Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.
Identifieur interne : 002886 ( PubMed/Corpus ); précédent : 002885; suivant : 002887Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.
Auteurs : Hirohisa Okabe ; Evan Delgado ; Jung Min Lee ; Jing Yang ; Hiroki Kinoshita ; Hiromitsu Hayashi ; Allan Tsung ; Jaideep Behari ; Toru Beppu ; Hideo Baba ; Satdarshan P. MongaSource :
- PloS one [ 1932-6203 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Biomarkers, Tumor (genetics), Biomarkers, Tumor (metabolism), Carcinoma, Hepatocellular (genetics), Carcinoma, Hepatocellular (metabolism), Humans, Intercellular Signaling Peptides and Proteins (genetics), Intercellular Signaling Peptides and Proteins (metabolism), Liver Neoplasms (genetics), Liver Neoplasms (metabolism), Mice, Mice, Knockout, beta Catenin (genetics), beta Catenin (metabolism).
- MESH :
- chemical , genetics : Biomarkers, Tumor, Intercellular Signaling Peptides and Proteins, beta Catenin.
- chemical , metabolism : Biomarkers, Tumor, Intercellular Signaling Peptides and Proteins, beta Catenin.
- genetics : Carcinoma, Hepatocellular, Liver Neoplasms.
- metabolism : Carcinoma, Hepatocellular, Liver Neoplasms.
- Animals, Humans, Mice, Mice, Knockout.
Abstract
We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28 ± 22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8 ± 21.1 ng/mL; n = 15) or healthy volunteers (33.2 ± 7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.
DOI: 10.1371/journal.pone.0098817
PubMed: 24892551
Links to Exploration step
pubmed:24892551Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.</title><author><name sortKey="Okabe, Hirohisa" sort="Okabe, Hirohisa" uniqKey="Okabe H" first="Hirohisa" last="Okabe">Hirohisa Okabe</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Delgado, Evan" sort="Delgado, Evan" uniqKey="Delgado E" first="Evan" last="Delgado">Evan Delgado</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><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, Pittsburgh, Pennsylvania, United States of America.</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, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Kinoshita, Hiroki" sort="Kinoshita, Hiroki" uniqKey="Kinoshita H" first="Hiroki" last="Kinoshita">Hiroki Kinoshita</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Hayashi, Hiromitsu" sort="Hayashi, Hiromitsu" uniqKey="Hayashi H" first="Hiromitsu" last="Hayashi">Hiromitsu Hayashi</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Tsung, Allan" sort="Tsung, Allan" uniqKey="Tsung A" first="Allan" last="Tsung">Allan Tsung</name><affiliation><nlm:affiliation>Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Behari, Jaideep" sort="Behari, Jaideep" uniqKey="Behari J" first="Jaideep" last="Behari">Jaideep Behari</name><affiliation><nlm:affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Beppu, Toru" sort="Beppu, Toru" uniqKey="Beppu T" first="Toru" last="Beppu">Toru Beppu</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan; Department of Multidisciplinary Treatment for Gastroenterological Cancer, Kumamoto University Hospital, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Baba, Hideo" sort="Baba, Hideo" uniqKey="Baba H" first="Hideo" last="Baba">Hideo Baba</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</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, Pittsburgh, Pennsylvania, United States of America; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:24892551</idno><idno type="pmid">24892551</idno><idno type="doi">10.1371/journal.pone.0098817</idno><idno type="wicri:Area/PubMed/Corpus">002886</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">002886</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.</title><author><name sortKey="Okabe, Hirohisa" sort="Okabe, Hirohisa" uniqKey="Okabe H" first="Hirohisa" last="Okabe">Hirohisa Okabe</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Delgado, Evan" sort="Delgado, Evan" uniqKey="Delgado E" first="Evan" last="Delgado">Evan Delgado</name><affiliation><nlm:affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><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, Pittsburgh, Pennsylvania, United States of America.</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, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Kinoshita, Hiroki" sort="Kinoshita, Hiroki" uniqKey="Kinoshita H" first="Hiroki" last="Kinoshita">Hiroki Kinoshita</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Hayashi, Hiromitsu" sort="Hayashi, Hiromitsu" uniqKey="Hayashi H" first="Hiromitsu" last="Hayashi">Hiromitsu Hayashi</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Tsung, Allan" sort="Tsung, Allan" uniqKey="Tsung A" first="Allan" last="Tsung">Allan Tsung</name><affiliation><nlm:affiliation>Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Behari, Jaideep" sort="Behari, Jaideep" uniqKey="Behari J" first="Jaideep" last="Behari">Jaideep Behari</name><affiliation><nlm:affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Beppu, Toru" sort="Beppu, Toru" uniqKey="Beppu T" first="Toru" last="Beppu">Toru Beppu</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan; Department of Multidisciplinary Treatment for Gastroenterological Cancer, Kumamoto University Hospital, Kumamoto, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Baba, Hideo" sort="Baba, Hideo" uniqKey="Baba H" first="Hideo" last="Baba">Hideo Baba</name><affiliation><nlm:affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</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, Pittsburgh, Pennsylvania, United States of America; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</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>Biomarkers, Tumor (genetics)</term><term>Biomarkers, Tumor (metabolism)</term><term>Carcinoma, Hepatocellular (genetics)</term><term>Carcinoma, Hepatocellular (metabolism)</term><term>Humans</term><term>Intercellular Signaling Peptides and Proteins (genetics)</term><term>Intercellular Signaling Peptides and Proteins (metabolism)</term><term>Liver Neoplasms (genetics)</term><term>Liver Neoplasms (metabolism)</term><term>Mice</term><term>Mice, Knockout</term><term>beta Catenin (genetics)</term><term>beta Catenin (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Biomarkers, Tumor</term><term>Intercellular Signaling Peptides and Proteins</term><term>beta Catenin</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Biomarkers, Tumor</term><term>Intercellular Signaling Peptides and Proteins</term><term>beta Catenin</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Hepatocellular</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Hepatocellular</term><term>Liver Neoplasms</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Humans</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28 ± 22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8 ± 21.1 ng/mL; n = 15) or healthy volunteers (33.2 ± 7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24892551</PMID><DateCreated><Year>2014</Year><Month>06</Month><Day>04</Day></DateCreated><DateCompleted><Year>2015</Year><Month>01</Month><Day>12</Day></DateCompleted><DateRevised><Year>2016</Year><Month>10</Month><Day>19</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>9</Volume><Issue>6</Issue><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Role of leukocyte cell-derived chemotaxin 2 as a biomarker in hepatocellular carcinoma.</ArticleTitle><Pagination><MedlinePgn>e98817</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0098817</ELocationID><Abstract><AbstractText>We sought to identify a secreted biomarker for β-catenin activation commonly seen in hepatocellular carcinoma (HCC). By examination of our previously published genearray of hepatocyte-specific β-catenin knockout (KO) livers, we identified secreted factors whose expression may be β-catenin-dependent. We verified expression and secretion of the leading factor in HCC cells transfected with mutated (Hep3BS33Y)-β-catenin. Serum levels of biomarker were next investigated in a mouse model of HCC with β-catenin gene (Ctnnb1) mutations and eventually in HCC patients. Leukocyte cell-derived chemotaxin-2 (LECT2) expression was decreased in KO livers. Hep3BS33Y expressed and secreted more LECT2 in media as compared to Hep3BWT. Mice developing HCC with Ctnnb1 mutations showed significantly higher serum LECT2 levels. However patients with CTNNB1 mutations showed LECT2 levels of 54.28 ± 22.32 ng/mL (Mean ± SD; n = 8) that were insignificantly different from patients with non-neoplastic chronic liver disease (32.8 ± 21.1 ng/mL; n = 15) or healthy volunteers (33.2 ± 7.2 ng/mL; n = 11). Intriguingly, patients without β-catenin mutations showed significantly higher serum LECT2 levels (54.26 ± 22.25 ng/mL; n = 46). While β-catenin activation was evident in a subset of non-mutant β-catenin HCC group with high LECT2 expression, serum LECT2 was unequivocally similar between β-catenin-active and -normal group. Further analysis showed that LECT2 levels greater than 50 ng/ml diagnosed HCC in patients irrespective of β-catenin mutations with specificity of 96.1% and positive predictive value of 97.0%. Thus, LECT2 is regulated by β-catenin in HCC in both mice and men, but serum LECT2 reflects β-catenin activity only in mice. Serum LECT2 could be a potential biomarker of HCC in patients.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Okabe</LastName><ForeName>Hirohisa</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Delgado</LastName><ForeName>Evan</ForeName><Initials>E</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Jung Min</ForeName><Initials>JM</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Yang</LastName><ForeName>Jing</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kinoshita</LastName><ForeName>Hiroki</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hayashi</LastName><ForeName>Hiromitsu</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tsung</LastName><ForeName>Allan</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Behari</LastName><ForeName>Jaideep</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Beppu</LastName><ForeName>Toru</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan; Department of Multidisciplinary Treatment for Gastroenterological Cancer, Kumamoto University Hospital, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baba</LastName><ForeName>Hideo</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Gastroenterological Surgery, Graduate School of Life Sciences, Kumamoto University, Kumamoto, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Monga</LastName><ForeName>Satdarshan P</ForeName><Initials>SP</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America; Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 DK100287</GrantID><Acronym>DK</Acronym><Agency>NIDDK NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>T32 HL094295</GrantID><Acronym>HL</Acronym><Agency>NHLBI 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><Grant><GrantID>R01DK100287</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>2014</Year><Month>06</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014408">Biomarkers, Tumor</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D036341">Intercellular Signaling Peptides and Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C103468">LECT2 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491213">Lect2 protein, mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051176">beta Catenin</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Lancet. 2012 Mar 31;379(9822):1245-55</RefSource><PMID Version="1">22353262</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>Mol Cell Biol. 2002 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Version="1">21778132</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Oncogene. 2001 Nov 22;20(53):7812-6</RefSource><PMID Version="1">11753661</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014408" MajorTopicYN="N">Biomarkers, Tumor</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006528" MajorTopicYN="N">Carcinoma, Hepatocellular</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D036341" MajorTopicYN="N">Intercellular Signaling Peptides and Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008113" MajorTopicYN="N">Liver Neoplasms</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018345" MajorTopicYN="N">Mice, Knockout</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051176" MajorTopicYN="N">beta Catenin</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading></MeshHeadingList><OtherID Source="NLM">PMC4043833</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2014</Year><Month>02</Month><Day>19</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2014</Year><Month>05</Month><Day>06</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>6</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>6</Month><Day>4</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>1</Month><Day>13</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>epublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24892551</ArticleId><ArticleId IdType="doi">10.1371/journal.pone.0098817</ArticleId><ArticleId IdType="pii">PONE-D-14-07658</ArticleId><ArticleId IdType="pmc">PMC4043833</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce 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