ChloroquineV1, PubMed, Curation, bibRecord, 000099

Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.

Identifieur interne : 000099 ( PubMed/Curation ); précédent : 000098; suivant : 000100

Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.

Auteurs : Tingting Lv [République populaire de Chine] ; Ziying Li [République populaire de Chine] ; Liang Xu [République populaire de Chine] ; Yingying Zhang [République populaire de Chine] ; Haijun Chen [République populaire de Chine] ; Yu Gao [République populaire de Chine]

Source :

Acta biomaterialia [ 1878-7568 ] ; 2018.

RBID : pubmed:29960010

Descripteurs français

English descriptors

KwdEn :
- Animals, Aptamers, Nucleotide (chemistry), Aptamers, Nucleotide (pharmacokinetics), Aptamers, Nucleotide (pharmacology), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (metabolism), Carcinoma, Non-Small-Cell Lung (pathology), Cell Line, Tumor, Chloroquine (chemistry), Chloroquine (pharmacokinetics), Chloroquine (pharmacology), Drug Resistance, Neoplasm (drug effects), Drug Resistance, Neoplasm (genetics), ErbB Receptors (genetics), ErbB Receptors (metabolism), Erlotinib Hydrochloride (chemistry), Erlotinib Hydrochloride (pharmacokinetics), Erlotinib Hydrochloride (pharmacology), Female, Humans, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (metabolism), Lung Neoplasms (pathology), Mice, Mice, Inbred BALB C, Mice, Nude, Mutation, Nanoparticles (chemistry), Nanoparticles (therapeutic use), Neoplasm Proteins (genetics), Neoplasm Proteins (metabolism), RNA, Small Interfering (chemistry), RNA, Small Interfering (pharmacokinetics), RNA, Small Interfering (pharmacology), Survivin, Xenograft Model Antitumor Assays.
MESH :
- chemical , chemistry : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemical , genetics : ErbB Receptors, Neoplasm Proteins.
- chemical , metabolism : ErbB Receptors, Neoplasm Proteins.
- chemical , pharmacokinetics : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemical , pharmacology : Aptamers, Nucleotide, Chloroquine, Erlotinib Hydrochloride, RNA, Small Interfering.
- chemistry : Nanoparticles.
- drug effects : Drug Resistance, Neoplasm.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Lung Neoplasms.
- metabolism : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- therapeutic use : Nanoparticles.
- Animals, Cell Line, Tumor, Female, Humans, Mice, Mice, Inbred BALB C, Mice, Nude, Mutation, Survivin, Xenograft Model Antitumor Assays.

Abstract

Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.

DOI: 10.1016/j.actbio.2018.06.034
PubMed: 29960010

Links toward previous steps (curation, corpus...)

to stream PubMed, to step Corpus: Pour aller vers cette notice dans l'étape Curation :000099

Links to Exploration step

pubmed:29960010

Le document en format XML

<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.</title>
<author><name sortKey="Lv, Tingting" sort="Lv, Tingting" uniqKey="Lv T" first="Tingting" last="Lv">Tingting Lv</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Li, Ziying" sort="Li, Ziying" uniqKey="Li Z" first="Ziying" last="Li">Ziying Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Xu, Liang" sort="Xu, Liang" uniqKey="Xu L" first="Liang" last="Xu">Liang Xu</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Zhang, Yingying" sort="Zhang, Yingying" uniqKey="Zhang Y" first="Yingying" last="Zhang">Yingying Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chen, Haijun" sort="Chen, Haijun" uniqKey="Chen H" first="Haijun" last="Chen">Haijun Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Gao, Yu" sort="Gao, Yu" uniqKey="Gao Y" first="Yu" last="Gao">Yu Gao</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China. Electronic address: hellogaoyu@126.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2018">2018</date>
<idno type="RBID">pubmed:29960010</idno>
<idno type="pmid">29960010</idno>
<idno type="doi">10.1016/j.actbio.2018.06.034</idno>
<idno type="wicri:Area/PubMed/Corpus">000099</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000099</idno>
<idno type="wicri:Area/PubMed/Curation">000099</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000099</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.</title>
<author><name sortKey="Lv, Tingting" sort="Lv, Tingting" uniqKey="Lv T" first="Tingting" last="Lv">Tingting Lv</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Li, Ziying" sort="Li, Ziying" uniqKey="Li Z" first="Ziying" last="Li">Ziying Li</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Xu, Liang" sort="Xu, Liang" uniqKey="Xu L" first="Liang" last="Xu">Liang Xu</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Zhang, Yingying" sort="Zhang, Yingying" uniqKey="Zhang Y" first="Yingying" last="Zhang">Yingying Zhang</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Chen, Haijun" sort="Chen, Haijun" uniqKey="Chen H" first="Haijun" last="Chen">Haijun Chen</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
<author><name sortKey="Gao, Yu" sort="Gao, Yu" uniqKey="Gao Y" first="Yu" last="Gao">Yu Gao</name>
<affiliation wicri:level="1"><nlm:affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China. Electronic address: hellogaoyu@126.com.</nlm:affiliation>
<country xml:lang="fr">République populaire de Chine</country>
<wicri:regionArea>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116</wicri:regionArea>
</affiliation>
</author>
</analytic>
<series><title level="j">Acta biomaterialia</title>
<idno type="eISSN">1878-7568</idno>
<imprint><date when="2018" type="published">2018</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Aptamers, Nucleotide (chemistry)</term>
<term>Aptamers, Nucleotide (pharmacokinetics)</term>
<term>Aptamers, Nucleotide (pharmacology)</term>
<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (metabolism)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>Cell Line, Tumor</term>
<term>Chloroquine (chemistry)</term>
<term>Chloroquine (pharmacokinetics)</term>
<term>Chloroquine (pharmacology)</term>
<term>Drug Resistance, Neoplasm (drug effects)</term>
<term>Drug Resistance, Neoplasm (genetics)</term>
<term>ErbB Receptors (genetics)</term>
<term>ErbB Receptors (metabolism)</term>
<term>Erlotinib Hydrochloride (chemistry)</term>
<term>Erlotinib Hydrochloride (pharmacokinetics)</term>
<term>Erlotinib Hydrochloride (pharmacology)</term>
<term>Female</term>
<term>Humans</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (metabolism)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Mutation</term>
<term>Nanoparticles (chemistry)</term>
<term>Nanoparticles (therapeutic use)</term>
<term>Neoplasm Proteins (genetics)</term>
<term>Neoplasm Proteins (metabolism)</term>
<term>RNA, Small Interfering (chemistry)</term>
<term>RNA, Small Interfering (pharmacokinetics)</term>
<term>RNA, Small Interfering (pharmacology)</term>
<term>Survivin</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term>
<term>Aptamères nucléotidiques ()</term>
<term>Aptamères nucléotidiques (pharmacocinétique)</term>
<term>Aptamères nucléotidiques (pharmacologie)</term>
<term>Carcinome pulmonaire non à petites cellules (anatomopathologie)</term>
<term>Carcinome pulmonaire non à petites cellules (génétique)</term>
<term>Carcinome pulmonaire non à petites cellules (métabolisme)</term>
<term>Carcinome pulmonaire non à petites cellules (traitement médicamenteux)</term>
<term>Chlorhydrate d'erlotinib ()</term>
<term>Chlorhydrate d'erlotinib (pharmacocinétique)</term>
<term>Chlorhydrate d'erlotinib (pharmacologie)</term>
<term>Chloroquine ()</term>
<term>Chloroquine (pharmacocinétique)</term>
<term>Chloroquine (pharmacologie)</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
<term>Nanoparticules ()</term>
<term>Nanoparticules (usage thérapeutique)</term>
<term>Petit ARN interférent ()</term>
<term>Petit ARN interférent (pharmacocinétique)</term>
<term>Petit ARN interférent (pharmacologie)</term>
<term>Protéines tumorales (génétique)</term>
<term>Protéines tumorales (métabolisme)</term>
<term>Récepteurs ErbB (génétique)</term>
<term>Récepteurs ErbB (métabolisme)</term>
<term>Résistance aux médicaments antinéoplasiques ()</term>
<term>Résistance aux médicaments antinéoplasiques (génétique)</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (métabolisme)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="chemistry" xml:lang="en"><term>Aptamers, Nucleotide</term>
<term>Chloroquine</term>
<term>Erlotinib Hydrochloride</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>ErbB Receptors</term>
<term>Neoplasm Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>ErbB Receptors</term>
<term>Neoplasm Proteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Aptamers, Nucleotide</term>
<term>Chloroquine</term>
<term>Erlotinib Hydrochloride</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Aptamers, Nucleotide</term>
<term>Chloroquine</term>
<term>Erlotinib Hydrochloride</term>
<term>RNA, Small Interfering</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="chemistry" xml:lang="en"><term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Drug Resistance, Neoplasm</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Drug Resistance, Neoplasm</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Protéines tumorales</term>
<term>Récepteurs ErbB</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Protéines tumorales</term>
<term>Récepteurs ErbB</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Carcinoma, Non-Small-Cell Lung</term>
<term>Lung Neoplasms</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacocinétique" xml:lang="fr"><term>Aptamères nucléotidiques</term>
<term>Chlorhydrate d'erlotinib</term>
<term>Chloroquine</term>
<term>Petit ARN interférent</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Aptamères nucléotidiques</term>
<term>Chlorhydrate d'erlotinib</term>
<term>Chloroquine</term>
<term>Petit ARN interférent</term>
</keywords>
<keywords scheme="MESH" qualifier="therapeutic use" xml:lang="en"><term>Nanoparticles</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Carcinome pulmonaire non à petites cellules</term>
<term>Tumeurs du poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Nanoparticules</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Cell Line, Tumor</term>
<term>Female</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Mice, Nude</term>
<term>Mutation</term>
<term>Survivin</term>
<term>Xenograft Model Antitumor Assays</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Aptamères nucléotidiques</term>
<term>Chlorhydrate d'erlotinib</term>
<term>Chloroquine</term>
<term>Femelle</term>
<term>Humains</term>
<term>Lignée cellulaire tumorale</term>
<term>Mutation</term>
<term>Nanoparticules</term>
<term>Petit ARN interférent</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Souris</term>
<term>Souris de lignée BALB C</term>
<term>Souris nude</term>
<term>Tests d'activité antitumorale sur modèle de xénogreffe</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29960010</PMID>
<DateCompleted><Year>2019</Year>
<Month>05</Month>
<Day>22</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>05</Month>
<Day>22</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1878-7568</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>76</Volume>
<PubDate><Year>2018</Year>
<Month>08</Month>
</PubDate>
</JournalIssue>
<Title>Acta biomaterialia</Title>
<ISOAbbreviation>Acta Biomater</ISOAbbreviation>
</Journal>
<ArticleTitle>Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.</ArticleTitle>
<Pagination><MedlinePgn>257-274</MedlinePgn>
</Pagination>
<ELocationID EIdType="pii" ValidYN="Y">S1742-7061(18)30380-5</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.1016/j.actbio.2018.06.034</ELocationID>
<Abstract><AbstractText>Although novel molecular targeted drugs have been recognized as an effective therapy for non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their efficacy fails to meet the expectation due to the acquired resistance in tumors. Up-regulation of the anti-apoptotic protein Survivin was shown to contribute to the resistance to EGFR tyrosine kinase inhibitors (TKI) in EGFR mutation-positive NSCLC. However, the unorganized tumor blood vessels impeded drug penetration into tumor tissue. The resulting insufficient intracellular drug/gene delivery in drug-resistant cancer cells remarkably weakened the drug efficacy in NSCLC. In this work, a multi-functional drug delivery system AP/ES was developed by using anti-EGFR aptamer (Apt)-modified polyamidoamine to co-deliver erlotinib and Survivin-shRNA. Chloroquine (CQ) was used in combination with AP/ES to normalize tumor vessels for sufficient drug/gene delivery to overcome drug resistance in NSCLC cells. The obtained AP/ES possessed desired physicochemical properties, good biostability, controlled drug release profiles, and strong selectivity to EGFR-mutated NSCLC mediated by Apt. CQ not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery and enhanced drug efficacy in erlotinib-resistant NSCLC cells. Our innovative gene/drug co-delivery system in combination with CQ showed a promising outcome in fighting against erlotinib resistance both in vitro and in vivo. This work indicates that normalization of tumor vessels could help intracellular erlotinib/Survivin-shRNA delivery and the down-regulation of Survivin could act synergistically with erlotinib for reversal of erlotinib resistance in EGFR mutation-positive NSCLC.</AbstractText>
<AbstractText Label="STATEMENT OF SIGNIFICANCE">NSCLC patients who benefited from EGFR-TKIs inevitably developed acquired resistance. Previous research focused on synthesis of new generation of molecular targeted drugs that could irreversibly inhibit EGFR with a particular gene mutation to overcome drug resistance. However, they failed to inhibit EGFR with other gene mutations. Activation of bypass signaling pathway and the changes of tumor microenvironment are identified as two of the mechanisms of acquired resistance to EGFR-TKIs. We therefore constructed multifunctional gene/drug co-delivery nanocomplexes AP/ES co-formulated with chloroquine that could target the both two mechanisms. We found that chloroquine not only enhanced endosomal escape ability of AP/ES for efficient gene transfection to inhibit Survivin, but also showed strong vessel-normalization ability to improve tumor microcirculation, which further promoted drug delivery into tumor tissue and enhanced drug efficacy in erlotinib-resistant NSCLC.</AbstractText>
<CopyrightInformation>Copyright © 2018 Acta Materialia Inc. Published by Elsevier Ltd. All rights reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lv</LastName>
<ForeName>Tingting</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Li</LastName>
<ForeName>Ziying</ForeName>
<Initials>Z</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Xu</LastName>
<ForeName>Liang</ForeName>
<Initials>L</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Zhang</LastName>
<ForeName>Yingying</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chen</LastName>
<ForeName>Haijun</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gao</LastName>
<ForeName>Yu</ForeName>
<Initials>Y</Initials>
<AffiliationInfo><Affiliation>Cancer Metastasis Alert and Prevention Center, and Pharmaceutical Photocatalysis of State Key Laboratory of Photocatalysis on Energy and Environment, College of Chemistry, Fujian Provincial Key Laboratory of Cancer Metastasis Chemoprevention and Chemotherapy, Fuzhou University, Fuzhou, Fujian 350116, China. Electronic address: hellogaoyu@126.com.</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>06</Month>
<Day>28</Day>
</ArticleDate>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>Acta Biomater</MedlineTA>
<NlmUniqueID>101233144</NlmUniqueID>
<ISSNLinking>1742-7061</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D052157">Aptamers, Nucleotide</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D009363">Neoplasm Proteins</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D034741">RNA, Small Interfering</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000077022">Survivin</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>886U3H6UFF</RegistryNumber>
<NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>DA87705X9K</RegistryNumber>
<NameOfSubstance UI="D000069347">Erlotinib Hydrochloride</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="C512478">EGFR protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>EC 2.7.10.1</RegistryNumber>
<NameOfSubstance UI="D066246">ErbB Receptors</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D052157" MajorTopicYN="Y">Aptamers, Nucleotide</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002289" MajorTopicYN="Y">Carcinoma, Non-Small-Cell Lung</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002738" MajorTopicYN="Y">Chloroquine</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
<QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000069347" MajorTopicYN="Y">Erlotinib Hydrochloride</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="Y">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008819" MajorTopicYN="N">Mice, Nude</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009154" MajorTopicYN="Y">Mutation</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D053758" MajorTopicYN="Y">Nanoparticles</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D009363" MajorTopicYN="N">Neoplasm Proteins</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D034741" MajorTopicYN="Y">RNA, Small Interfering</DescriptorName>
<QualifierName UI="Q000737" MajorTopicYN="N">chemistry</QualifierName>
<QualifierName UI="Q000493" MajorTopicYN="N">pharmacokinetics</QualifierName>
<QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077022" MajorTopicYN="Y">Survivin</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D023041" MajorTopicYN="N">Xenograft Model Antitumor Assays</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="Y">Chloroquine</Keyword>
<Keyword MajorTopicYN="Y">EGFR</Keyword>
<Keyword MajorTopicYN="Y">Erlotinib</Keyword>
<Keyword MajorTopicYN="Y">NSCLC</Keyword>
<Keyword MajorTopicYN="Y">Polyamidoamine</Keyword>
<Keyword MajorTopicYN="Y">Survivin</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="received"><Year>2018</Year>
<Month>02</Month>
<Day>06</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="revised"><Year>2018</Year>
<Month>05</Month>
<Day>23</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="accepted"><Year>2018</Year>
<Month>06</Month>
<Day>26</Day>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed"><Year>2018</Year>
<Month>7</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline"><Year>2019</Year>
<Month>5</Month>
<Day>23</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="entrez"><Year>2018</Year>
<Month>7</Month>
<Day>1</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList><ArticleId IdType="pubmed">29960010</ArticleId>
<ArticleId IdType="pii">S1742-7061(18)30380-5</ArticleId>
<ArticleId IdType="doi">10.1016/j.actbio.2018.06.034</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/PubMed/Curation

HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 000099 | SxmlIndent | more

HfdSelect -h $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd -nk 000099 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    PubMed
   |étape=   Curation
   |type=    RBID
   |clé=     pubmed:29960010
   |texte=   Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.
}}

Pour générer des pages wiki

HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Curation/RBID.i   -Sk "pubmed:29960010" \
       | HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Curation/biblio.hfd   \
       | NlmPubMed2Wicri -a ChloroquineV1

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021

	Serveur d'exploration Chloroquine
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.

Serveur d'exploration Chloroquine

Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.

Chloroquine in combination with aptamer-modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin shRNA co-delivery to overcome drug resistance in EGFR-mutated non-small cell lung cancer.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Links to Exploration step

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki