RapamycinFungusV1, Main, Exploration, bibRecord, 000295

Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.

Identifieur interne : 000295 ( Main/Exploration ); précédent : 000294; suivant : 000296

Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.

Auteurs : Gabrielle V. Rushing [États-Unis] ; Asa A. Brockman [États-Unis] ; Madelyn K. Bollig [États-Unis] ; Nalin Leelatian [États-Unis] ; Bret C. Mobley [États-Unis] ; Jonathan M. Irish [États-Unis] ; Kevin C. Ess [États-Unis] ; Cary Fu [États-Unis] ; Rebecca A. Ihrie [États-Unis]

Source :

Life science alliance [ 2575-1077 ] ; 2019.

RBID : pubmed:30910807

Descripteurs français

English descriptors

KwdEn :
- Adolescent (MeSH), Animals (MeSH), Astrocytoma (metabolism), Astrocytoma (pathology), Carcinogenesis (metabolism), Cells, Cultured (MeSH), Child (MeSH), Child, Preschool (MeSH), Disease Susceptibility (metabolism), Female (MeSH), Humans (MeSH), Lateral Ventricles (cytology), Male (MeSH), Mechanistic Target of Rapamycin Complex 1 (metabolism), Mice (MeSH), Mice, Inbred C57BL (MeSH), Neural Stem Cells (metabolism), Signal Transduction (MeSH), Thyroid Nuclear Factor 1 (metabolism), Tuberous Sclerosis (pathology).
MESH :
- chemical , metabolism : Mechanistic Target of Rapamycin Complex 1, Thyroid Nuclear Factor 1.
- cytology : Lateral Ventricles.
- metabolism : Astrocytoma, Carcinogenesis, Disease Susceptibility, Neural Stem Cells.
- pathology : Astrocytoma, Tuberous Sclerosis.
- Adolescent, Animals, Cells, Cultured, Child, Child, Preschool, Female, Humans, Male, Mice, Mice, Inbred C57BL, Signal Transduction.

Abstract

Neural stem/progenitor cells (NSPCs) of the ventricular-subventricular zone (V-SVZ) are candidate cells of origin for many brain tumors. However, whether NSPCs in different locations within the V-SVZ differ in susceptibility to tumorigenic mutations is unknown. Here, single-cell measurements of signal transduction intermediates in the mechanistic target of rapamycin complex 1 (mTORC1) pathway reveal that ventral NSPCs have higher levels of signaling than dorsal NSPCs. These features are linked with differences in mTORC1-driven disease severity: introduction of a pathognomonic Tsc2 mutation only results in formation of tumor-like masses from the ventral V-SVZ. We propose a direct link between location-dependent intrinsic growth properties imbued by mTORC1 and predisposition to tumor development.

DOI: 10.26508/lsa.201800218
PubMed: 30910807
PubMed Central: PMC6435042

Affiliations:

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Le document en format XML

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<author><name sortKey="Irish, Jonathan M" sort="Irish, Jonathan M" uniqKey="Irish J" first="Jonathan M" last="Irish">Jonathan M. Irish</name>
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<author><name sortKey="Ess, Kevin C" sort="Ess, Kevin C" uniqKey="Ess K" first="Kevin C" last="Ess">Kevin C. Ess</name>
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<author><name sortKey="Fu, Cary" sort="Fu, Cary" uniqKey="Fu C" first="Cary" last="Fu">Cary Fu</name>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Neurological Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.</nlm:affiliation>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.</title>
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<author><name sortKey="Brockman, Asa A" sort="Brockman, Asa A" uniqKey="Brockman A" first="Asa A" last="Brockman">Asa A. Brockman</name>
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<author><name sortKey="Bollig, Madelyn K" sort="Bollig, Madelyn K" uniqKey="Bollig M" first="Madelyn K" last="Bollig">Madelyn K. Bollig</name>
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<author><name sortKey="Leelatian, Nalin" sort="Leelatian, Nalin" uniqKey="Leelatian N" first="Nalin" last="Leelatian">Nalin Leelatian</name>
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<author><name sortKey="Mobley, Bret C" sort="Mobley, Bret C" uniqKey="Mobley B" first="Bret C" last="Mobley">Bret C. Mobley</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Immunology, and Microbiology, Vanderbilt University School of Medicine, Nashville, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Pathology, Immunology, and Microbiology, Vanderbilt University School of Medicine, Nashville, TN</wicri:regionArea>
<placeName><region type="state">Tennessee</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Irish, Jonathan M" sort="Irish, Jonathan M" uniqKey="Irish J" first="Jonathan M" last="Irish">Jonathan M. Irish</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN</wicri:regionArea>
<placeName><region type="state">Tennessee</region>
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</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pathology, Immunology, and Microbiology, Vanderbilt University School of Medicine, Nashville, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<placeName><region type="state">Tennessee</region>
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<author><name sortKey="Ess, Kevin C" sort="Ess, Kevin C" uniqKey="Ess K" first="Kevin C" last="Ess">Kevin C. Ess</name>
<affiliation wicri:level="2"><nlm:affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<wicri:regionArea>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN</wicri:regionArea>
<placeName><region type="state">Tennessee</region>
</placeName>
</affiliation>
<affiliation wicri:level="2"><nlm:affiliation>Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA.</nlm:affiliation>
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<author><name sortKey="Fu, Cary" sort="Fu, Cary" uniqKey="Fu C" first="Cary" last="Fu">Cary Fu</name>
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</placeName>
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<author><name sortKey="Ihrie, Rebecca A" sort="Ihrie, Rebecca A" uniqKey="Ihrie R" first="Rebecca A" last="Ihrie">Rebecca A. Ihrie</name>
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<wicri:regionArea>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN</wicri:regionArea>
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</placeName>
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<affiliation wicri:level="2"><nlm:affiliation>Department of Neurological Surgery, Vanderbilt University Medical Center, Nashville, TN, USA.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
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<series><title level="j">Life science alliance</title>
<idno type="eISSN">2575-1077</idno>
<imprint><date when="2019" type="published">2019</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent (MeSH)</term>
<term>Animals (MeSH)</term>
<term>Astrocytoma (metabolism)</term>
<term>Astrocytoma (pathology)</term>
<term>Carcinogenesis (metabolism)</term>
<term>Cells, Cultured (MeSH)</term>
<term>Child (MeSH)</term>
<term>Child, Preschool (MeSH)</term>
<term>Disease Susceptibility (metabolism)</term>
<term>Female (MeSH)</term>
<term>Humans (MeSH)</term>
<term>Lateral Ventricles (cytology)</term>
<term>Male (MeSH)</term>
<term>Mechanistic Target of Rapamycin Complex 1 (metabolism)</term>
<term>Mice (MeSH)</term>
<term>Mice, Inbred C57BL (MeSH)</term>
<term>Neural Stem Cells (metabolism)</term>
<term>Signal Transduction (MeSH)</term>
<term>Thyroid Nuclear Factor 1 (metabolism)</term>
<term>Tuberous Sclerosis (pathology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Adolescent (MeSH)</term>
<term>Animaux (MeSH)</term>
<term>Astrocytome (anatomopathologie)</term>
<term>Astrocytome (métabolisme)</term>
<term>Carcinogenèse (métabolisme)</term>
<term>Cellules cultivées (MeSH)</term>
<term>Cellules souches neurales (métabolisme)</term>
<term>Complexe de la sclérose tubéreuse (anatomopathologie)</term>
<term>Complexe-1 cible mécanistique de la rapamycine (métabolisme)</term>
<term>Enfant (MeSH)</term>
<term>Enfant d'âge préscolaire (MeSH)</term>
<term>Facteur-1 de transcription de la thyroïde (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Mâle (MeSH)</term>
<term>Prédisposition aux maladies (métabolisme)</term>
<term>Souris (MeSH)</term>
<term>Souris de lignée C57BL (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
<term>Ventricules latéraux (cytologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Mechanistic Target of Rapamycin Complex 1</term>
<term>Thyroid Nuclear Factor 1</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Astrocytome</term>
<term>Complexe de la sclérose tubéreuse</term>
</keywords>
<keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Ventricules latéraux</term>
</keywords>
<keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Lateral Ventricles</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Astrocytoma</term>
<term>Carcinogenesis</term>
<term>Disease Susceptibility</term>
<term>Neural Stem Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Astrocytome</term>
<term>Carcinogenèse</term>
<term>Cellules souches neurales</term>
<term>Complexe-1 cible mécanistique de la rapamycine</term>
<term>Facteur-1 de transcription de la thyroïde</term>
<term>Prédisposition aux maladies</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Astrocytoma</term>
<term>Tuberous Sclerosis</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Adolescent</term>
<term>Animals</term>
<term>Cells, Cultured</term>
<term>Child</term>
<term>Child, Preschool</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Adolescent</term>
<term>Animaux</term>
<term>Cellules cultivées</term>
<term>Enfant</term>
<term>Enfant d'âge préscolaire</term>
<term>Femelle</term>
<term>Humains</term>
<term>Mâle</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Transduction du signal</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Neural stem/progenitor cells (NSPCs) of the ventricular-subventricular zone (V-SVZ) are candidate cells of origin for many brain tumors. However, whether NSPCs in different locations within the V-SVZ differ in susceptibility to tumorigenic mutations is unknown. Here, single-cell measurements of signal transduction intermediates in the mechanistic target of rapamycin complex 1 (mTORC1) pathway reveal that ventral NSPCs have higher levels of signaling than dorsal NSPCs<i>.</i>
 These features are linked with differences in mTORC1-driven disease severity: introduction of a pathognomonic <i>Tsc2</i>
 mutation only results in formation of tumor-like masses from the ventral V-SVZ. We propose a direct link between location-dependent intrinsic growth properties imbued by mTORC1 and predisposition to tumor development.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">30910807</PMID>
<DateCompleted><Year>2020</Year>
<Month>02</Month>
<Day>26</Day>
</DateCompleted>
<DateRevised><Year>2020</Year>
<Month>05</Month>
<Day>28</Day>
</DateRevised>
<Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">2575-1077</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>2</Volume>
<Issue>2</Issue>
<PubDate><Year>2019</Year>
<Month>04</Month>
</PubDate>
</JournalIssue>
<Title>Life science alliance</Title>
<ISOAbbreviation>Life Sci Alliance</ISOAbbreviation>
</Journal>
<ArticleTitle>Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">e201800218</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.26508/lsa.201800218</ELocationID>
<Abstract><AbstractText>Neural stem/progenitor cells (NSPCs) of the ventricular-subventricular zone (V-SVZ) are candidate cells of origin for many brain tumors. However, whether NSPCs in different locations within the V-SVZ differ in susceptibility to tumorigenic mutations is unknown. Here, single-cell measurements of signal transduction intermediates in the mechanistic target of rapamycin complex 1 (mTORC1) pathway reveal that ventral NSPCs have higher levels of signaling than dorsal NSPCs<i>.</i>
 These features are linked with differences in mTORC1-driven disease severity: introduction of a pathognomonic <i>Tsc2</i>
 mutation only results in formation of tumor-like masses from the ventral V-SVZ. We propose a direct link between location-dependent intrinsic growth properties imbued by mTORC1 and predisposition to tumor development.</AbstractText>
<CopyrightInformation>© 2019 Rushing et al.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rushing</LastName>
<ForeName>Gabrielle V</ForeName>
<Initials>GV</Initials>
<Identifier Source="ORCID">0000-0002-6114-883X</Identifier>
<AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Brockman</LastName>
<ForeName>Asa A</ForeName>
<Initials>AA</Initials>
<AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bollig</LastName>
<ForeName>Madelyn K</ForeName>
<Initials>MK</Initials>
<Identifier Source="ORCID">0000-0002-1910-1675</Identifier>
<AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Leelatian</LastName>
<ForeName>Nalin</ForeName>
<Initials>N</Initials>
<Identifier Source="ORCID">0000-0003-4284-8272</Identifier>
<AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mobley</LastName>
<ForeName>Bret C</ForeName>
<Initials>BC</Initials>
<Identifier Source="ORCID">0000-0002-8138-5330</Identifier>
<AffiliationInfo><Affiliation>Department of Pathology, Immunology, and Microbiology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Irish</LastName>
<ForeName>Jonathan M</ForeName>
<Initials>JM</Initials>
<Identifier Source="ORCID">0000-0001-9428-8866</Identifier>
<AffiliationInfo><Affiliation>Department of Cell and Developmental Biology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pathology, Immunology, and Microbiology, Vanderbilt University School of Medicine, Nashville, TN, USA.</Affiliation>
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   |texte=   Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.
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	Serveur d'exploration sur la rapamycine et les champignons
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Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.

Location-dependent maintenance of intrinsic susceptibility to mTORC1-driven tumorigenesis.

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