ChloroquineV1, PubMed, Curation, bibRecord, 000150

Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.

Identifieur interne : 000150 ( PubMed/Curation ); précédent : 000149; suivant : 000151

Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.

Auteurs : Bernhard Englinger [Autriche] ; Sebastian Kallus [Autriche] ; Julia Senkiv [Autriche] ; Daniela Heilos [Autriche] ; Lisa Gabler [Autriche] ; Sushilla Van Schoonhoven [Autriche] ; Alessio Terenzi [Autriche] ; Patrick Moser [Autriche] ; Christine Pirker [Autriche] ; Gerald Timelthaler [Autriche] ; Walter J Ger [Autriche] ; Christian R. Kowol [Autriche] ; Petra Heffeter [Autriche] ; Michael Grusch [Autriche] ; Walter Berger [Autriche]

Source :

Journal of experimental & clinical cancer research : CR [ 1756-9966 ] ; 2017.

RBID : pubmed:28882160

Descripteurs français

KwdFr :
- Animaux, Fluorescence, Humains, Indoles (administration et posologie), Indoles (pharmacocinétique), Lignée cellulaire tumorale, Lysosomes (), Lysosomes (métabolisme), Macrolides (administration et posologie), Phosphorylation (), Poumon (), Poumon (anatomopathologie), Prolifération cellulaire (), Protocoles de polychimiothérapie antinéoplasique (administration et posologie), Récepteur facteur croissance fibroblaste (antagonistes et inhibiteurs), Récepteur facteur croissance fibroblaste (génétique), Souris, Synergie des médicaments, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal (), Tumeurs du poumon (anatomopathologie), Tumeurs du poumon (génétique), Tumeurs du poumon (traitement médicamenteux).
MESH :
- administration et posologie : Indoles, Macrolides, Protocoles de polychimiothérapie antinéoplasique.
- anatomopathologie : Poumon, Tumeurs du poumon.
- antagonistes et inhibiteurs : Récepteur facteur croissance fibroblaste.
- génétique : Récepteur facteur croissance fibroblaste, Tumeurs du poumon.
- métabolisme : Lysosomes.
- pharmacocinétique : Indoles.
- traitement médicamenteux : Tumeurs du poumon.
- Animaux, Fluorescence, Humains, Lignée cellulaire tumorale, Lysosomes, Phosphorylation, Poumon, Prolifération cellulaire, Souris, Synergie des médicaments, Tests d'activité antitumorale sur modèle de xénogreffe, Transduction du signal.

English descriptors

KwdEn :
- Animals, Antineoplastic Combined Chemotherapy Protocols (administration & dosage), Cell Line, Tumor, Cell Proliferation (drug effects), Drug Synergism, Fluorescence, Humans, Indoles (administration & dosage), Indoles (pharmacokinetics), Lung (drug effects), Lung (pathology), Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), Lysosomes (drug effects), Lysosomes (metabolism), Macrolides (administration & dosage), Mice, Phosphorylation (drug effects), Receptors, Fibroblast Growth Factor (antagonists & inhibitors), Receptors, Fibroblast Growth Factor (genetics), Signal Transduction (drug effects), Xenograft Model Antitumor Assays.
MESH :
- chemical , administration & dosage : Indoles, Macrolides.
- administration & dosage : Antineoplastic Combined Chemotherapy Protocols.
- chemical , antagonists & inhibitors : Receptors, Fibroblast Growth Factor.
- drug effects : Cell Proliferation, Lung, Lysosomes, Phosphorylation, Signal Transduction.
- drug therapy : Lung Neoplasms.
- genetics : Lung Neoplasms, Receptors, Fibroblast Growth Factor.
- metabolism : Lysosomes.
- pathology : Lung, Lung Neoplasms.
- chemical , pharmacokinetics : Indoles.
- Animals, Cell Line, Tumor, Drug Synergism, Fluorescence, Humans, Mice, Xenograft Model Antitumor Assays.

Abstract

Studying the intracellular distribution of pharmacological agents, including anticancer compounds, is of central importance in biomedical research. It constitutes a prerequisite for a better understanding of the molecular mechanisms underlying drug action and resistance development. Hyperactivated fibroblast growth factor receptors (FGFRs) constitute a promising therapy target in several types of malignancies including lung cancer. The clinically approved small-molecule FGFR inhibitor nintedanib exerts strong cytotoxicity in FGFR-driven lung cancer cells. However, subcellular pharmacokinetics of this compound and its impact on therapeutic efficacy remain obscure.

DOI: 10.1186/s13046-017-0592-3
PubMed: 28882160

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Le document en format XML

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<author><name sortKey="J Ger, Walter" sort="J Ger, Walter" uniqKey="J Ger W" first="Walter" last="J Ger">Walter J Ger</name>
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<author><name sortKey="Kowol, Christian R" sort="Kowol, Christian R" uniqKey="Kowol C" first="Christian R" last="Kowol">Christian R. Kowol</name>
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<term>Drug Synergism</term>
<term>Fluorescence</term>
<term>Humans</term>
<term>Indoles (administration & dosage)</term>
<term>Indoles (pharmacokinetics)</term>
<term>Lung (drug effects)</term>
<term>Lung (pathology)</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Lysosomes (drug effects)</term>
<term>Lysosomes (metabolism)</term>
<term>Macrolides (administration & dosage)</term>
<term>Mice</term>
<term>Phosphorylation (drug effects)</term>
<term>Receptors, Fibroblast Growth Factor (antagonists & inhibitors)</term>
<term>Receptors, Fibroblast Growth Factor (genetics)</term>
<term>Signal Transduction (drug effects)</term>
<term>Xenograft Model Antitumor Assays</term>
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<term>Fluorescence</term>
<term>Humains</term>
<term>Indoles (administration et posologie)</term>
<term>Indoles (pharmacocinétique)</term>
<term>Lignée cellulaire tumorale</term>
<term>Lysosomes ()</term>
<term>Lysosomes (métabolisme)</term>
<term>Macrolides (administration et posologie)</term>
<term>Phosphorylation ()</term>
<term>Poumon ()</term>
<term>Poumon (anatomopathologie)</term>
<term>Prolifération cellulaire ()</term>
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<term>Récepteur facteur croissance fibroblaste (antagonistes et inhibiteurs)</term>
<term>Récepteur facteur croissance fibroblaste (génétique)</term>
<term>Souris</term>
<term>Synergie des médicaments</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
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<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
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<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Indoles</term>
<term>Macrolides</term>
<term>Protocoles de polychimiothérapie antinéoplasique</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Poumon</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Récepteur facteur croissance fibroblaste</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Receptors, Fibroblast Growth Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Proliferation</term>
<term>Lung</term>
<term>Lysosomes</term>
<term>Phosphorylation</term>
<term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Lung Neoplasms</term>
<term>Receptors, Fibroblast Growth Factor</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Récepteur facteur croissance fibroblaste</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Lysosomes</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacocinétique" xml:lang="fr"><term>Indoles</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Indoles</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Drug Synergism</term>
<term>Fluorescence</term>
<term>Humans</term>
<term>Mice</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Fluorescence</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Lysosomes</term>
<term>Phosphorylation</term>
<term>Poumon</term>
<term>Prolifération cellulaire</term>
<term>Souris</term>
<term>Synergie des médicaments</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">Studying the intracellular distribution of pharmacological agents, including anticancer compounds, is of central importance in biomedical research. It constitutes a prerequisite for a better understanding of the molecular mechanisms underlying drug action and resistance development. Hyperactivated fibroblast growth factor receptors (FGFRs) constitute a promising therapy target in several types of malignancies including lung cancer. The clinically approved small-molecule FGFR inhibitor nintedanib exerts strong cytotoxicity in FGFR-driven lung cancer cells. However, subcellular pharmacokinetics of this compound and its impact on therapeutic efficacy remain obscure.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28882160</PMID>
<DateCompleted><Year>2018</Year>
<Month>05</Month>
<Day>10</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1756-9966</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>36</Volume>
<Issue>1</Issue>
<PubDate><Year>2017</Year>
<Month>09</Month>
<Day>07</Day>
</PubDate>
</JournalIssue>
<Title>Journal of experimental & clinical cancer research : CR</Title>
<ISOAbbreviation>J. Exp. Clin. Cancer Res.</ISOAbbreviation>
</Journal>
<ArticleTitle>Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.</ArticleTitle>
<Pagination><MedlinePgn>122</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1186/s13046-017-0592-3</ELocationID>
<Abstract><AbstractText Label="BACKGROUND">Studying the intracellular distribution of pharmacological agents, including anticancer compounds, is of central importance in biomedical research. It constitutes a prerequisite for a better understanding of the molecular mechanisms underlying drug action and resistance development. Hyperactivated fibroblast growth factor receptors (FGFRs) constitute a promising therapy target in several types of malignancies including lung cancer. The clinically approved small-molecule FGFR inhibitor nintedanib exerts strong cytotoxicity in FGFR-driven lung cancer cells. However, subcellular pharmacokinetics of this compound and its impact on therapeutic efficacy remain obscure.</AbstractText>
<AbstractText Label="METHODS">3-dimensional fluorescence spectroscopy was conducted to asses cell-free nintedanib fluorescence properties. MTT assay was used to determine the impact of the lysosome-targeting agents bafilomycin A1 and chloroquine combined with nintedanib on lung cancer cell viability. Flow cytometry and live cell as well as confocal microscopy were performed to analyze uptake kinetics as well as subcellular distribution of nintedanib. Western blot was conducted to investigate protein expression. Cryosections of subcutaneous tumor allografts were generated to detect intratumoral nintedanib in mice after oral drug administration.</AbstractText>
<AbstractText Label="RESULTS">Here, we report for the first time drug-intrinsic fluorescence properties of nintedanib in living and fixed cancer cells as well as in cryosections derived from allograft tumors of orally treated mice. Using this feature in conjunction with flow cytometry and confocal microscopy allowed to determine cellular drug accumulation levels, impact of the ABCB1 efflux pump and to uncover nintedanib trapping into lysosomes. Lysosomal sequestration - resulting in an organelle-specific and pH-dependent nintedanib fluorescence - was identified as an intrinsic resistance mechanism in FGFR-driven lung cancer cells. Accordingly, combination of nintedanib with agents compromising lysosomal acidification (bafilomycin A1, chloroquine) exerted distinctly synergistic growth inhibitory effects.</AbstractText>
<AbstractText Label="CONCLUSION">Our findings provide a powerful tool to dissect molecular factors impacting organismal and intracellular pharmacokinetics of nintedanib. Regarding clinical application, prevention of lysosomal trapping via lysosome-alkalization might represent a promising strategy to circumvent cancer cell-intrinsic nintedanib resistance.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Englinger</LastName>
<ForeName>Bernhard</ForeName>
<Initials>B</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kallus</LastName>
<ForeName>Sebastian</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institute of Inorganic Chemistry, University of Vienna, Waehringer Str. 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Research Cluster "Translational Cancer Therapy Research", University of Vienna, Waehringer Strasse 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Senkiv</LastName>
<ForeName>Julia</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Institute of Cell Biology NAS of Ukraine, Drahomanova str 14/16, 79005, Lviv, Ukraine.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heilos</LastName>
<ForeName>Daniela</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Pharmacology and Toxicology, University of Vienna, Althanstr. 14, 1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gabler</LastName>
<ForeName>Lisa</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>van Schoonhoven</LastName>
<ForeName>Sushilla</ForeName>
<Initials>S</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Terenzi</LastName>
<ForeName>Alessio</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Institute of Inorganic Chemistry, University of Vienna, Waehringer Str. 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Moser</LastName>
<ForeName>Patrick</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Pirker</LastName>
<ForeName>Christine</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Timelthaler</LastName>
<ForeName>Gerald</ForeName>
<Initials>G</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Jäger</LastName>
<ForeName>Walter</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Department of Pharmaceutical Chemistry, Division of Clinical Pharmacy and Diagnostics, University of Vienna, Althanstrasse 14, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Kowol</LastName>
<ForeName>Christian R</ForeName>
<Initials>CR</Initials>
<AffiliationInfo><Affiliation>Institute of Inorganic Chemistry, University of Vienna, Waehringer Str. 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Research Cluster "Translational Cancer Therapy Research", University of Vienna, Waehringer Strasse 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Heffeter</LastName>
<ForeName>Petra</ForeName>
<Initials>P</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Research Cluster "Translational Cancer Therapy Research", University of Vienna, Waehringer Strasse 42, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Grusch</LastName>
<ForeName>Michael</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Berger</LastName>
<ForeName>Walter</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Institute of Cancer Research and Comprehensive Cancer Center, Department of Medicine I, Medical University of Vienna, Borschkegasse 8a, A-1090, Vienna, Austria. walter.berger@meduniwien.ac.at.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Research Cluster "Translational Cancer Therapy Research", University of Vienna, Waehringer Strasse 42, A-1090, Vienna, Austria. walter.berger@meduniwien.ac.at.</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>2017</Year>
<Month>09</Month>
<Day>07</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>J Exp Clin Cancer Res</MedlineTA>
<NlmUniqueID>8308647</NlmUniqueID>
<ISSNLinking>0392-9078</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D007211">Indoles</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D018942">Macrolides</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D017468">Receptors, Fibroblast Growth Factor</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>88899-55-2</RegistryNumber>
<NameOfSubstance UI="C040929">bafilomycin A1</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>G6HRD2P839</RegistryNumber>
<NameOfSubstance UI="C530716">nintedanib</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000971" MajorTopicYN="N">Antineoplastic Combined Chemotherapy Protocols</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004357" MajorTopicYN="N">Drug Synergism</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005453" MajorTopicYN="N">Fluorescence</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D007211" MajorTopicYN="N">Indoles</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
<QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName>
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<MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</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="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008247" MajorTopicYN="N">Lysosomes</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D018942" MajorTopicYN="N">Macrolides</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D010766" MajorTopicYN="N">Phosphorylation</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D017468" MajorTopicYN="N">Receptors, Fibroblast Growth Factor</DescriptorName>
<QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">FGFR1</Keyword>
<Keyword MajorTopicYN="Y">Fluorescence</Keyword>
<Keyword MajorTopicYN="Y">Lysosomes</Keyword>
<Keyword MajorTopicYN="Y">Nintedanib</Keyword>
<Keyword MajorTopicYN="Y">Resistance</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year>
<Month>06</Month>
<Day>21</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2017</Year>
<Month>09</Month>
<Day>01</Day>
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   |texte=   Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.
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Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.

Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer.

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