ChloroquineV1, PubMed, Curation, bibRecord, 000109

Loss of C/EBP-β LIP drives cisplatin resistance in malignant pleural mesothelioma.

Identifieur interne : 000109 ( PubMed/Curation ); précédent : 000108; suivant : 000110

Loss of C/EBP-β LIP drives cisplatin resistance in malignant pleural mesothelioma.

Auteurs : Joanna Kopecka [Italie] ; Iris C. Salaroglio [Italie] ; Luisella Righi [Italie] ; Roberta Libener [Italie] ; Sara Orecchia [Italie] ; Federica Grosso [Italie] ; Vladan Milosevic [Italie] ; Preeta Ananthanarayanan [Italie] ; Luisa Ricci [Italie] ; Enrica Capelletto [Italie] ; Monica Pradotto [Italie] ; Francesca Napoli [Italie] ; Massimo Di Maio [Italie] ; Silvia Novello [Italie] ; Menachem Rubinstein [Israël] ; Giorgio V. Scagliotti [Italie] ; Chiara Riganti [Italie]

Source :

Lung cancer (Amsterdam, Netherlands) [ 1872-8332 ] ; 2018.

RBID : pubmed:29748013

Descripteurs français

English descriptors

KwdEn :
- Adaptor Proteins, Signal Transducing (genetics), Adaptor Proteins, Signal Transducing (metabolism), Antineoplastic Agents (therapeutic use), Apoptosis, CCAAT-Enhancer-Binding Protein-beta (genetics), CCAAT-Enhancer-Binding Protein-beta (metabolism), CD8-Positive T-Lymphocytes (immunology), Cisplatin (therapeutic use), Dendritic Cells (immunology), Drug Resistance, Neoplasm (genetics), Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (mortality), Lymphocyte Activation, Mesothelioma (drug therapy), Mesothelioma (genetics), Mesothelioma (mortality), Oligopeptides (pharmacology), Pleural Neoplasms (drug therapy), Pleural Neoplasms (mortality), Prognosis, Proteolysis, Survival Analysis, Tumor Cells, Cultured, Ubiquitination.
MESH :
- chemical , genetics : Adaptor Proteins, Signal Transducing, CCAAT-Enhancer-Binding Protein-beta.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, CCAAT-Enhancer-Binding Protein-beta.
- chemical , pharmacology : Oligopeptides.
- chemical , therapeutic use : Antineoplastic Agents, Cisplatin.
- drug therapy : Lung Neoplasms, Mesothelioma, Pleural Neoplasms.
- genetics : Drug Resistance, Neoplasm, Lung Neoplasms, Mesothelioma.
- immunology : CD8-Positive T-Lymphocytes, Dendritic Cells.
- mortality : Lung Neoplasms, Mesothelioma, Pleural Neoplasms.
- Apoptosis, Humans, Lymphocyte Activation, Prognosis, Proteolysis, Survival Analysis, Tumor Cells, Cultured, Ubiquitination.

Abstract

Cisplatin-based chemotherapy is moderately active in malignant pleural mesothelioma (MPM) due to intrinsic drug resistance and to low immunogenicity of MPM cells. CAAT/enhancer binding protein (C/EBP)-β LIP is a pro-apoptotic and chemosensitizing transcription factor activated in response to endoplasmic reticulum (ER) stress.

DOI: 10.1016/j.lungcan.2018.03.022
PubMed: 29748013

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<country xml:lang="fr">Italie</country>
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<country xml:lang="fr">Italie</country>
<wicri:regionArea>Medical Oncology Division, Department of Oncology at Mauriziano Hospital, Largo Filippo Turati 62, 10128, University of Torino</wicri:regionArea>
</affiliation>
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<country xml:lang="fr">Italie</country>
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<country xml:lang="fr">Israël</country>
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<country xml:lang="fr">Italie</country>
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<author><name sortKey="Riganti, Chiara" sort="Riganti, Chiara" uniqKey="Riganti C" first="Chiara" last="Riganti">Chiara Riganti</name>
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<country xml:lang="fr">Italie</country>
<wicri:regionArea>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino</wicri:regionArea>
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<series><title level="j">Lung cancer (Amsterdam, Netherlands)</title>
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<imprint><date when="2018" type="published">2018</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (genetics)</term>
<term>Adaptor Proteins, Signal Transducing (metabolism)</term>
<term>Antineoplastic Agents (therapeutic use)</term>
<term>Apoptosis</term>
<term>CCAAT-Enhancer-Binding Protein-beta (genetics)</term>
<term>CCAAT-Enhancer-Binding Protein-beta (metabolism)</term>
<term>CD8-Positive T-Lymphocytes (immunology)</term>
<term>Cisplatin (therapeutic use)</term>
<term>Dendritic Cells (immunology)</term>
<term>Drug Resistance, Neoplasm (genetics)</term>
<term>Humans</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (mortality)</term>
<term>Lymphocyte Activation</term>
<term>Mesothelioma (drug therapy)</term>
<term>Mesothelioma (genetics)</term>
<term>Mesothelioma (mortality)</term>
<term>Oligopeptides (pharmacology)</term>
<term>Pleural Neoplasms (drug therapy)</term>
<term>Pleural Neoplasms (mortality)</term>
<term>Prognosis</term>
<term>Proteolysis</term>
<term>Survival Analysis</term>
<term>Tumor Cells, Cultured</term>
<term>Ubiquitination</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Analyse de survie</term>
<term>Antinéoplasiques (usage thérapeutique)</term>
<term>Apoptose</term>
<term>Cellules cancéreuses en culture</term>
<term>Cellules dendritiques (immunologie)</term>
<term>Cisplatine (usage thérapeutique)</term>
<term>Humains</term>
<term>Lymphocytes T CD8+ (immunologie)</term>
<term>Mésothéliome (génétique)</term>
<term>Mésothéliome (mortalité)</term>
<term>Mésothéliome (traitement médicamenteux)</term>
<term>Oligopeptides (pharmacologie)</term>
<term>Pronostic</term>
<term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (génétique)</term>
<term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT (métabolisme)</term>
<term>Protéines adaptatrices de la transduction du signal (génétique)</term>
<term>Protéines adaptatrices de la transduction du signal (métabolisme)</term>
<term>Protéolyse</term>
<term>Résistance aux médicaments antinéoplasiques (génétique)</term>
<term>Tumeurs de la plèvre (mortalité)</term>
<term>Tumeurs de la plèvre (traitement médicamenteux)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (mortalité)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
<term>Ubiquitinylation</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>CCAAT-Enhancer-Binding Protein-beta</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term>
<term>CCAAT-Enhancer-Binding Protein-beta</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Oligopeptides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antineoplastic Agents</term>
<term>Cisplatin</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term>
<term>Mesothelioma</term>
<term>Pleural Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Drug Resistance, Neoplasm</term>
<term>Lung Neoplasms</term>
<term>Mesothelioma</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Mésothéliome</term>
<term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT</term>
<term>Protéines adaptatrices de la transduction du signal</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules dendritiques</term>
<term>Lymphocytes T CD8+</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
<term>Dendritic Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="mortality" xml:lang="en"><term>Lung Neoplasms</term>
<term>Mesothelioma</term>
<term>Pleural Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="mortalité" xml:lang="fr"><term>Mésothéliome</term>
<term>Tumeurs de la plèvre</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéine bêta de liaison aux séquences stimulatrices de type CCAAT</term>
<term>Protéines adaptatrices de la transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Oligopeptides</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Mésothéliome</term>
<term>Tumeurs de la plèvre</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Antinéoplasiques</term>
<term>Cisplatine</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Apoptosis</term>
<term>Humans</term>
<term>Lymphocyte Activation</term>
<term>Prognosis</term>
<term>Proteolysis</term>
<term>Survival Analysis</term>
<term>Tumor Cells, Cultured</term>
<term>Ubiquitination</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Activation des lymphocytes</term>
<term>Analyse de survie</term>
<term>Apoptose</term>
<term>Cellules cancéreuses en culture</term>
<term>Humains</term>
<term>Pronostic</term>
<term>Protéolyse</term>
<term>Ubiquitinylation</term>
</keywords>
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<front><div type="abstract" xml:lang="en">Cisplatin-based chemotherapy is moderately active in malignant pleural mesothelioma (MPM) due to intrinsic drug resistance and to low immunogenicity of MPM cells. CAAT/enhancer binding protein (C/EBP)-β LIP is a pro-apoptotic and chemosensitizing transcription factor activated in response to endoplasmic reticulum (ER) stress.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29748013</PMID>
<DateCompleted><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>07</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1872-8332</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>120</Volume>
<PubDate><Year>2018</Year>
<Month>06</Month>
</PubDate>
</JournalIssue>
<Title>Lung cancer (Amsterdam, Netherlands)</Title>
<ISOAbbreviation>Lung Cancer</ISOAbbreviation>
</Journal>
<ArticleTitle>Loss of C/EBP-β LIP drives cisplatin resistance in malignant pleural mesothelioma.</ArticleTitle>
<Pagination><MedlinePgn>34-45</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S0169-5002(18)30311-8</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lungcan.2018.03.022</ELocationID>
<Abstract><AbstractText Label="OBJECTIVES">Cisplatin-based chemotherapy is moderately active in malignant pleural mesothelioma (MPM) due to intrinsic drug resistance and to low immunogenicity of MPM cells. CAAT/enhancer binding protein (C/EBP)-β LIP is a pro-apoptotic and chemosensitizing transcription factor activated in response to endoplasmic reticulum (ER) stress.</AbstractText>
<AbstractText Label="MATERIALS AND METHODS">We investigated if LIP levels can predict the clinical response to cisplatin and survival of MPM patients receiving cisplatin-based chemotherapy. We studied the LIP-dependent mechanisms determining cisplatin-resistance and we identified pharmacological approaches targeting LIP, able to restore cisplatin sensitiveness, in patient-derived MPM cells and animal models. Results were analyzed by a one-way analysis of variance test.</AbstractText>
<AbstractText Label="RESULTS">We found that LIP was degraded by constitutive ubiquitination in primary MPM cells derived from patients poorly responsive to cisplatin. LIP ubiquitination was directly correlated with cisplatin chemosensitivity and was associated with patients' survival after chemotherapy. Overexpression of LIP restored cisplatin's pro-apoptotic effect by activating CHOP/TRB3/caspase 3 axis and up-regulating calreticulin, that triggered MPM cell phagocytosis by dendritic cells and expanded autologous anti-tumor CD8<sup>+</sup>
CD107<sup>+</sup>
T-cytotoxic lymphocytes. Proteasome inhibitor carfilzomib and lysosome inhibitor chloroquine prevented LIP degradation. The triple combination of carfilzomib, chloroquine and cisplatin increased ER stress-triggered apoptosis and immunogenic cell death in patients' samples, and reduced tumor growth in cisplatin-resistant MPM preclinical models.</AbstractText>
<AbstractText Label="CONCLUSION">The loss of LIP mediates cisplatin resistance, rendering LIP a possible predictor of cisplatin response in MPM patients. The association of proteasome and lysosome inhibitors reverses cisplatin resistance by restoring LIP levels and may represent a new adjuvant strategy in MPM treatment.</AbstractText>
<CopyrightInformation>Copyright © 2018 Elsevier B.V. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kopecka</LastName>
<ForeName>Joanna</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: joanna.kopecka@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Salaroglio</LastName>
<ForeName>Iris C</ForeName>
<Initials>IC</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: irischiara.salaroglio@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Righi</LastName>
<ForeName>Luisella</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Pathology Unit, Department of Oncology at San Luigi Hospital, University of Torino, Regione Gonzole 10, 10043, Orbassano, Italy. Electronic address: luisella.righi@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Libener</LastName>
<ForeName>Roberta</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Pathology Division, S. Antonio and Biagio Hospital, Spalto Marengo, 15121, Alessandria, Italy. Electronic address: rlibener@ospedale.al.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Orecchia</LastName>
<ForeName>Sara</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Pathology Division, S. Antonio and Biagio Hospital, Spalto Marengo, 15121, Alessandria, Italy. Electronic address: sorecchia@ospedale.al.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Grosso</LastName>
<ForeName>Federica</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Oncology Division, S. Antonio and Biagio Hospital, Spalto Marengo, 15121, Alessandria, Italy. Electronic address: fgrosso@ospedale.al.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Milosevic</LastName>
<ForeName>Vladan</ForeName>
<Initials>V</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: vladan.milosevic@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ananthanarayanan</LastName>
<ForeName>Preeta</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: preeta.ananthanarayanan@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ricci</LastName>
<ForeName>Luisa</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: luisa.ricci@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Capelletto</LastName>
<ForeName>Enrica</ForeName>
<Initials>E</Initials>
<AffiliationInfo><Affiliation>Thoracic Unit and Medical Oncology Division, Department of Oncology at San Luigi Hospital, Regione Gonzole 10, University of Torino, Orbassano, Italy. Electronic address: enrica.capelletto@gmail.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pradotto</LastName>
<ForeName>Monica</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Thoracic Unit and Medical Oncology Division, Department of Oncology at San Luigi Hospital, Regione Gonzole 10, University of Torino, Orbassano, Italy. Electronic address: monica.pradotto@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Napoli</LastName>
<ForeName>Francesca</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Pathology Unit, Department of Oncology at San Luigi Hospital, University of Torino, Regione Gonzole 10, 10043, Orbassano, Italy. Electronic address: francesca.napoli@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Di Maio</LastName>
<ForeName>Massimo</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Medical Oncology Division, Department of Oncology at Mauriziano Hospital, Largo Filippo Turati 62, 10128, University of Torino, Italy. Electronic address: massimo.dimaio@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Novello</LastName>
<ForeName>Silvia</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Thoracic Unit and Medical Oncology Division, Department of Oncology at San Luigi Hospital, Regione Gonzole 10, University of Torino, Orbassano, Italy. Electronic address: silvia.novello@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rubinstein</LastName>
<ForeName>Menachem</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Department of Molecular Genetics, The Weizmann Institute of Science, Herzl Street 234, 76100, Rehovot, Israel. Electronic address: menachem.rubinstein@weizmann.ac.il.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Scagliotti</LastName>
<ForeName>Giorgio V</ForeName>
<Initials>GV</Initials>
<AffiliationInfo><Affiliation>Thoracic Unit and Medical Oncology Division, Department of Oncology at San Luigi Hospital, Regione Gonzole 10, University of Torino, Orbassano, Italy. Electronic address: giorgio.scagliotti@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Riganti</LastName>
<ForeName>Chiara</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Torino, via Santena 5/bis, 10126, Torino, Italy. Electronic address: chiara.riganti@unito.it.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2018</Year>
<Month>03</Month>
<Day>26</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>Ireland</Country>
<MedlineTA>Lung Cancer</MedlineTA>
<NlmUniqueID>8800805</NlmUniqueID>
<ISSNLinking>0169-5002</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D022782">CCAAT-Enhancer-Binding Protein-beta</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C545012">CEBPB protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D009842">Oligopeptides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C094398">PPFIA1 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>72X6E3J5AR</RegistryNumber>
<NameOfSubstance UI="C524865">carfilzomib</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>Q20Q21Q62J</RegistryNumber>
<NameOfSubstance UI="D002945">Cisplatin</NameOfSubstance>
</Chemical>
</ChemicalList>
<SupplMeshList><SupplMeshName Type="Disease" UI="C562839">Mesothelioma, Malignant</SupplMeshName>
</SupplMeshList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017209" MajorTopicYN="N">Apoptosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D022782" MajorTopicYN="N">CCAAT-Enhancer-Binding Protein-beta</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018414" MajorTopicYN="N">CD8-Positive T-Lymphocytes</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002945" MajorTopicYN="N">Cisplatin</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003713" MajorTopicYN="N">Dendritic Cells</DescriptorName>
<QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008213" MajorTopicYN="N">Lymphocyte Activation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008654" MajorTopicYN="N">Mesothelioma</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009842" MajorTopicYN="N">Oligopeptides</DescriptorName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010997" MajorTopicYN="N">Pleural Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D011379" MajorTopicYN="N">Prognosis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D059748" MajorTopicYN="N">Proteolysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D016019" MajorTopicYN="N">Survival Analysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D014407" MajorTopicYN="N">Tumor Cells, Cultured</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D054875" MajorTopicYN="N">Ubiquitination</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">CAAT/enhancer binding protein</Keyword>
<Keyword MajorTopicYN="Y">Cisplatin resistance</Keyword>
<Keyword MajorTopicYN="Y">Endoplasmic reticulum stress</Keyword>
<Keyword MajorTopicYN="Y">Immunogenic cell death</Keyword>
<Keyword MajorTopicYN="Y">Malignant pleural mesothelioma</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>11</Month>
<Day>15</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>03</Month>
<Day>13</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>03</Month>
<Day>22</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>5</Month>
<Day>12</Day>
<Hour>6</Hour>
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<Hour>6</Hour>
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<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>7</Month>
<Day>23</Day>
<Hour>6</Hour>
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<ArticleId IdType="pii">S0169-5002(18)30311-8</ArticleId>
<ArticleId IdType="doi">10.1016/j.lungcan.2018.03.022</ArticleId>
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Loss of C/EBP-β LIP drives cisplatin resistance in malignant pleural mesothelioma.

Loss of C/EBP-β LIP drives cisplatin resistance in malignant pleural mesothelioma.

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