ChloroquineV1, PubMed, Checkpoint, bibRecord, 000111

Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.

Identifieur interne : 000111 ( PubMed/Checkpoint ); précédent : 000110; suivant : 000112

Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.

Auteurs : Dana Wai Yi Tsui [Royaume-Uni] ; Muhammed Murtaza [Royaume-Uni] ; Alvin Seng Cheong Wong [Singapour] ; Oscar M. Rueda [Royaume-Uni] ; Christopher G. Smith [Royaume-Uni] ; Dineika Chandrananda [Royaume-Uni] ; Ross A. Soo [Singapour] ; Hong Liang Lim [Singapour] ; Boon Cher Goh [Singapour] ; Carlos Caldas [Royaume-Uni] ; Tim Forshew [Royaume-Uni] ; Davina Gale [Royaume-Uni] ; Wei Liu [Royaume-Uni] ; James Morris [Royaume-Uni] ; Francesco Marass [Royaume-Uni] ; Tim Eisen [Royaume-Uni] ; Tan Min Chin [Singapour] ; Nitzan Rosenfeld [Singapour]

Source :

EMBO molecular medicine [ 1757-4684 ] ; 2018.

RBID : pubmed:29848757

Descripteurs français

English descriptors

KwdEn :
- Antineoplastic Agents (therapeutic use), Carcinoma, Non-Small-Cell Lung (drug therapy), Carcinoma, Non-Small-Cell Lung (genetics), Carcinoma, Non-Small-Cell Lung (pathology), DNA Copy Number Variations, DNA Mutational Analysis, DNA, Neoplasm (blood), Drug Resistance, Neoplasm (genetics), ErbB Receptors (genetics), Gefitinib (therapeutic use), Humans, Hydroxychloroquine (therapeutic use), Longitudinal Studies, Lung Neoplasms (drug therapy), Lung Neoplasms (genetics), Lung Neoplasms (pathology), Mutation, Prognosis, Survival Analysis, Treatment Outcome, Tumor Suppressor Protein p53 (chemistry), Tumor Suppressor Protein p53 (genetics).
MESH :
- chemical , blood : DNA, Neoplasm.
- chemical , chemistry : Tumor Suppressor Protein p53.
- chemical , genetics : ErbB Receptors, Tumor Suppressor Protein p53.
- chemical , therapeutic use : Antineoplastic Agents, Gefitinib, Hydroxychloroquine.
- drug therapy : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- genetics : Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Lung Neoplasms.
- pathology : Carcinoma, Non-Small-Cell Lung, Lung Neoplasms.
- DNA Copy Number Variations, DNA Mutational Analysis, Humans, Longitudinal Studies, Mutation, Prognosis, Survival Analysis, Treatment Outcome.

Abstract

Tumour heterogeneity leads to the development of multiple resistance mechanisms during targeted therapies. Identifying the dominant driver(s) is critical for treatment decision. We studied the relative dynamics of multiple oncogenic drivers in longitudinal plasma of 50 EGFR-mutant non-small-cell lung cancer patients receiving gefitinib and hydroxychloroquine. We performed digital PCR and targeted sequencing on samples from all patients and shallow whole-genome sequencing on samples from three patients who underwent histological transformation to small-cell lung cancer. In 43 patients with known EGFR mutations from tumour, we identified them accurately in plasma of 41 patients (95%, 41/43). We also found additional mutations, including EGFR T790M (31/50, 62%), TP53 (23/50, 46%), PIK3CA (7/50, 14%) and PTEN (4/50, 8%). Patients with both TP53 and EGFR mutations before treatment had worse overall survival than those with only EGFR Patients who progressed without T790M had worse PFS during TKI continuation and developed alternative alterations, including small-cell lung cancer-associated copy number changes and TP53 mutations, that tracked subsequent treatment responses. Longitudinal plasma analysis can help identify dominant resistance mechanisms, including non-druggable genetic information that may guide clinical management.

DOI: 10.15252/emmm.201707945
PubMed: 29848757

Affiliations:

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Le document en format XML

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<author><name sortKey="Liu, Wei" sort="Liu, Wei" uniqKey="Liu W" first="Wei" last="Liu">Wei Liu</name>
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<author><name sortKey="Morris, James" sort="Morris, James" uniqKey="Morris J" first="James" last="Morris">James Morris</name>
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<author><name sortKey="Marass, Francesco" sort="Marass, Francesco" uniqKey="Marass F" first="Francesco" last="Marass">Francesco Marass</name>
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<author><name sortKey="Eisen, Tim" sort="Eisen, Tim" uniqKey="Eisen T" first="Tim" last="Eisen">Tim Eisen</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.</title>
<author><name sortKey="Tsui, Dana Wai Yi" sort="Tsui, Dana Wai Yi" uniqKey="Tsui D" first="Dana Wai Yi" last="Tsui">Dana Wai Yi Tsui</name>
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<orgName type="university">Université de Cambridge</orgName>
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</placeName>
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<author><name sortKey="Murtaza, Muhammed" sort="Murtaza, Muhammed" uniqKey="Murtaza M" first="Muhammed" last="Murtaza">Muhammed Murtaza</name>
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<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
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<author><name sortKey="Wong, Alvin Seng Cheong" sort="Wong, Alvin Seng Cheong" uniqKey="Wong A" first="Alvin Seng Cheong" last="Wong">Alvin Seng Cheong Wong</name>
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<author><name sortKey="Smith, Christopher G" sort="Smith, Christopher G" uniqKey="Smith C" first="Christopher G" last="Smith">Christopher G. Smith</name>
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<author><name sortKey="Chandrananda, Dineika" sort="Chandrananda, Dineika" uniqKey="Chandrananda D" first="Dineika" last="Chandrananda">Dineika Chandrananda</name>
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<author><name sortKey="Soo, Ross A" sort="Soo, Ross A" uniqKey="Soo R" first="Ross A" last="Soo">Ross A. Soo</name>
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<author><name sortKey="Lim, Hong Liang" sort="Lim, Hong Liang" uniqKey="Lim H" first="Hong Liang" last="Lim">Hong Liang Lim</name>
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<author><name sortKey="Goh, Boon Cher" sort="Goh, Boon Cher" uniqKey="Goh B" first="Boon Cher" last="Goh">Boon Cher Goh</name>
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<author><name sortKey="Caldas, Carlos" sort="Caldas, Carlos" uniqKey="Caldas C" first="Carlos" last="Caldas">Carlos Caldas</name>
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<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
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<author><name sortKey="Forshew, Tim" sort="Forshew, Tim" uniqKey="Forshew T" first="Tim" last="Forshew">Tim Forshew</name>
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<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
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<author><name sortKey="Gale, Davina" sort="Gale, Davina" uniqKey="Gale D" first="Davina" last="Gale">Davina Gale</name>
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<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
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<author><name sortKey="Liu, Wei" sort="Liu, Wei" uniqKey="Liu W" first="Wei" last="Liu">Wei Liu</name>
<affiliation wicri:level="4"><nlm:affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</nlm:affiliation>
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<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
</placeName>
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<author><name sortKey="Morris, James" sort="Morris, James" uniqKey="Morris J" first="James" last="Morris">James Morris</name>
<affiliation wicri:level="4"><nlm:affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
<wicri:regionArea>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Marass, Francesco" sort="Marass, Francesco" uniqKey="Marass F" first="Francesco" last="Marass">Francesco Marass</name>
<affiliation wicri:level="4"><nlm:affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</nlm:affiliation>
<country xml:lang="fr">Royaume-Uni</country>
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</placeName>
</affiliation>
</author>
<author><name sortKey="Eisen, Tim" sort="Eisen, Tim" uniqKey="Eisen T" first="Tim" last="Eisen">Tim Eisen</name>
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<wicri:regionArea>Department of Oncology, University of Cambridge, Cambridge</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Chin, Tan Min" sort="Chin, Tan Min" uniqKey="Chin T" first="Tan Min" last="Chin">Tan Min Chin</name>
<affiliation wicri:level="1"><nlm:affiliation>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore, Singapore csictm@nus.edu.sg nitzan.rosenfeld@cruk.cam.ac.uk.</nlm:affiliation>
<country wicri:rule="url">Singapour</country>
<wicri:regionArea>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore</wicri:regionArea>
<wicri:noRegion>Singapore</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Rosenfeld, Nitzan" sort="Rosenfeld, Nitzan" uniqKey="Rosenfeld N" first="Nitzan" last="Rosenfeld">Nitzan Rosenfeld</name>
<affiliation wicri:level="4"><nlm:affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK csictm@nus.edu.sg nitzan.rosenfeld@cruk.cam.ac.uk.</nlm:affiliation>
<country wicri:rule="url">Singapour</country>
<wicri:regionArea>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge</wicri:regionArea>
<orgName type="university">Université de Cambridge</orgName>
<placeName><settlement type="city">Cambridge</settlement>
<region type="country">Angleterre</region>
<region type="région" nuts="1">Angleterre de l'Est</region>
</placeName>
</affiliation>
</author>
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<series><title level="j">EMBO molecular medicine</title>
<idno type="eISSN">1757-4684</idno>
<imprint><date when="2018" type="published">2018</date>
</imprint>
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<term>Carcinoma, Non-Small-Cell Lung (drug therapy)</term>
<term>Carcinoma, Non-Small-Cell Lung (genetics)</term>
<term>Carcinoma, Non-Small-Cell Lung (pathology)</term>
<term>DNA Copy Number Variations</term>
<term>DNA Mutational Analysis</term>
<term>DNA, Neoplasm (blood)</term>
<term>Drug Resistance, Neoplasm (genetics)</term>
<term>ErbB Receptors (genetics)</term>
<term>Gefitinib (therapeutic use)</term>
<term>Humans</term>
<term>Hydroxychloroquine (therapeutic use)</term>
<term>Longitudinal Studies</term>
<term>Lung Neoplasms (drug therapy)</term>
<term>Lung Neoplasms (genetics)</term>
<term>Lung Neoplasms (pathology)</term>
<term>Mutation</term>
<term>Prognosis</term>
<term>Survival Analysis</term>
<term>Treatment Outcome</term>
<term>Tumor Suppressor Protein p53 (chemistry)</term>
<term>Tumor Suppressor Protein p53 (genetics)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ADN tumoral (sang)</term>
<term>Analyse de mutations d'ADN</term>
<term>Analyse de survie</term>
<term>Antinéoplasiques (usage thérapeutique)</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 (traitement médicamenteux)</term>
<term>Humains</term>
<term>Hydroxychloroquine (usage thérapeutique)</term>
<term>Mutation</term>
<term>Pronostic</term>
<term>Protéine p53 suppresseur de tumeur ()</term>
<term>Protéine p53 suppresseur de tumeur (génétique)</term>
<term>Récepteurs ErbB (génétique)</term>
<term>Résistance aux médicaments antinéoplasiques (génétique)</term>
<term>Résultat thérapeutique</term>
<term>Tumeurs du poumon (anatomopathologie)</term>
<term>Tumeurs du poumon (génétique)</term>
<term>Tumeurs du poumon (traitement médicamenteux)</term>
<term>Variations de nombre de copies de segment d'ADN</term>
<term>Études longitudinales</term>
</keywords>
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<term>Tumor Suppressor Protein p53</term>
</keywords>
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<term>Gefitinib</term>
<term>Hydroxychloroquine</term>
</keywords>
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<term>Tumeurs du poumon</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>
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<term>Protéine p53 suppresseur de tumeur</term>
<term>Récepteurs ErbB</term>
<term>Résistance aux médicaments antinéoplasiques</term>
<term>Tumeurs du poumon</term>
</keywords>
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<term>Lung Neoplasms</term>
</keywords>
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</keywords>
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<term>Hydroxychloroquine</term>
</keywords>
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<term>DNA Mutational Analysis</term>
<term>Humans</term>
<term>Longitudinal Studies</term>
<term>Mutation</term>
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<term>Survival Analysis</term>
<term>Treatment Outcome</term>
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<term>Mutation</term>
<term>Pronostic</term>
<term>Protéine p53 suppresseur de tumeur</term>
<term>Résultat thérapeutique</term>
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<front><div type="abstract" xml:lang="en">Tumour heterogeneity leads to the development of multiple resistance mechanisms during targeted therapies. Identifying the dominant driver(s) is critical for treatment decision. We studied the relative dynamics of multiple oncogenic drivers in longitudinal plasma of 50 <i>EGFR</i>
-mutant non-small-cell lung cancer patients receiving gefitinib and hydroxychloroquine. We performed digital PCR and targeted sequencing on samples from all patients and shallow whole-genome sequencing on samples from three patients who underwent histological transformation to small-cell lung cancer. In 43 patients with known EGFR mutations from tumour, we identified them accurately in plasma of 41 patients (95%, 41/43). We also found additional mutations, including <i>EGFR</i>
 T790M (31/50, 62%), <i>TP53</i>
 (23/50, 46%), <i>PIK3CA</i>
 (7/50, 14%) and <i>PTEN</i>
 (4/50, 8%). Patients with both <i>TP53</i>
 and <i>EGFR</i>
 mutations before treatment had worse overall survival than those with only <i>EGFR</i>
 Patients who progressed without T790M had worse PFS during TKI continuation and developed alternative alterations, including small-cell lung cancer-associated copy number changes and <i>TP53</i>
 mutations, that tracked subsequent treatment responses. Longitudinal plasma analysis can help identify dominant resistance mechanisms, including non-druggable genetic information that may guide clinical management.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">29848757</PMID>
<DateCompleted><Year>2019</Year>
<Month>04</Month>
<Day>23</Day>
</DateCompleted>
<DateRevised><Year>2019</Year>
<Month>04</Month>
<Day>23</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1757-4684</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>10</Volume>
<Issue>6</Issue>
<PubDate><Year>2018</Year>
<Month>06</Month>
</PubDate>
</JournalIssue>
<Title>EMBO molecular medicine</Title>
<ISOAbbreviation>EMBO Mol Med</ISOAbbreviation>
</Journal>
<ArticleTitle>Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.</ArticleTitle>
<ELocationID EIdType="pii" ValidYN="Y">e7945</ELocationID>
<ELocationID EIdType="doi" ValidYN="Y">10.15252/emmm.201707945</ELocationID>
<Abstract><AbstractText>Tumour heterogeneity leads to the development of multiple resistance mechanisms during targeted therapies. Identifying the dominant driver(s) is critical for treatment decision. We studied the relative dynamics of multiple oncogenic drivers in longitudinal plasma of 50 <i>EGFR</i>
-mutant non-small-cell lung cancer patients receiving gefitinib and hydroxychloroquine. We performed digital PCR and targeted sequencing on samples from all patients and shallow whole-genome sequencing on samples from three patients who underwent histological transformation to small-cell lung cancer. In 43 patients with known EGFR mutations from tumour, we identified them accurately in plasma of 41 patients (95%, 41/43). We also found additional mutations, including <i>EGFR</i>
 T790M (31/50, 62%), <i>TP53</i>
 (23/50, 46%), <i>PIK3CA</i>
 (7/50, 14%) and <i>PTEN</i>
 (4/50, 8%). Patients with both <i>TP53</i>
 and <i>EGFR</i>
 mutations before treatment had worse overall survival than those with only <i>EGFR</i>
 Patients who progressed without T790M had worse PFS during TKI continuation and developed alternative alterations, including small-cell lung cancer-associated copy number changes and <i>TP53</i>
 mutations, that tracked subsequent treatment responses. Longitudinal plasma analysis can help identify dominant resistance mechanisms, including non-druggable genetic information that may guide clinical management.</AbstractText>
<CopyrightInformation>© 2018 The Authors. Published under the terms of the CC BY 4.0 license.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Tsui</LastName>
<ForeName>Dana Wai Yi</ForeName>
<Initials>DWY</Initials>
<Identifier Source="ORCID">0000-0002-0595-6664</Identifier>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Murtaza</LastName>
<ForeName>Muhammed</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Oncology, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Wong</LastName>
<ForeName>Alvin Seng Cheong</ForeName>
<Initials>ASC</Initials>
<AffiliationInfo><Affiliation>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rueda</LastName>
<ForeName>Oscar M</ForeName>
<Initials>OM</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Smith</LastName>
<ForeName>Christopher G</ForeName>
<Initials>CG</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chandrananda</LastName>
<ForeName>Dineika</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Soo</LastName>
<ForeName>Ross A</ForeName>
<Initials>RA</Initials>
<AffiliationInfo><Affiliation>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Science Institute, Centre for Translational Medicine, National University of Singapore, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lim</LastName>
<ForeName>Hong Liang</ForeName>
<Initials>HL</Initials>
<AffiliationInfo><Affiliation>Parkway Cancer Center, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Goh</LastName>
<ForeName>Boon Cher</ForeName>
<Initials>BC</Initials>
<AffiliationInfo><Affiliation>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Science Institute, Centre for Translational Medicine, National University of Singapore, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Caldas</LastName>
<ForeName>Carlos</ForeName>
<Initials>C</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Oncology, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Oncology, Addenbrooke's Hospital, Cambridge University Health Partners, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Forshew</LastName>
<ForeName>Tim</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Gale</LastName>
<ForeName>Davina</ForeName>
<Initials>D</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Liu</LastName>
<ForeName>Wei</ForeName>
<Initials>W</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Morris</LastName>
<ForeName>James</ForeName>
<Initials>J</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marass</LastName>
<ForeName>Francesco</ForeName>
<Initials>F</Initials>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Eisen</LastName>
<ForeName>Tim</ForeName>
<Initials>T</Initials>
<AffiliationInfo><Affiliation>Department of Oncology, University of Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Department of Oncology, Addenbrooke's Hospital, Cambridge University Health Partners, Cambridge, UK.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Oncology Early Clinical Development, AstraZeneca, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chin</LastName>
<ForeName>Tan Min</ForeName>
<Initials>TM</Initials>
<Identifier Source="ORCID">0000-0002-3289-8498</Identifier>
<AffiliationInfo><Affiliation>Department of Haematology-Oncology, National University Cancer Institute, National University Health System, Singapore, Singapore csictm@nus.edu.sg nitzan.rosenfeld@cruk.cam.ac.uk.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Science Institute, Centre for Translational Medicine, National University of Singapore, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Raffles Cancer Centre, Raffles Hospital, Singapore, Singapore.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Rosenfeld</LastName>
<ForeName>Nitzan</ForeName>
<Initials>N</Initials>
<Identifier Source="ORCID">0000-0002-2825-4788</Identifier>
<AffiliationInfo><Affiliation>Cancer Research UK Cambridge Institute, Li Ka Shing Centre, University of Cambridge, Cambridge, UK csictm@nus.edu.sg nitzan.rosenfeld@cruk.cam.ac.uk.</Affiliation>
</AffiliationInfo>
<AffiliationInfo><Affiliation>Cancer Research UK Major Center - Cambridge, Cambridge, UK.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<GrantList CompleteYN="Y"><Grant><GrantID>337905</GrantID>
<Agency>European Research Council</Agency>
<Country>International</Country>
</Grant>
<Grant><GrantID>A11906</GrantID>
<Agency>Cancer Research UK</Agency>
<Country>United Kingdom</Country>
</Grant>
<Grant><GrantID>A20240</GrantID>
<Agency>Cancer Research UK</Agency>
<Country>United Kingdom</Country>
</Grant>
</GrantList>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
<PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo><Country>England</Country>
<MedlineTA>EMBO Mol Med</MedlineTA>
<NlmUniqueID>101487380</NlmUniqueID>
<ISSNLinking>1757-4676</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList><Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D000970">Antineoplastic Agents</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D004273">DNA, Neoplasm</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="C495901">TP53 protein, human</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>0</RegistryNumber>
<NameOfSubstance UI="D016159">Tumor Suppressor Protein p53</NameOfSubstance>
</Chemical>
<Chemical><RegistryNumber>4QWG6N8QKH</RegistryNumber>
<NameOfSubstance UI="D006886">Hydroxychloroquine</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>
<Chemical><RegistryNumber>S65743JHBS</RegistryNumber>
<NameOfSubstance UI="D000077156">Gefitinib</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
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<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D002289" MajorTopicYN="N">Carcinoma, Non-Small-Cell Lung</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D056915" MajorTopicYN="N">DNA Copy Number Variations</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004252" MajorTopicYN="N">DNA Mutational Analysis</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D004273" MajorTopicYN="N">DNA, Neoplasm</DescriptorName>
<QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D066246" MajorTopicYN="N">ErbB Receptors</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D000077156" MajorTopicYN="N">Gefitinib</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006886" MajorTopicYN="N">Hydroxychloroquine</DescriptorName>
<QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008137" MajorTopicYN="N">Longitudinal Studies</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008175" MajorTopicYN="N">Lung Neoplasms</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
<QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName>
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Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.

Dynamics of multiple resistance mechanisms in plasma DNA during EGFR-targeted therapies in non-small cell lung cancer.

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