Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.
Identifieur interne : 000590 ( PubMed/Curation ); précédent : 000589; suivant : 000591Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.
Auteurs : Kristina Ibá Ez [Espagne] ; César Boullosa [Espagne] ; Rafael Tabarés-Seisdedos [Espagne] ; Anaïs Baudot [France] ; Alfonso Valencia [Espagne]Source :
- PLoS genetics [ 1553-7404 ] ; 2014.
English descriptors
- KwdEn :
- Alzheimer Disease (epidemiology), Alzheimer Disease (genetics), Alzheimer Disease (pathology), Central Nervous System (pathology), Comorbidity, Gene Expression Profiling, Gene Expression Regulation, Humans, NIMA-Interacting Peptidylprolyl Isomerase, Neoplasms (epidemiology), Neoplasms (genetics), Neoplasms (pathology), Parkinson Disease (epidemiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Peptidylprolyl Isomerase (genetics), Schizophrenia (epidemiology), Schizophrenia (genetics), Schizophrenia (pathology), Signal Transduction.
- MESH :
- chemical , genetics : Peptidylprolyl Isomerase.
- chemical : NIMA-Interacting Peptidylprolyl Isomerase.
- epidemiology : Alzheimer Disease, Neoplasms, Parkinson Disease, Schizophrenia.
- genetics : Alzheimer Disease, Neoplasms, Parkinson Disease, Schizophrenia.
- pathology : Alzheimer Disease, Central Nervous System, Neoplasms, Parkinson Disease, Schizophrenia.
- Comorbidity, Gene Expression Profiling, Gene Expression Regulation, Humans, Signal Transduction.
Abstract
There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.
DOI: 10.1371/journal.pgen.1004173
PubMed: 24586201
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pubmed:24586201Le document en format XML
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sort="Boullosa, Cesar" uniqKey="Boullosa C" first="César" last="Boullosa">César Boullosa</name><affiliation wicri:level="1"><nlm:affiliation>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid</wicri:regionArea></affiliation></author><author><name sortKey="Tabares Seisdedos, Rafael" sort="Tabares Seisdedos, Rafael" uniqKey="Tabares Seisdedos R" first="Rafael" last="Tabarés-Seisdedos">Rafael Tabarés-Seisdedos</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine, University of Valencia, CIBERSAM, INCLIVA, Valencia, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Medicine, University of Valencia, CIBERSAM, INCLIVA, Valencia</wicri:regionArea></affiliation></author><author><name sortKey="Baudot, Anais" sort="Baudot, Anais" uniqKey="Baudot A" first="Anaïs" last="Baudot">Anaïs Baudot</name><affiliation wicri:level="1"><nlm:affiliation>Aix-Marseille Université, CNRS, I2M, UMR 7373, Marseille, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Aix-Marseille Université, CNRS, I2M, UMR 7373, Marseille</wicri:regionArea></affiliation></author><author><name sortKey="Valencia, Alfonso" sort="Valencia, Alfonso" uniqKey="Valencia A" first="Alfonso" last="Valencia">Alfonso Valencia</name><affiliation wicri:level="1"><nlm:affiliation>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid</wicri:regionArea></affiliation></author></analytic><series><title level="j">PLoS genetics</title><idno 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scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidylprolyl Isomerase</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>NIMA-Interacting Peptidylprolyl Isomerase</term></keywords><keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Alzheimer Disease</term><term>Neoplasms</term><term>Parkinson Disease</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Alzheimer Disease</term><term>Neoplasms</term><term>Parkinson Disease</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Alzheimer Disease</term><term>Central Nervous System</term><term>Neoplasms</term><term>Parkinson Disease</term><term>Schizophrenia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Comorbidity</term><term>Gene Expression Profiling</term><term>Gene Expression Regulation</term><term>Humans</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24586201</PMID><DateCreated><Year>2014</Year><Month>03</Month><Day>03</Day></DateCreated><DateCompleted><Year>2014</Year><Month>12</Month><Day>15</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7404</ISSN><JournalIssue CitedMedium="Internet"><Volume>10</Volume><Issue>2</Issue><PubDate><Year>2014</Year><Month>Feb</Month></PubDate></JournalIssue><Title>PLoS genetics</Title><ISOAbbreviation>PLoS Genet.</ISOAbbreviation></Journal><ArticleTitle>Molecular evidence for the inverse comorbidity between central nervous system disorders and cancers detected by transcriptomic meta-analyses.</ArticleTitle><Pagination><MedlinePgn>e1004173</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pgen.1004173</ELocationID><Abstract><AbstractText>There is epidemiological evidence that patients with certain Central Nervous System (CNS) disorders have a lower than expected probability of developing some types of Cancer. We tested here the hypothesis that this inverse comorbidity is driven by molecular processes common to CNS disorders and Cancers, and that are deregulated in opposite directions. We conducted transcriptomic meta-analyses of three CNS disorders (Alzheimer's disease, Parkinson's disease and Schizophrenia) and three Cancer types (Lung, Prostate, Colorectal) previously described with inverse comorbidities. A significant overlap was observed between the genes upregulated in CNS disorders and downregulated in Cancers, as well as between the genes downregulated in CNS disorders and upregulated in Cancers. We also observed expression deregulations in opposite directions at the level of pathways. Our analysis points to specific genes and pathways, the upregulation of which could increase the incidence of CNS disorders and simultaneously lower the risk of developing Cancer, while the downregulation of another set of genes and pathways could contribute to a decrease in the incidence of CNS disorders while increasing the Cancer risk. These results reinforce the previously proposed involvement of the PIN1 gene, Wnt and P53 pathways, and reveal potential new candidates, in particular related with protein degradation processes.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ibáñez</LastName><ForeName>Kristina</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Boullosa</LastName><ForeName>César</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tabarés-Seisdedos</LastName><ForeName>Rafael</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Medicine, University of Valencia, CIBERSAM, INCLIVA, Valencia, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Baudot</LastName><ForeName>Anaïs</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Aix-Marseille Université, CNRS, I2M, UMR 7373, Marseille, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Valencia</LastName><ForeName>Alfonso</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Structural Biology and Biocomputing Programme, Spanish National Cancer, Research Centre (CNIO), Madrid, Spain.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>02</Month><Day>20</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Genet</MedlineTA><NlmUniqueID>101239074</NlmUniqueID><ISSNLinking>1553-7390</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000072340">NIMA-Interacting Peptidylprolyl Isomerase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 5.2.1.8</RegistryNumber><NameOfSubstance UI="C000606846">PIN1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 5.2.1.8</RegistryNumber><NameOfSubstance UI="D019696">Peptidylprolyl Isomerase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Eur J Hum Genet. 2003 Dec;11(12):937-44</RefSource><PMID Version="1">14508504</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Bioinformatics. 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RefType="Cites"><RefSource>Bioinformatics. 2004 Feb 12;20(3):307-15</RefSource><PMID Version="1">14960456</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000453" MajorTopicYN="N">epidemiology</QualifierName><QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002490" MajorTopicYN="N">Central Nervous System</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015897" MajorTopicYN="Y">Comorbidity</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020869" MajorTopicYN="N">Gene Expression Profiling</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression 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