Natural killer cells are essential for the ability of BRAF inhibitors to control BRAFV600E-mutant metastatic melanoma.
Identifieur interne : 003251 ( PubMed/Corpus ); précédent : 003250; suivant : 003252Natural killer cells are essential for the ability of BRAF inhibitors to control BRAFV600E-mutant metastatic melanoma.
Auteurs : Lucas Ferrari De Andrade ; Shin F. Ngiow ; Kimberley Stannard ; Sylvie Rusakiewicz ; Murugan Kalimutho ; Kum Kum Khanna ; Siok-Keen Tey ; Kazuyoshi Takeda ; Laurence Zitvogel ; Ludovic Martinet ; Mark J. SmythSource :
- Cancer research [ 1538-7445 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Cell Line, Tumor, Cell Proliferation (genetics), Drug Resistance, Neoplasm (genetics), Drug Resistance, Neoplasm (immunology), Humans, Immunotherapy, Killer Cells, Natural (metabolism), Killer Cells, Natural (pathology), Melanoma (genetics), Melanoma (immunology), Melanoma (pathology), Melanoma (therapy), Mice, Mutation, Neoplasm Metastasis (genetics), Neoplasm Metastasis (immunology), Neoplasm Metastasis (pathology), Proto-Oncogene Proteins B-raf (antagonists & inhibitors), Proto-Oncogene Proteins B-raf (genetics), Signal Transduction (genetics).
- MESH :
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins B-raf.
- genetics : Cell Proliferation, Drug Resistance, Neoplasm, Melanoma, Neoplasm Metastasis, Proto-Oncogene Proteins B-raf, Signal Transduction.
- immunology : Drug Resistance, Neoplasm, Melanoma, Neoplasm Metastasis.
- metabolism : Killer Cells, Natural.
- pathology : Killer Cells, Natural, Melanoma, Neoplasm Metastasis.
- therapy : Melanoma.
- Animals, Cell Line, Tumor, Humans, Immunotherapy, Mice, Mutation.
Abstract
BRAF(V600E) is a major oncogenic mutation found in approximately 50% of human melanoma that confers constitutive activation of the MAPK pathway and increased melanoma growth. Inhibition of BRAF(V600E) by oncogene targeting therapy increases overall survival of patients with melanoma, but is unable to produce many durable responses. Adaptive drug resistance remains the main limitation to BRAF(V600E) inhibitor clinical efficacy and immune-based strategies could be useful to overcome disease relapse. Tumor microenvironment greatly differs between visceral metastasis and primary cutaneous melanoma, and the mechanisms involved in the antimetastatic efficacy of BRAF(V600E) inhibitors remain to be determined. To address this question, we developed a metastatic BRAF(V600E)-mutant melanoma cell line and demonstrated that the antimetastatic properties of BRAF inhibitor PLX4720 (a research analogue of vemurafenib) require host natural killer (NK) cells and perforin. Indeed, PLX4720 not only directly limited BRAF(V600E)-induced tumor cell proliferation, but also affected NK cell functions. We showed that PLX4720 increases the phosphorylation of ERK1/2, CD69 expression, and proliferation of mouse NK cells in vitro. NK cell frequencies were significantly enhanced by PLX4720 specifically in the lungs of mice with BRAF(V600E) lung metastases. Furthermore, PLX4720 also increased human NK cell pERK1/2, CD69 expression, and IFNγ release in the context of anti-NKp30 and IL2 stimulation. Overall, this study supports the idea that additional NK cell-based immunotherapy (by checkpoint blockade or agonists or cytokines) may combine well with BRAF(V600E) inhibitor therapy to promote more durable responses in melanoma.
DOI: 10.1158/0008-5472.CAN-14-1339
PubMed: 25351955
Links to Exploration step
pubmed:25351955Le document en format XML
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Ngiow</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Stannard, Kimberley" sort="Stannard, Kimberley" uniqKey="Stannard K" first="Kimberley" last="Stannard">Kimberley Stannard</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Rusakiewicz, Sylvie" sort="Rusakiewicz, Sylvie" uniqKey="Rusakiewicz S" first="Sylvie" last="Rusakiewicz">Sylvie Rusakiewicz</name><affiliation><nlm:affiliation>Gustave Roussy Cancer Campus, Villejuif, France. INSERM U1015, Villejuif, France. 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School of Medicine, University of Queensland, Herston, Queensland, Australia. mark.smyth@qimrberghofer.edu.au.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25351955</idno><idno type="pmid">25351955</idno><idno type="doi">10.1158/0008-5472.CAN-14-1339</idno><idno type="wicri:Area/PubMed/Corpus">003251</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">003251</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Natural killer cells are essential for the ability of BRAF inhibitors to control BRAFV600E-mutant metastatic melanoma.</title><author><name sortKey="Ferrari De Andrade, Lucas" sort="Ferrari De Andrade, Lucas" uniqKey="Ferrari De Andrade L" first="Lucas" last="Ferrari De Andrade">Lucas Ferrari De Andrade</name><affiliation><nlm:affiliation>Laboratorio de Pesquisa em Células Inflamatórias e Neoplásicas Group, Universidade Federal do Paraná, Curitiba, Paraná, Brazil. Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Ngiow, Shin F" sort="Ngiow, Shin F" uniqKey="Ngiow S" first="Shin F" last="Ngiow">Shin F. Ngiow</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Stannard, Kimberley" sort="Stannard, Kimberley" uniqKey="Stannard K" first="Kimberley" last="Stannard">Kimberley Stannard</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Rusakiewicz, Sylvie" sort="Rusakiewicz, Sylvie" uniqKey="Rusakiewicz S" first="Sylvie" last="Rusakiewicz">Sylvie Rusakiewicz</name><affiliation><nlm:affiliation>Gustave Roussy Cancer Campus, Villejuif, France. INSERM U1015, Villejuif, France. Center of Clinical Investigations in Biotherapies of Cancer (CICBT) 1428, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Kalimutho, Murugan" sort="Kalimutho, Murugan" uniqKey="Kalimutho M" first="Murugan" last="Kalimutho">Murugan Kalimutho</name><affiliation><nlm:affiliation>Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Khanna, Kum Kum" sort="Khanna, Kum Kum" uniqKey="Khanna K" first="Kum Kum" last="Khanna">Kum Kum Khanna</name><affiliation><nlm:affiliation>Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Tey, Siok Keen" sort="Tey, Siok Keen" uniqKey="Tey S" first="Siok-Keen" last="Tey">Siok-Keen Tey</name><affiliation><nlm:affiliation>Bone Marrow Transplant Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Takeda, Kazuyoshi" sort="Takeda, Kazuyoshi" uniqKey="Takeda K" first="Kazuyoshi" last="Takeda">Kazuyoshi Takeda</name><affiliation><nlm:affiliation>Department of Immunology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo, Japan.</nlm:affiliation></affiliation></author><author><name sortKey="Zitvogel, Laurence" sort="Zitvogel, Laurence" uniqKey="Zitvogel L" first="Laurence" last="Zitvogel">Laurence Zitvogel</name><affiliation><nlm:affiliation>Gustave Roussy Cancer Campus, Villejuif, France. INSERM U1015, Villejuif, France. Université Paris Sud-XI, Faculté de Médecine, Le Kremlin Bicêtre, France. Department of Medical Oncology, IGR, Villejuif, France.</nlm:affiliation></affiliation></author><author><name sortKey="Martinet, Ludovic" sort="Martinet, Ludovic" uniqKey="Martinet L" first="Ludovic" last="Martinet">Ludovic Martinet</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Smyth, Mark J" sort="Smyth, Mark J" uniqKey="Smyth M" first="Mark J" last="Smyth">Mark J. Smyth</name><affiliation><nlm:affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia. School of Medicine, University of Queensland, Herston, Queensland, Australia. mark.smyth@qimrberghofer.edu.au.</nlm:affiliation></affiliation></author></analytic><series><title level="j">Cancer research</title><idno type="eISSN">1538-7445</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Cell Proliferation (genetics)</term><term>Drug Resistance, Neoplasm (genetics)</term><term>Drug Resistance, Neoplasm (immunology)</term><term>Humans</term><term>Immunotherapy</term><term>Killer Cells, Natural (metabolism)</term><term>Killer Cells, Natural (pathology)</term><term>Melanoma (genetics)</term><term>Melanoma (immunology)</term><term>Melanoma (pathology)</term><term>Melanoma (therapy)</term><term>Mice</term><term>Mutation</term><term>Neoplasm Metastasis (genetics)</term><term>Neoplasm Metastasis (immunology)</term><term>Neoplasm Metastasis (pathology)</term><term>Proto-Oncogene Proteins B-raf (antagonists & inhibitors)</term><term>Proto-Oncogene Proteins B-raf (genetics)</term><term>Signal Transduction (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Proto-Oncogene Proteins B-raf</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cell Proliferation</term><term>Drug Resistance, Neoplasm</term><term>Melanoma</term><term>Neoplasm Metastasis</term><term>Proto-Oncogene Proteins B-raf</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Drug Resistance, Neoplasm</term><term>Melanoma</term><term>Neoplasm Metastasis</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Killer Cells, Natural</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Killer Cells, Natural</term><term>Melanoma</term><term>Neoplasm Metastasis</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Melanoma</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Cell Line, Tumor</term><term>Humans</term><term>Immunotherapy</term><term>Mice</term><term>Mutation</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">BRAF(V600E) is a major oncogenic mutation found in approximately 50% of human melanoma that confers constitutive activation of the MAPK pathway and increased melanoma growth. Inhibition of BRAF(V600E) by oncogene targeting therapy increases overall survival of patients with melanoma, but is unable to produce many durable responses. Adaptive drug resistance remains the main limitation to BRAF(V600E) inhibitor clinical efficacy and immune-based strategies could be useful to overcome disease relapse. Tumor microenvironment greatly differs between visceral metastasis and primary cutaneous melanoma, and the mechanisms involved in the antimetastatic efficacy of BRAF(V600E) inhibitors remain to be determined. To address this question, we developed a metastatic BRAF(V600E)-mutant melanoma cell line and demonstrated that the antimetastatic properties of BRAF inhibitor PLX4720 (a research analogue of vemurafenib) require host natural killer (NK) cells and perforin. Indeed, PLX4720 not only directly limited BRAF(V600E)-induced tumor cell proliferation, but also affected NK cell functions. We showed that PLX4720 increases the phosphorylation of ERK1/2, CD69 expression, and proliferation of mouse NK cells in vitro. NK cell frequencies were significantly enhanced by PLX4720 specifically in the lungs of mice with BRAF(V600E) lung metastases. Furthermore, PLX4720 also increased human NK cell pERK1/2, CD69 expression, and IFNγ release in the context of anti-NKp30 and IL2 stimulation. Overall, this study supports the idea that additional NK cell-based immunotherapy (by checkpoint blockade or agonists or cytokines) may combine well with BRAF(V600E) inhibitor therapy to promote more durable responses in melanoma.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25351955</PMID><DateCreated><Year>2014</Year><Month>12</Month><Day>16</Day></DateCreated><DateCompleted><Year>2015</Year><Month>02</Month><Day>10</Day></DateCompleted><DateRevised><Year>2014</Year><Month>12</Month><Day>16</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1538-7445</ISSN><JournalIssue CitedMedium="Internet"><Volume>74</Volume><Issue>24</Issue><PubDate><Year>2014</Year><Month>Dec</Month><Day>15</Day></PubDate></JournalIssue><Title>Cancer research</Title><ISOAbbreviation>Cancer Res.</ISOAbbreviation></Journal><ArticleTitle>Natural killer cells are essential for the ability of BRAF inhibitors to control BRAFV600E-mutant metastatic melanoma.</ArticleTitle><Pagination><MedlinePgn>7298-308</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1158/0008-5472.CAN-14-1339</ELocationID><Abstract><AbstractText>BRAF(V600E) is a major oncogenic mutation found in approximately 50% of human melanoma that confers constitutive activation of the MAPK pathway and increased melanoma growth. Inhibition of BRAF(V600E) by oncogene targeting therapy increases overall survival of patients with melanoma, but is unable to produce many durable responses. Adaptive drug resistance remains the main limitation to BRAF(V600E) inhibitor clinical efficacy and immune-based strategies could be useful to overcome disease relapse. Tumor microenvironment greatly differs between visceral metastasis and primary cutaneous melanoma, and the mechanisms involved in the antimetastatic efficacy of BRAF(V600E) inhibitors remain to be determined. To address this question, we developed a metastatic BRAF(V600E)-mutant melanoma cell line and demonstrated that the antimetastatic properties of BRAF inhibitor PLX4720 (a research analogue of vemurafenib) require host natural killer (NK) cells and perforin. Indeed, PLX4720 not only directly limited BRAF(V600E)-induced tumor cell proliferation, but also affected NK cell functions. We showed that PLX4720 increases the phosphorylation of ERK1/2, CD69 expression, and proliferation of mouse NK cells in vitro. NK cell frequencies were significantly enhanced by PLX4720 specifically in the lungs of mice with BRAF(V600E) lung metastases. Furthermore, PLX4720 also increased human NK cell pERK1/2, CD69 expression, and IFNγ release in the context of anti-NKp30 and IL2 stimulation. Overall, this study supports the idea that additional NK cell-based immunotherapy (by checkpoint blockade or agonists or cytokines) may combine well with BRAF(V600E) inhibitor therapy to promote more durable responses in melanoma.</AbstractText><CopyrightInformation>©2014 American Association for Cancer Research.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ferrari de Andrade</LastName><ForeName>Lucas</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratorio de Pesquisa em Células Inflamatórias e Neoplásicas Group, Universidade Federal do Paraná, Curitiba, Paraná, Brazil. Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ngiow</LastName><ForeName>Shin F</ForeName><Initials>SF</Initials><AffiliationInfo><Affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Stannard</LastName><ForeName>Kimberley</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rusakiewicz</LastName><ForeName>Sylvie</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Gustave Roussy Cancer Campus, Villejuif, France. INSERM U1015, Villejuif, France. Center of Clinical Investigations in Biotherapies of Cancer (CICBT) 1428, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kalimutho</LastName><ForeName>Murugan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Khanna</LastName><ForeName>Kum Kum</ForeName><Initials>KK</Initials><AffiliationInfo><Affiliation>Signal Transduction Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Tey</LastName><ForeName>Siok-Keen</ForeName><Initials>SK</Initials><AffiliationInfo><Affiliation>Bone Marrow Transplant Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Takeda</LastName><ForeName>Kazuyoshi</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Immunology, Juntendo University School of Medicine, Hongo, Bunkyo-ku, Tokyo, Japan.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zitvogel</LastName><ForeName>Laurence</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Gustave Roussy Cancer Campus, Villejuif, France. INSERM U1015, Villejuif, France. Université Paris Sud-XI, Faculté de Médecine, Le Kremlin Bicêtre, France. Department of Medical Oncology, IGR, Villejuif, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Martinet</LastName><ForeName>Ludovic</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smyth</LastName><ForeName>Mark J</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>Immunology in Cancer and Infection Laboratory, QIMR Berghofer Medical Research Institute, Herston, Queensland, Australia. School of Medicine, University of Queensland, Herston, Queensland, Australia. mark.smyth@qimrberghofer.edu.au.</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>2014</Year><Month>10</Month><Day>28</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Cancer Res</MedlineTA><NlmUniqueID>2984705R</NlmUniqueID><ISSNLinking>0008-5472</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="C482119">BRAF protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.1</RegistryNumber><NameOfSubstance UI="D048493">Proto-Oncogene Proteins B-raf</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D045744" MajorTopicYN="N">Cell Line, Tumor</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019008" MajorTopicYN="N">Drug Resistance, Neoplasm</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007167" MajorTopicYN="Y">Immunotherapy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007694" MajorTopicYN="N">Killer Cells, Natural</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008545" MajorTopicYN="N">Melanoma</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000628" MajorTopicYN="Y">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009154" MajorTopicYN="N">Mutation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009362" MajorTopicYN="N">Neoplasm Metastasis</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048493" MajorTopicYN="N">Proto-Oncogene Proteins B-raf</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="Q000235" MajorTopicYN="N">genetics</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2014</Year><Month>10</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2014</Year><Month>10</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2015</Year><Month>2</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">25351955</ArticleId><ArticleId IdType="pii">0008-5472.CAN-14-1339</ArticleId><ArticleId IdType="doi">10.1158/0008-5472.CAN-14-1339</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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