups, there was no statistical difference in all four measurements.
Conclusions H. pylori infection may induce the overexpression of hTR, hTERT, c‐myc and stimulate cell proliferation. Eradication of H. pylori may reverse the aberrant expression of these oncoproteins and thus correct the abnormal cell proliferation.</description><subject>Adult</subject><subject>Aged</subject><subject>Bacterial diseases</subject><subject>Bacterial diseases of the digestive system and abdomen</subject><subject>Biological and medical sciences</subject><subject>c-myc</subject><subject>Cell Proliferation - drug effects</subject><subject>eradication therapy</subject><subject>Female</subject><subject>Gastric Mucosa - pathology</subject><subject>Gastritis, Atrophic - drug therapy</subject><subject>Gastritis, Atrophic - genetics</subject><subject>Gene Expression</subject><subject>General aspects</subject><subject>Helicobacter Infections - drug therapy</subject><subject>Helicobacter Infections - genetics</subject><subject>Helicobacter Infections - pathology</subject><subject>Helicobacter pylori</subject><subject>Human bacterial diseases</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Infectious diseases</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Oncogenes - drug effects</subject><subject>proliferating cell nuclear antigen</subject><subject>Proliferating Cell Nuclear Antigen - metabolism</subject><subject>RNA - metabolism</subject><subject>Telomerase - metabolism</subject><subject>telomerase reverse transcriptase</subject><subject>telomerase RNA</subject><subject>Treatment Outcome</subject><issn>0014-2972</issn><issn>1365-2362</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><recordid>eNqNkElv2zAQRomgReKm-QsBL-lNChdx0SGHwnCTAEkXoNuNoKhhQEeWHFJG7X9fKjbcawkCJMj3zQweQpiSkuZ1vSwpl6JgXLKSEaJLQmutyu0Jmh0_3qAZIbQqWK3YGXqX0pJkknJ2is6o1lwprmfoceE9uBEPHt9BF9zQWDdCxOtdN8SAIdo2ODuGocev2w1P0EPCtm-xg67D6zh0wWduYt6jt952CS4O5zn68WnxfX5XPHy5vZ9_fChcJaUqdC0aC8QrJkBVllPRQH5oBbTSW0mdc6KpHGNOCtlUtgFfO2lrXbXMM8v5Ofqwr5u7v2wgjWYV0jSO7WHYJENrKbiSNIN6D7o4pBTBm3UMKxt3hhIzqTRLMxkzkzEzqTSvKs02Ry8PPTbNCtp_wYO7DFwdAJuc7Xy0vQvpyDEiiWZiGvZmz_0JHez-ewCzmN9Pt5wv9vmQRtge8zY-G6m4EubX51vzjdKv4vdPYSr-F7Yyn4w</recordid><startdate>200809</startdate><enddate>200809</enddate><creator>Zhu, Y.</creator><creator>Shu, X.</creator><creator>Chen, J.</creator><creator>Xie, Y.</creator><creator>Xu, P.</creator><creator>Huang, D.-Q.</creator><creator>Lu, N.-H.</creator><general>Blackwell Publishing Ltd</general><general>Blackwell</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7TO</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>200809</creationdate><title>Effect of Helicobacter pylori eradication on oncogenes and cell proliferation</title><author>Zhu, Y. ; Shu, X. ; Chen, J. ; Xie, Y. ; Xu, P. ; Huang, D.-Q. ; Lu, N.-H.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4667-895bae0f725e74a315bebaed5ed6fa61ccc5b4c22c656b4abef9c6a984d2f2a33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Bacterial diseases</topic><topic>Bacterial diseases of the digestive system and abdomen</topic><topic>Biological and medical sciences</topic><topic>c-myc</topic><topic>Cell Proliferation - drug effects</topic><topic>eradication therapy</topic><topic>Female</topic><topic>Gastric Mucosa - pathology</topic><topic>Gastritis, Atrophic - drug therapy</topic><topic>Gastritis, Atrophic - genetics</topic><topic>Gene Expression</topic><topic>General aspects</topic><topic>Helicobacter Infections - drug therapy</topic><topic>Helicobacter Infections - genetics</topic><topic>Helicobacter Infections - pathology</topic><topic>Helicobacter pylori</topic><topic>Human bacterial diseases</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Infectious diseases</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Oncogenes - drug effects</topic><topic>proliferating cell nuclear antigen</topic><topic>Proliferating Cell Nuclear Antigen - metabolism</topic><topic>RNA - metabolism</topic><topic>Telomerase - metabolism</topic><topic>telomerase reverse transcriptase</topic><topic>telomerase RNA</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Y.</creatorcontrib><creatorcontrib>Shu, X.</creatorcontrib><creatorcontrib>Chen, J.</creatorcontrib><creatorcontrib>Xie, Y.</creatorcontrib><creatorcontrib>Xu, P.</creatorcontrib><creatorcontrib>Huang, D.-Q.</creatorcontrib><creatorcontrib>Lu, N.-H.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>European journal of clinical investigation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Y.</au><au>Shu, X.</au><au>Chen, J.</au><au>Xie, Y.</au><au>Xu, P.</au><au>Huang, D.-Q.</au><au>Lu, N.-H.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of Helicobacter pylori eradication on oncogenes and cell proliferation</atitle><jtitle>European journal of clinical investigation</jtitle><addtitle>Eur J Clin Invest</addtitle><date>2008-09</date><risdate>2008</risdate><volume>38</volume><issue>9</issue><spage>628</spage><epage>633</epage><pages>628-633</pages><issn>0014-2972</issn><eissn>1365-2362</eissn><abstract>Background Helicobacter pylori , the main cause of chronic gastritis, is a class 1 gastric carcinogen. However, it remains unclear whether H. pylori affects molecular alterations in chronic gastritis. Thus, this study was designed to investigate the effect of H. pylori eradication on the expression of human telomerase RNA (hTR), human telomerase reverse transcriptase (hTERT), c‐myc and proliferation nuclear cell antigen (PCNA) in H. pylori associated chronic gastritis.
Materials and methods hTR was determined by in situ hybridization, hTERT, c‐myc and PCNA were detected by immunohistochemistry using stomach tissues obtained from 39 H. pylori‐infected and 21 H. pylori‐negative patients with chronic gastritis before and after H. pylori eradication therapy or treatment for symptom relief only.
Results Levels of hTR, hTERT, c‐myc and PCNA were significantly higher in H. pylori‐infected mucosa (51·3%, 53·8%, 53·8% and 16·8 ± 5·8, respectively) when compared to H. pylori‐negative mucosa before therapy (19·0%, 23·8%, 28·6%, 8·8 ± 3·4, respectively; P < 0·05 in all cases). In patients with successful eradication of H. pylori the levels of hTR, hTERT, c‐myc and PCNA (55·5%, 59·3%, 59·3%, 16·8 ± 5·8, respectively) were significantly reduced after the therapy (22·2%, 22·2%, 14·8%, 7·0 ± 5·0, respectively; P < 0·05 in all cases). In the H. pylori failed eradication and H. pylori‐negative groups, there was no statistical difference in all four measurements.
Conclusions H. pylori infection may induce the overexpression of hTR, hTERT, c‐myc and stimulate cell proliferation. Eradication of H. pylori may reverse the aberrant expression of these oncoproteins and thus correct the abnormal cell proliferation.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>18837738</pmid><doi>10.1111/j.1365-2362.2008.01987.x</doi><tpages>6</tpages></addata></record> |
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| subjects | Adult Aged Bacterial diseases Bacterial diseases of the digestive system and abdomen Biological and medical sciences c-myc Cell Proliferation - drug effects eradication therapy Female Gastric Mucosa - pathology Gastritis, Atrophic - drug therapy Gastritis, Atrophic - genetics Gene Expression General aspects Helicobacter Infections - drug therapy Helicobacter Infections - genetics Helicobacter Infections - pathology Helicobacter pylori Human bacterial diseases Humans Immunohistochemistry Infectious diseases Male Medical sciences Middle Aged Oncogenes - drug effects proliferating cell nuclear antigen Proliferating Cell Nuclear Antigen - metabolism RNA - metabolism Telomerase - metabolism telomerase reverse transcriptase telomerase RNA Treatment Outcome |
| title | Effect of Helicobacter pylori eradication on oncogenes and cell proliferation |
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