β-Catenin signaling in hepatocellular cancer: Implications in inflammation, fibrosis, and proliferation.
Identifieur interne : 003B88 ( PubMed/Corpus ); précédent : 003B87; suivant : 003B89β-Catenin signaling in hepatocellular cancer: Implications in inflammation, fibrosis, and proliferation.
Auteurs : Jung Min Lee ; Jing Yang ; Pippa Newell ; Sucha Singh ; Anil Parwani ; Scott L. Friedman ; Kari Nichole Nejak-Bowen ; Satdarshan P. MongaSource :
- Cancer letters [ 1872-7980 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Carcinoma, Hepatocellular (metabolism), Cell Line, Tumor, Cell Proliferation, Cytoplasm (metabolism), DNA Methylation, Female, Fibrosis (pathology), Glutamate-Ammonia Ligase (metabolism), Humans, Immunohistochemistry, Inflammation, Liver Neoplasms (metabolism), Male, Mice, Mice, Transgenic, Mutation, Signal Transduction, beta Catenin (metabolism).
- MESH :
- chemical , metabolism : Glutamate-Ammonia Ligase, beta Catenin.
- metabolism : Carcinoma, Hepatocellular, Cytoplasm, Liver Neoplasms.
- pathology : Fibrosis.
- Animals, Cell Line, Tumor, Cell Proliferation, DNA Methylation, Female, Humans, Immunohistochemistry, Inflammation, Male, Mice, Mice, Transgenic, Mutation, Signal Transduction.
Abstract
β-Catenin signaling is implicated in hepatocellular carcinoma (HCC), although its role in inflammation, fibrosis, and proliferation is unclear. Commercially available HCC tissue microarray (TMA) of 89 cases was assessed for β-catenin, one of its transcriptional targets glutamine synthetase (GS), proliferation (PCNA), inflammation (CD45), and fibrosis (Sirius Red). HCC cells transfected with wild-type (WT) or mutant-β-catenin were evaluated for β-catenin-T cell factor transactivation by TOPFlash reporter activity and expression of certain targets. Hepatocyte-specific-serine-45-mutated β-catenin transgenic mice (TG) and controls (Con) were used to study thioacetamide (TAA)-induced hepatic fibrosis and tumorigenesis. Sustained β-catenin activation was only observed in mutant-, not WT-β-catenin transfected HCC cells. Aberrant intratumoral β-catenin stabilization was evident in 33% cases with 9% showing predominant nuclear with some cytoplasmic (N/C) localization and 24% displaying predominant cytoplasmic with occasional nuclear (C/N) localization. N/C β-catenin was associated with reduced fibrosis (p=0.017) and tumor-wide GS staining (p<0.001) while C/N correlated with increased intratumoral inflammation (p=0.064) and proliferation (p=0.029). A small subset of HCC patients (15.5%) lacked β-catenin staining and exhibited low inflammation and fibrosis (p<0.05). TG and Con mice exposed to TAA showed comparable development of fibrosis and progression to cirrhosis and HCC. Taken together the data suggests a complex relationship of β-catenin, inflammation, fibrosis and HCC. GS staining is highly sensitive in identifying HCC with nuclear β-catenin, which may in turn represent β-catenin mutations, and does so with high negative predictive value. Also, β-catenin mutations and cirrhosis do not appear to cooperate in HCC pathogenesis in mice and men.
DOI: 10.1016/j.canlet.2013.09.020
PubMed: 24071572
Links to Exploration step
pubmed:24071572Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">β-Catenin signaling in hepatocellular cancer: Implications in inflammation, fibrosis, and proliferation.</title><author><name sortKey="Lee, Jung Min" sort="Lee, Jung Min" uniqKey="Lee J" first="Jung Min" last="Lee">Jung Min Lee</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jing" sort="Yang, Jing" uniqKey="Yang J" first="Jing" last="Yang">Jing Yang</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Newell, Pippa" sort="Newell, Pippa" uniqKey="Newell P" first="Pippa" last="Newell">Pippa Newell</name><affiliation><nlm:affiliation>Hepatobiliary and Pancreatic Surgery Program, Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OR, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Singh, Sucha" sort="Singh, Sucha" uniqKey="Singh S" first="Sucha" last="Singh">Sucha Singh</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Parwani, Anil" sort="Parwani, Anil" uniqKey="Parwani A" first="Anil" last="Parwani">Anil Parwani</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Friedman, Scott L" sort="Friedman, Scott L" uniqKey="Friedman S" first="Scott L" last="Friedman">Scott L. Friedman</name><affiliation><nlm:affiliation>Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nejak Bowen, Kari Nichole" sort="Nejak Bowen, Kari Nichole" uniqKey="Nejak Bowen K" first="Kari Nichole" last="Nejak-Bowen">Kari Nichole Nejak-Bowen</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Monga, Satdarshan P" sort="Monga, Satdarshan P" uniqKey="Monga S" first="Satdarshan P" last="Monga">Satdarshan P. Monga</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: smonga@pitt.edu.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24071572</idno><idno type="pmid">24071572</idno><idno type="doi">10.1016/j.canlet.2013.09.020</idno><idno type="wicri:Area/PubMed/Corpus">003B88</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003B88</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">β-Catenin signaling in hepatocellular cancer: Implications in inflammation, fibrosis, and proliferation.</title><author><name sortKey="Lee, Jung Min" sort="Lee, Jung Min" uniqKey="Lee J" first="Jung Min" last="Lee">Jung Min Lee</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Yang, Jing" sort="Yang, Jing" uniqKey="Yang J" first="Jing" last="Yang">Jing Yang</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Newell, Pippa" sort="Newell, Pippa" uniqKey="Newell P" first="Pippa" last="Newell">Pippa Newell</name><affiliation><nlm:affiliation>Hepatobiliary and Pancreatic Surgery Program, Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OR, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Singh, Sucha" sort="Singh, Sucha" uniqKey="Singh S" first="Sucha" last="Singh">Sucha Singh</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Parwani, Anil" sort="Parwani, Anil" uniqKey="Parwani A" first="Anil" last="Parwani">Anil Parwani</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Friedman, Scott L" sort="Friedman, Scott L" uniqKey="Friedman S" first="Scott L" last="Friedman">Scott L. Friedman</name><affiliation><nlm:affiliation>Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Nejak Bowen, Kari Nichole" sort="Nejak Bowen, Kari Nichole" uniqKey="Nejak Bowen K" first="Kari Nichole" last="Nejak-Bowen">Kari Nichole Nejak-Bowen</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</nlm:affiliation></affiliation></author><author><name sortKey="Monga, Satdarshan P" sort="Monga, Satdarshan P" uniqKey="Monga S" first="Satdarshan P" last="Monga">Satdarshan P. Monga</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: smonga@pitt.edu.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cancer letters</title><idno type="eISSN">1872-7980</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Carcinoma, Hepatocellular (metabolism)</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>Cytoplasm (metabolism)</term><term>DNA Methylation</term><term>Female</term><term>Fibrosis (pathology)</term><term>Glutamate-Ammonia Ligase (metabolism)</term><term>Humans</term><term>Immunohistochemistry</term><term>Inflammation</term><term>Liver Neoplasms (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation</term><term>Signal Transduction</term><term>beta Catenin (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Glutamate-Ammonia Ligase</term><term>beta Catenin</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Hepatocellular</term><term>Cytoplasm</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Fibrosis</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Cell Proliferation</term><term>DNA Methylation</term><term>Female</term><term>Humans</term><term>Immunohistochemistry</term><term>Inflammation</term><term>Male</term><term>Mice</term><term>Mice, Transgenic</term><term>Mutation</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">β-Catenin signaling is implicated in hepatocellular carcinoma (HCC), although its role in inflammation, fibrosis, and proliferation is unclear. Commercially available HCC tissue microarray (TMA) of 89 cases was assessed for β-catenin, one of its transcriptional targets glutamine synthetase (GS), proliferation (PCNA), inflammation (CD45), and fibrosis (Sirius Red). HCC cells transfected with wild-type (WT) or mutant-β-catenin were evaluated for β-catenin-T cell factor transactivation by TOPFlash reporter activity and expression of certain targets. Hepatocyte-specific-serine-45-mutated β-catenin transgenic mice (TG) and controls (Con) were used to study thioacetamide (TAA)-induced hepatic fibrosis and tumorigenesis. Sustained β-catenin activation was only observed in mutant-, not WT-β-catenin transfected HCC cells. Aberrant intratumoral β-catenin stabilization was evident in 33% cases with 9% showing predominant nuclear with some cytoplasmic (N/C) localization and 24% displaying predominant cytoplasmic with occasional nuclear (C/N) localization. N/C β-catenin was associated with reduced fibrosis (p=0.017) and tumor-wide GS staining (p<0.001) while C/N correlated with increased intratumoral inflammation (p=0.064) and proliferation (p=0.029). A small subset of HCC patients (15.5%) lacked β-catenin staining and exhibited low inflammation and fibrosis (p<0.05). TG and Con mice exposed to TAA showed comparable development of fibrosis and progression to cirrhosis and HCC. Taken together the data suggests a complex relationship of β-catenin, inflammation, fibrosis and HCC. GS staining is highly sensitive in identifying HCC with nuclear β-catenin, which may in turn represent β-catenin mutations, and does so with high negative predictive value. Also, β-catenin mutations and cirrhosis do not appear to cooperate in HCC pathogenesis in mice and men.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24071572</PMID><DateCreated><Year>2013</Year><Month>12</Month><Day>27</Day></DateCreated><DateCompleted><Year>2014</Year><Month>02</Month><Day>20</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-7980</ISSN><JournalIssue CitedMedium="Internet"><Volume>343</Volume><Issue>1</Issue><PubDate><Year>2014</Year><Month>Feb</Month><Day>01</Day></PubDate></JournalIssue><Title>Cancer letters</Title><ISOAbbreviation>Cancer Lett.</ISOAbbreviation></Journal><ArticleTitle>β-Catenin signaling in hepatocellular cancer: Implications in inflammation, fibrosis, and proliferation.</ArticleTitle><Pagination><MedlinePgn>90-7</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.canlet.2013.09.020</ELocationID><ELocationID EIdType="pii" ValidYN="Y">S0304-3835(13)00674-5</ELocationID><Abstract><AbstractText>β-Catenin signaling is implicated in hepatocellular carcinoma (HCC), although its role in inflammation, fibrosis, and proliferation is unclear. Commercially available HCC tissue microarray (TMA) of 89 cases was assessed for β-catenin, one of its transcriptional targets glutamine synthetase (GS), proliferation (PCNA), inflammation (CD45), and fibrosis (Sirius Red). HCC cells transfected with wild-type (WT) or mutant-β-catenin were evaluated for β-catenin-T cell factor transactivation by TOPFlash reporter activity and expression of certain targets. Hepatocyte-specific-serine-45-mutated β-catenin transgenic mice (TG) and controls (Con) were used to study thioacetamide (TAA)-induced hepatic fibrosis and tumorigenesis. Sustained β-catenin activation was only observed in mutant-, not WT-β-catenin transfected HCC cells. Aberrant intratumoral β-catenin stabilization was evident in 33% cases with 9% showing predominant nuclear with some cytoplasmic (N/C) localization and 24% displaying predominant cytoplasmic with occasional nuclear (C/N) localization. N/C β-catenin was associated with reduced fibrosis (p=0.017) and tumor-wide GS staining (p<0.001) while C/N correlated with increased intratumoral inflammation (p=0.064) and proliferation (p=0.029). A small subset of HCC patients (15.5%) lacked β-catenin staining and exhibited low inflammation and fibrosis (p<0.05). TG and Con mice exposed to TAA showed comparable development of fibrosis and progression to cirrhosis and HCC. Taken together the data suggests a complex relationship of β-catenin, inflammation, fibrosis and HCC. GS staining is highly sensitive in identifying HCC with nuclear β-catenin, which may in turn represent β-catenin mutations, and does so with high negative predictive value. Also, β-catenin mutations and cirrhosis do not appear to cooperate in HCC pathogenesis in mice and men.</AbstractText><CopyrightInformation>Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Jung Min</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Newell</LastName><ForeName>Pippa</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Hepatobiliary and Pancreatic Surgery Program, Earle A. Chiles Research Institute, Providence Portland Medical Center, Portland, OR, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Singh</LastName><ForeName>Sucha</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Parwani</LastName><ForeName>Anil</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Friedman</LastName><ForeName>Scott L</ForeName><Initials>SL</Initials><AffiliationInfo><Affiliation>Department of Medicine, Mount Sinai School of Medicine, New York, NY, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nejak-Bowen</LastName><ForeName>Kari Nichole</ForeName><Initials>KN</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Monga</LastName><ForeName>Satdarshan P</ForeName><Initials>SP</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: smonga@pitt.edu.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 DK056621</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>UL1 TR000005</GrantID><Acronym>TR</Acronym><Agency>NCATS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R01DK100287</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R01DK56621</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK062277</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AA020709</GrantID><Acronym>AA</Acronym><Agency>NIAAA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK100287</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 DK037340</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>1R01DK62277</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>09</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>Ireland</Country><MedlineTA>Cancer Lett</MedlineTA><NlmUniqueID>7600053</NlmUniqueID><ISSNLinking>0304-3835</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051176">beta Catenin</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 6.3.1.2</RegistryNumber><NameOfSubstance UI="D005974">Glutamate-Ammonia Ligase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Hepatology. 2009 Mar;49(3):821-31</RefSource><PMID Version="1">19101982</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Clin Invest. 2012 Feb;122(2):586-99</RefSource><PMID Version="1">22251704</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hepatology. 2007 May;45(5):1298-305</RefSource><PMID Version="1">17464972</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Gastroenterology. 2011 Aug;141(2):707-18, 718.e1-5</RefSource><PMID Version="1">21679710</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Carcinogenesis. 2011 Jan;32(1):52-7</RefSource><PMID 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Version="1">16496320</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hepatology. 1994 Sep;20(3):684-91</RefSource><PMID Version="1">7915704</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2004 Dec 7;101(49):17216-21</RefSource><PMID Version="1">15563600</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D006528" MajorTopicYN="N">Carcinoma, Hepatocellular</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D003593" MajorTopicYN="N">Cytoplasm</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019175" MajorTopicYN="N">DNA Methylation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005355" MajorTopicYN="N">Fibrosis</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005974" MajorTopicYN="N">Glutamate-Ammonia Ligase</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007150" MajorTopicYN="N">Immunohistochemistry</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007249" 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