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Alteration in the Wnt/β-catenin signaling pathway in gastric neoplasias of fundic gland (chief cell predominant) type
Summary Gastric neoplasia of chief cell–predominant type (GN-CCP) has been reported as a new, rare variant of gastric tumor. GN-CCPs were defined as tumors consisting of irregular anastomosing glands of columnar cells mimicking chief cells of fundic gland with nuclear atypia and prolapse-type submuc...
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| Published in: | Human pathology 2013-11, Vol.44 (11), p.2438-2448 |
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| creator | Hidaka, Yasuhiro, MD Mitomi, Hiroyuki, MD, PhD Saito, Tsuyoshi, MD, PhD Takahashi, Michiko, TBSc Lee, Se-yong, MD Matsumoto, Kenshi, MD Yao, Takashi, MD, PhD Watanabe, Sumio, MD, PhD |
| description | Summary Gastric neoplasia of chief cell–predominant type (GN-CCP) has been reported as a new, rare variant of gastric tumor. GN-CCPs were defined as tumors consisting of irregular anastomosing glands of columnar cells mimicking chief cells of fundic gland with nuclear atypia and prolapse-type submucosal involvement. We comparatively evaluated clinicopathologic features between 31 GN-CCPs and 130 cases of conventional gastric adenocarcinoma invading into submucosa (CGA-SM) in additon to nuclear β -catenin immunolabeling and direct sequencing of members of the Wnt/ β -catenin pathway, CTNNB1 , APC , and AXIN , in a subset of these tumors. GN-CCP presented as small protruded lesions located in the upper third of the stomach, with minimal involvement into the submucosa and rare lymphovascular invasion. None of the lesions have demonstrated a recurrence of disease or metastasis on follow-up. Nuclear β -catenin immunolabeling was higher in GN-CCP (labeling index [LI]: median, 19.3%; high expresser [LI >30%], 7/27 cases [26%]) than CGA-SM (median LI, 14.7%; high expresser, 1/19 cases [6%]). Missense mutation of APC was observed in 1 GN-CCP but not CGA-SM. Missense or nonsense mutations of CTNNB1 and AXIN1 were higher in GN-CCPs (14.8%, both) than CGA-SMs (5.3%, both). Missense mutations of AXIN2 were higher in GN-CCPs (25.9%) than in CGA-SMs (10.5%). Overall, 14 (51.9%) of 27 GN-CCPs and 5 (26.3%) of 19 CGA-SM cases harbored at least 1 of these gene mutations. In conclusion, GN-CCPs as a unique variant of nonaggressive tumor are characterized by nuclear β -catenin accumulation and mutation of CTNNB1 or AXIN gene, suggesting activation of the Wnt/ β -catenin pathway. |
| doi_str_mv | 10.1016/j.humpath.2013.06.002 |
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GN-CCPs were defined as tumors consisting of irregular anastomosing glands of columnar cells mimicking chief cells of fundic gland with nuclear atypia and prolapse-type submucosal involvement. We comparatively evaluated clinicopathologic features between 31 GN-CCPs and 130 cases of conventional gastric adenocarcinoma invading into submucosa (CGA-SM) in additon to nuclear β -catenin immunolabeling and direct sequencing of members of the Wnt/ β -catenin pathway, CTNNB1 , APC , and AXIN , in a subset of these tumors. GN-CCP presented as small protruded lesions located in the upper third of the stomach, with minimal involvement into the submucosa and rare lymphovascular invasion. None of the lesions have demonstrated a recurrence of disease or metastasis on follow-up. Nuclear β -catenin immunolabeling was higher in GN-CCP (labeling index [LI]: median, 19.3%; high expresser [LI >30%], 7/27 cases [26%]) than CGA-SM (median LI, 14.7%; high expresser, 1/19 cases [6%]). Missense mutation of APC was observed in 1 GN-CCP but not CGA-SM. Missense or nonsense mutations of CTNNB1 and AXIN1 were higher in GN-CCPs (14.8%, both) than CGA-SMs (5.3%, both). Missense mutations of AXIN2 were higher in GN-CCPs (25.9%) than in CGA-SMs (10.5%). Overall, 14 (51.9%) of 27 GN-CCPs and 5 (26.3%) of 19 CGA-SM cases harbored at least 1 of these gene mutations. In conclusion, GN-CCPs as a unique variant of nonaggressive tumor are characterized by nuclear β -catenin accumulation and mutation of CTNNB1 or AXIN gene, suggesting activation of the Wnt/ β -catenin pathway.</description><identifier>ISSN: 0046-8177</identifier><identifier>EISSN: 1532-8392</identifier><identifier>DOI: 10.1016/j.humpath.2013.06.002</identifier><identifier>PMID: 24011952</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adenocarcinoma ; Adenocarcinoma - genetics ; Adenocarcinoma - metabolism ; Adenocarcinoma - pathology ; Adenocarcinoma - surgery ; Adenoma ; Adenomatous Polyposis Coli Protein - genetics ; Adenomatous Polyposis Coli Protein - metabolism ; Adult ; Aged ; Aged, 80 and over ; APC ; AXIN ; Axin Protein - genetics ; Axin Protein - metabolism ; beta Catenin - genetics ; beta Catenin - metabolism ; Cell Nucleus - genetics ; Cell Nucleus - metabolism ; Chief Cells, Gastric - metabolism ; Chief Cells, Gastric - pathology ; DNA Mutational Analysis ; Female ; Fundic gland/chief cell differentiation ; Gastric Mucosa - metabolism ; Gastric Mucosa - pathology ; Humans ; Japan ; Male ; Middle Aged ; Mutation ; Neoplasm Recurrence, Local ; Pathology ; Signal Transduction ; Stomach ; Stomach Neoplasms - genetics ; Stomach Neoplasms - metabolism ; Stomach Neoplasms - pathology ; Stomach Neoplasms - surgery ; Wnt Proteins - genetics ; Wnt Proteins - metabolism ; Wnt Signaling Pathway ; Wnt/β-Catenin</subject><ispartof>Human pathology, 2013-11, Vol.44 (11), p.2438-2448</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>2013.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-e315e719275c54bc404b430cf621a3e2a7ba5ffcdb29fbb309e504b29bbb3fc3</citedby><cites>FETCH-LOGICAL-c420t-e315e719275c54bc404b430cf621a3e2a7ba5ffcdb29fbb309e504b29bbb3fc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24011952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hidaka, Yasuhiro, MD</creatorcontrib><creatorcontrib>Mitomi, Hiroyuki, MD, PhD</creatorcontrib><creatorcontrib>Saito, Tsuyoshi, MD, PhD</creatorcontrib><creatorcontrib>Takahashi, Michiko, TBSc</creatorcontrib><creatorcontrib>Lee, Se-yong, MD</creatorcontrib><creatorcontrib>Matsumoto, Kenshi, MD</creatorcontrib><creatorcontrib>Yao, Takashi, MD, PhD</creatorcontrib><creatorcontrib>Watanabe, Sumio, MD, PhD</creatorcontrib><title>Alteration in the Wnt/β-catenin signaling pathway in gastric neoplasias of fundic gland (chief cell predominant) type</title><title>Human pathology</title><addtitle>Hum Pathol</addtitle><description>Summary Gastric neoplasia of chief cell–predominant type (GN-CCP) has been reported as a new, rare variant of gastric tumor. GN-CCPs were defined as tumors consisting of irregular anastomosing glands of columnar cells mimicking chief cells of fundic gland with nuclear atypia and prolapse-type submucosal involvement. We comparatively evaluated clinicopathologic features between 31 GN-CCPs and 130 cases of conventional gastric adenocarcinoma invading into submucosa (CGA-SM) in additon to nuclear β -catenin immunolabeling and direct sequencing of members of the Wnt/ β -catenin pathway, CTNNB1 , APC , and AXIN , in a subset of these tumors. GN-CCP presented as small protruded lesions located in the upper third of the stomach, with minimal involvement into the submucosa and rare lymphovascular invasion. None of the lesions have demonstrated a recurrence of disease or metastasis on follow-up. Nuclear β -catenin immunolabeling was higher in GN-CCP (labeling index [LI]: median, 19.3%; high expresser [LI >30%], 7/27 cases [26%]) than CGA-SM (median LI, 14.7%; high expresser, 1/19 cases [6%]). Missense mutation of APC was observed in 1 GN-CCP but not CGA-SM. Missense or nonsense mutations of CTNNB1 and AXIN1 were higher in GN-CCPs (14.8%, both) than CGA-SMs (5.3%, both). Missense mutations of AXIN2 were higher in GN-CCPs (25.9%) than in CGA-SMs (10.5%). Overall, 14 (51.9%) of 27 GN-CCPs and 5 (26.3%) of 19 CGA-SM cases harbored at least 1 of these gene mutations. In conclusion, GN-CCPs as a unique variant of nonaggressive tumor are characterized by nuclear β -catenin accumulation and mutation of CTNNB1 or AXIN gene, suggesting activation of the Wnt/ β -catenin pathway.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - metabolism</subject><subject>Adenocarcinoma - pathology</subject><subject>Adenocarcinoma - surgery</subject><subject>Adenoma</subject><subject>Adenomatous Polyposis Coli Protein - genetics</subject><subject>Adenomatous Polyposis Coli Protein - metabolism</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>APC</subject><subject>AXIN</subject><subject>Axin Protein - genetics</subject><subject>Axin Protein - metabolism</subject><subject>beta Catenin - genetics</subject><subject>beta Catenin - metabolism</subject><subject>Cell Nucleus - genetics</subject><subject>Cell Nucleus - metabolism</subject><subject>Chief Cells, Gastric - metabolism</subject><subject>Chief Cells, Gastric - pathology</subject><subject>DNA Mutational Analysis</subject><subject>Female</subject><subject>Fundic gland/chief cell differentiation</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - pathology</subject><subject>Humans</subject><subject>Japan</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Mutation</subject><subject>Neoplasm Recurrence, Local</subject><subject>Pathology</subject><subject>Signal Transduction</subject><subject>Stomach</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - metabolism</subject><subject>Stomach Neoplasms - pathology</subject><subject>Stomach Neoplasms - surgery</subject><subject>Wnt Proteins - genetics</subject><subject>Wnt Proteins - metabolism</subject><subject>Wnt Signaling Pathway</subject><subject>Wnt/β-Catenin</subject><issn>0046-8177</issn><issn>1532-8392</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><recordid>eNqFUU1v1DAQtSoqurT8hCIfyyGpP5PNBVRV0CJV4kClHi3HGe96SZxgO0X7t_gh_CYc7cKBS08ej96bN_MeQpeUlJTQ6npXbudh0mlbMkJ5SaqSEHaCVlRyVqx5w16hFSGiKta0rs_Qmxh3hFAqhXyNzpjIZSPZCj3f9AmCTm702HmctoCffLr-_aswOoHPreg2XvfOb_Ci9lPvF9xGxxScwR7GqdfR6YhHi-3su9zc9Np3-MpsHVhsoO_xFKAbB-e1T-9x2k9wgU6t7iO8Pb7n6PHzp8fb--Lh692X25uHwghGUgGcSqhpw2pppGiNIKIVnBhbMao5MF23WlprupY1tm05aUBmCGva_LGGn6Orw9gpjD9miEkNLi4b6bz4HBUVggvC5LrKUHmAmjDGGMCqKbhBh72iRC2Oq506Oq4WxxWpVHY8894dJeZ2gO4f66_FGfDxAIB857ODoKJx4A10LoBJqhvdixIf_ptgch7O6P477CHuxjnkhPI1KjJF1Lcl9iV1yjNbsob_AY68rAk</recordid><startdate>20131101</startdate><enddate>20131101</enddate><creator>Hidaka, Yasuhiro, MD</creator><creator>Mitomi, Hiroyuki, MD, PhD</creator><creator>Saito, Tsuyoshi, MD, PhD</creator><creator>Takahashi, Michiko, TBSc</creator><creator>Lee, Se-yong, MD</creator><creator>Matsumoto, Kenshi, MD</creator><creator>Yao, Takashi, MD, PhD</creator><creator>Watanabe, Sumio, MD, PhD</creator><general>Elsevier Inc</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></search><sort><creationdate>20131101</creationdate><title>Alteration in the Wnt/β-catenin signaling pathway in gastric neoplasias of fundic gland (chief cell predominant) type</title><author>Hidaka, Yasuhiro, MD ; Mitomi, Hiroyuki, MD, PhD ; Saito, Tsuyoshi, MD, PhD ; Takahashi, Michiko, TBSc ; Lee, Se-yong, MD ; Matsumoto, Kenshi, MD ; Yao, Takashi, MD, PhD ; Watanabe, Sumio, MD, PhD</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-e315e719275c54bc404b430cf621a3e2a7ba5ffcdb29fbb309e504b29bbb3fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - metabolism</topic><topic>Adenocarcinoma - pathology</topic><topic>Adenocarcinoma - surgery</topic><topic>Adenoma</topic><topic>Adenomatous Polyposis Coli Protein - genetics</topic><topic>Adenomatous Polyposis Coli Protein - metabolism</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>APC</topic><topic>AXIN</topic><topic>Axin Protein - genetics</topic><topic>Axin Protein - metabolism</topic><topic>beta Catenin - genetics</topic><topic>beta Catenin - metabolism</topic><topic>Cell Nucleus - genetics</topic><topic>Cell Nucleus - metabolism</topic><topic>Chief Cells, Gastric - metabolism</topic><topic>Chief Cells, Gastric - pathology</topic><topic>DNA Mutational Analysis</topic><topic>Female</topic><topic>Fundic gland/chief cell differentiation</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - pathology</topic><topic>Humans</topic><topic>Japan</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Mutation</topic><topic>Neoplasm Recurrence, Local</topic><topic>Pathology</topic><topic>Signal Transduction</topic><topic>Stomach</topic><topic>Stomach Neoplasms - genetics</topic><topic>Stomach Neoplasms - metabolism</topic><topic>Stomach Neoplasms - pathology</topic><topic>Stomach Neoplasms - surgery</topic><topic>Wnt Proteins - genetics</topic><topic>Wnt Proteins - metabolism</topic><topic>Wnt Signaling Pathway</topic><topic>Wnt/β-Catenin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hidaka, Yasuhiro, MD</creatorcontrib><creatorcontrib>Mitomi, Hiroyuki, MD, PhD</creatorcontrib><creatorcontrib>Saito, Tsuyoshi, MD, PhD</creatorcontrib><creatorcontrib>Takahashi, Michiko, TBSc</creatorcontrib><creatorcontrib>Lee, Se-yong, MD</creatorcontrib><creatorcontrib>Matsumoto, Kenshi, MD</creatorcontrib><creatorcontrib>Yao, Takashi, MD, PhD</creatorcontrib><creatorcontrib>Watanabe, Sumio, MD, PhD</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><jtitle>Human pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hidaka, Yasuhiro, MD</au><au>Mitomi, Hiroyuki, MD, PhD</au><au>Saito, Tsuyoshi, MD, PhD</au><au>Takahashi, Michiko, TBSc</au><au>Lee, Se-yong, MD</au><au>Matsumoto, Kenshi, MD</au><au>Yao, Takashi, MD, PhD</au><au>Watanabe, Sumio, MD, PhD</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Alteration in the Wnt/β-catenin signaling pathway in gastric neoplasias of fundic gland (chief cell predominant) type</atitle><jtitle>Human pathology</jtitle><addtitle>Hum Pathol</addtitle><date>2013-11-01</date><risdate>2013</risdate><volume>44</volume><issue>11</issue><spage>2438</spage><epage>2448</epage><pages>2438-2448</pages><issn>0046-8177</issn><eissn>1532-8392</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Summary Gastric neoplasia of chief cell–predominant type (GN-CCP) has been reported as a new, rare variant of gastric tumor. GN-CCPs were defined as tumors consisting of irregular anastomosing glands of columnar cells mimicking chief cells of fundic gland with nuclear atypia and prolapse-type submucosal involvement. We comparatively evaluated clinicopathologic features between 31 GN-CCPs and 130 cases of conventional gastric adenocarcinoma invading into submucosa (CGA-SM) in additon to nuclear β -catenin immunolabeling and direct sequencing of members of the Wnt/ β -catenin pathway, CTNNB1 , APC , and AXIN , in a subset of these tumors. GN-CCP presented as small protruded lesions located in the upper third of the stomach, with minimal involvement into the submucosa and rare lymphovascular invasion. None of the lesions have demonstrated a recurrence of disease or metastasis on follow-up. Nuclear β -catenin immunolabeling was higher in GN-CCP (labeling index [LI]: median, 19.3%; high expresser [LI >30%], 7/27 cases [26%]) than CGA-SM (median LI, 14.7%; high expresser, 1/19 cases [6%]). Missense mutation of APC was observed in 1 GN-CCP but not CGA-SM. Missense or nonsense mutations of CTNNB1 and AXIN1 were higher in GN-CCPs (14.8%, both) than CGA-SMs (5.3%, both). Missense mutations of AXIN2 were higher in GN-CCPs (25.9%) than in CGA-SMs (10.5%). Overall, 14 (51.9%) of 27 GN-CCPs and 5 (26.3%) of 19 CGA-SM cases harbored at least 1 of these gene mutations. In conclusion, GN-CCPs as a unique variant of nonaggressive tumor are characterized by nuclear β -catenin accumulation and mutation of CTNNB1 or AXIN gene, suggesting activation of the Wnt/ β -catenin pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>24011952</pmid><doi>10.1016/j.humpath.2013.06.002</doi><tpages>11</tpages></addata></record> |
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| subjects | Adenocarcinoma Adenocarcinoma - genetics Adenocarcinoma - metabolism Adenocarcinoma - pathology Adenocarcinoma - surgery Adenoma Adenomatous Polyposis Coli Protein - genetics Adenomatous Polyposis Coli Protein - metabolism Adult Aged Aged, 80 and over APC AXIN Axin Protein - genetics Axin Protein - metabolism beta Catenin - genetics beta Catenin - metabolism Cell Nucleus - genetics Cell Nucleus - metabolism Chief Cells, Gastric - metabolism Chief Cells, Gastric - pathology DNA Mutational Analysis Female Fundic gland/chief cell differentiation Gastric Mucosa - metabolism Gastric Mucosa - pathology Humans Japan Male Middle Aged Mutation Neoplasm Recurrence, Local Pathology Signal Transduction Stomach Stomach Neoplasms - genetics Stomach Neoplasms - metabolism Stomach Neoplasms - pathology Stomach Neoplasms - surgery Wnt Proteins - genetics Wnt Proteins - metabolism Wnt Signaling Pathway Wnt/β-Catenin |
| title | Alteration in the Wnt/β-catenin signaling pathway in gastric neoplasias of fundic gland (chief cell predominant) type |
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