Methylation of PTCH1a gene in a subset of gastric cancers
To establish if PTCH1a transcriptional regulation region (TRR) is methylated in gastric cancer and its influence in gastric tumorigenesis. The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a...
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| Veröffentlicht in: | World journal of gastroenterology : WJG 2009-08, Vol.15 (30), p.3799-3806 |
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| creator | Du, Peng Ye, Hai-Rong Gao, Jun Chen, Wei Wang, Zhong-Chuan Jiang, Hong-Hua Xu, Ji Zhang, Ji-We Zhang, Jian-Cheng Cui, Long |
| description | To establish if PTCH1a transcriptional regulation region (TRR) is methylated in gastric cancer and its influence in gastric tumorigenesis.
The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a was designated as 0) that contained 19 CpG sites was chosen for bisulfite-sequencing PCR (BSP) and methylation-specific PCR (MSP) detection. The gastric cancer cell line AGS was treated with 5-aza-2'-deoxycytidine (5-Aza-dC; 1 micromol/L) for 3 d. Alterations in PTCH1a TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide (PI) staining or annexin V/PI double staining. The prevalence of PTCH1a TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients' clinical features was analyzed.
Methylation of PTCH1a TRR was observed in AGS cells and a subset of gastric cancer tissues (32%, 55/170), while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1a TRR was correlated negatively with PTCH1 expression (Spearman's r = -0.380, P = 0.000). However, methylation of PTCH1a TRR was not related to the gastric cancer patients' clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCH1a TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression (5.3 +/- 2.5 times; n = 3) and apoptosis rate (3.0 +/- 0.26 times; P < 0.05; n = 3).
Methylation of PTCH1a TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gastric tumorigenesis and a new treatment target. |
| doi_str_mv | 10.3748/wjg.15.3799 |
| format | Article |
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The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a was designated as 0) that contained 19 CpG sites was chosen for bisulfite-sequencing PCR (BSP) and methylation-specific PCR (MSP) detection. The gastric cancer cell line AGS was treated with 5-aza-2'-deoxycytidine (5-Aza-dC; 1 micromol/L) for 3 d. Alterations in PTCH1a TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide (PI) staining or annexin V/PI double staining. The prevalence of PTCH1a TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients' clinical features was analyzed.
Methylation of PTCH1a TRR was observed in AGS cells and a subset of gastric cancer tissues (32%, 55/170), while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1a TRR was correlated negatively with PTCH1 expression (Spearman's r = -0.380, P = 0.000). However, methylation of PTCH1a TRR was not related to the gastric cancer patients' clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCH1a TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression (5.3 +/- 2.5 times; n = 3) and apoptosis rate (3.0 +/- 0.26 times; P < 0.05; n = 3).
Methylation of PTCH1a TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gastric tumorigenesis and a new treatment target.</description><identifier>ISSN: 1007-9327</identifier><identifier>EISSN: 2219-2840</identifier><identifier>DOI: 10.3748/wjg.15.3799</identifier><identifier>PMID: 19673023</identifier><language>eng</language><publisher>United States: Department of Surgery,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Anesthesiology,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Gastroenterology,Changhai Hospital,Second Military Medical University,Shanghai 200433,China%Division of Ship Hygiene,Navy Medical Research Institute,Shanghai 200433,China</publisher><subject>Base Sequence ; Brief ; Cell Line, Tumor ; CpG Islands ; DNA Methylation ; Gene Expression Regulation, Neoplastic ; Humans ; Patched Receptors ; Patched-1 Receptor ; Protein Isoforms - genetics ; Receptors, Cell Surface - genetics ; Sequence Analysis, DNA ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Stomach Neoplasms - physiopathology</subject><ispartof>World journal of gastroenterology : WJG, 2009-08, Vol.15 (30), p.3799-3806</ispartof><rights>Copyright © Wanfang Data Co. Ltd. All Rights Reserved.</rights><rights>2009 The WJG Press and Baishideng. All rights reserved. 2009</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-340c74712c7fbbe699587e0c5f0f7c73076ed3061bb757576fbbaebb08dc60c43</citedby><cites>FETCH-LOGICAL-c474t-340c74712c7fbbe699587e0c5f0f7c73076ed3061bb757576fbbaebb08dc60c43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.wanfangdata.com.cn/images/PeriodicalImages/wjg/wjg.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726460/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726460/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19673023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Du, Peng</creatorcontrib><creatorcontrib>Ye, Hai-Rong</creatorcontrib><creatorcontrib>Gao, Jun</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Wang, Zhong-Chuan</creatorcontrib><creatorcontrib>Jiang, Hong-Hua</creatorcontrib><creatorcontrib>Xu, Ji</creatorcontrib><creatorcontrib>Zhang, Ji-We</creatorcontrib><creatorcontrib>Zhang, Jian-Cheng</creatorcontrib><creatorcontrib>Cui, Long</creatorcontrib><title>Methylation of PTCH1a gene in a subset of gastric cancers</title><title>World journal of gastroenterology : WJG</title><addtitle>World J Gastroenterol</addtitle><description>To establish if PTCH1a transcriptional regulation region (TRR) is methylated in gastric cancer and its influence in gastric tumorigenesis.
The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a was designated as 0) that contained 19 CpG sites was chosen for bisulfite-sequencing PCR (BSP) and methylation-specific PCR (MSP) detection. The gastric cancer cell line AGS was treated with 5-aza-2'-deoxycytidine (5-Aza-dC; 1 micromol/L) for 3 d. Alterations in PTCH1a TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide (PI) staining or annexin V/PI double staining. The prevalence of PTCH1a TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients' clinical features was analyzed.
Methylation of PTCH1a TRR was observed in AGS cells and a subset of gastric cancer tissues (32%, 55/170), while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1a TRR was correlated negatively with PTCH1 expression (Spearman's r = -0.380, P = 0.000). However, methylation of PTCH1a TRR was not related to the gastric cancer patients' clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCH1a TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression (5.3 +/- 2.5 times; n = 3) and apoptosis rate (3.0 +/- 0.26 times; P < 0.05; n = 3).
Methylation of PTCH1a TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gastric tumorigenesis and a new treatment target.</description><subject>Base Sequence</subject><subject>Brief</subject><subject>Cell Line, Tumor</subject><subject>CpG Islands</subject><subject>DNA Methylation</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Patched Receptors</subject><subject>Patched-1 Receptor</subject><subject>Protein Isoforms - genetics</subject><subject>Receptors, Cell Surface - genetics</subject><subject>Sequence Analysis, DNA</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach Neoplasms - physiopathology</subject><issn>1007-9327</issn><issn>2219-2840</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkUtLAzEUhYMotlZX7mUW4kam3jwmmWwEKb6gogtdh0yamU6ZZmoyY-m_N6XFB1nchPvdcw85CJ1jGFPB8pv1ohrjLN6lPEBDQrBMSc7gEA0xgEglJWKATkJYABBKM3KMBlhyQeNriOSL7eabRnd165K2TN7eJ09YJ5V1NqldopPQF8F221alQ-drkxjtjPXhFB2Vugn2bF9H6OPhPk6n09fH58ndNDVMsC6lDIxgAhMjyqKwXMosFxZMVkIpTHQhuJ1R4LgoRBYPj5S2RQH5zHAwjI7Q7U531RdLOzPWdV43auXrpfYb1epa_e-4eq6q9ksRQTjjEAUudwJr7UrtKrVoe--iZRV_jgBICoBpxK72e3z72dvQqWUdjG0a7WzbB8WjuVwAj-D1DjS-DcHb8scLBrVNZKurcKa2iUT64q_9X3YfAf0GuJqGFg</recordid><startdate>20090814</startdate><enddate>20090814</enddate><creator>Du, Peng</creator><creator>Ye, Hai-Rong</creator><creator>Gao, Jun</creator><creator>Chen, Wei</creator><creator>Wang, Zhong-Chuan</creator><creator>Jiang, Hong-Hua</creator><creator>Xu, Ji</creator><creator>Zhang, Ji-We</creator><creator>Zhang, Jian-Cheng</creator><creator>Cui, Long</creator><general>Department of Surgery,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Anesthesiology,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Gastroenterology,Changhai Hospital,Second Military Medical University,Shanghai 200433,China%Division of Ship Hygiene,Navy Medical Research Institute,Shanghai 200433,China</general><general>The WJG Press and Baishideng</general><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>7X8</scope><scope>2B.</scope><scope>4A8</scope><scope>92I</scope><scope>93N</scope><scope>PSX</scope><scope>TCJ</scope><scope>5PM</scope></search><sort><creationdate>20090814</creationdate><title>Methylation of PTCH1a gene in a subset of gastric cancers</title><author>Du, Peng ; Ye, Hai-Rong ; Gao, Jun ; Chen, Wei ; Wang, Zhong-Chuan ; Jiang, Hong-Hua ; Xu, Ji ; Zhang, Ji-We ; Zhang, Jian-Cheng ; Cui, Long</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-340c74712c7fbbe699587e0c5f0f7c73076ed3061bb757576fbbaebb08dc60c43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Base Sequence</topic><topic>Brief</topic><topic>Cell Line, Tumor</topic><topic>CpG Islands</topic><topic>DNA Methylation</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Patched Receptors</topic><topic>Patched-1 Receptor</topic><topic>Protein Isoforms - genetics</topic><topic>Receptors, Cell Surface - genetics</topic><topic>Sequence Analysis, DNA</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach Neoplasms - physiopathology</topic><toplevel>online_resources</toplevel><creatorcontrib>Du, Peng</creatorcontrib><creatorcontrib>Ye, Hai-Rong</creatorcontrib><creatorcontrib>Gao, Jun</creatorcontrib><creatorcontrib>Chen, Wei</creatorcontrib><creatorcontrib>Wang, Zhong-Chuan</creatorcontrib><creatorcontrib>Jiang, Hong-Hua</creatorcontrib><creatorcontrib>Xu, Ji</creatorcontrib><creatorcontrib>Zhang, Ji-We</creatorcontrib><creatorcontrib>Zhang, Jian-Cheng</creatorcontrib><creatorcontrib>Cui, Long</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Wanfang Data Journals - Hong Kong</collection><collection>WANFANG Data Centre</collection><collection>Wanfang Data Journals</collection><collection>万方数据期刊 - 香港版</collection><collection>China Online Journals (COJ)</collection><collection>China Online Journals (COJ)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>World journal of gastroenterology : WJG</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Du, Peng</au><au>Ye, Hai-Rong</au><au>Gao, Jun</au><au>Chen, Wei</au><au>Wang, Zhong-Chuan</au><au>Jiang, Hong-Hua</au><au>Xu, Ji</au><au>Zhang, Ji-We</au><au>Zhang, Jian-Cheng</au><au>Cui, Long</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Methylation of PTCH1a gene in a subset of gastric cancers</atitle><jtitle>World journal of gastroenterology : WJG</jtitle><addtitle>World J Gastroenterol</addtitle><date>2009-08-14</date><risdate>2009</risdate><volume>15</volume><issue>30</issue><spage>3799</spage><epage>3806</epage><pages>3799-3806</pages><issn>1007-9327</issn><eissn>2219-2840</eissn><abstract>To establish if PTCH1a transcriptional regulation region (TRR) is methylated in gastric cancer and its influence in gastric tumorigenesis.
The CpG islands in PTCH1a TRR were analyzed by Methyl Primer Express v1.0 software. The region from -643 to -355 bp (the transcription initiation site of PTCH1a was designated as 0) that contained 19 CpG sites was chosen for bisulfite-sequencing PCR (BSP) and methylation-specific PCR (MSP) detection. The gastric cancer cell line AGS was treated with 5-aza-2'-deoxycytidine (5-Aza-dC; 1 micromol/L) for 3 d. Alterations in PTCH1a TRR methylation in treated AGS cells was measured through BSP clone sequences, and their PTCH1 expression was measured by quantitative RT-PCR. The cell cycle and apoptosis were observed with flow cytometry through propidium iodide (PI) staining or annexin V/PI double staining. The prevalence of PTCH1a TRR methylation was investigated in 170 gastric cancer tissue samples and the adjacent normal tissues by MSP. The correlation of PTCH1a TRR methylation with PTCH1 expression or with patients' clinical features was analyzed.
Methylation of PTCH1a TRR was observed in AGS cells and a subset of gastric cancer tissues (32%, 55/170), while no methylation amplification products were observed in any normal tissues by MSP. The methylation of PTCH1a TRR was correlated negatively with PTCH1 expression (Spearman's r = -0.380, P = 0.000). However, methylation of PTCH1a TRR was not related to the gastric cancer patients' clinical features, such as sex, age of onset, clinical stage, lymph node metastasis or histological grade. The methylation of PTCH1a TRR in AGS cells was almost converted to non-methylation after 5-Aza-dC treatment, which increased PTCH1 expression (5.3 +/- 2.5 times; n = 3) and apoptosis rate (3.0 +/- 0.26 times; P < 0.05; n = 3).
Methylation of PTCH1a TRR is present in a subset of gastric cancers and correlated negatively with PTCH1 expression. This may be an early event in gastric tumorigenesis and a new treatment target.</abstract><cop>United States</cop><pub>Department of Surgery,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Anesthesiology,Shanghai Xinhua Hospital,Shanghai Jiao Tong University School of Medicine,1665 Kong Jiang Road,Shanghai 200092,China%Department of Gastroenterology,Changhai Hospital,Second Military Medical University,Shanghai 200433,China%Division of Ship Hygiene,Navy Medical Research Institute,Shanghai 200433,China</pub><pmid>19673023</pmid><doi>10.3748/wjg.15.3799</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Baishideng "World Journal of" online journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection |
| subjects | Base Sequence Brief Cell Line, Tumor CpG Islands DNA Methylation Gene Expression Regulation, Neoplastic Humans Patched Receptors Patched-1 Receptor Protein Isoforms - genetics Receptors, Cell Surface - genetics Sequence Analysis, DNA Stomach Neoplasms - genetics Stomach Neoplasms - pathology Stomach Neoplasms - physiopathology |
| title | Methylation of PTCH1a gene in a subset of gastric cancers |
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