Immune Responses to BRAF-Targeted Therapy in Melanoma: Is Targeted Therapy Immunotherapy?
Identifieur interne : 001819 ( Main/Exploration ); précédent : 001818; suivant : 001820Immune Responses to BRAF-Targeted Therapy in Melanoma: Is Targeted Therapy Immunotherapy?
Auteurs : Mark C. Kelley [États-Unis]Source :
- Critical reviews in oncogenesis [ 0893-9675 ] ; 2016.
Descripteurs français
- KwdFr :
- Anticorps monoclonaux (pharmacologie), Anticorps monoclonaux (usage thérapeutique), Antinéoplasiques (pharmacologie), Antinéoplasiques (usage thérapeutique), Charge tumorale (effets des médicaments et des substances chimiques), Humains (MeSH), Immunothérapie (méthodes), Inhibiteurs de protéines kinases (pharmacologie), Inhibiteurs de protéines kinases (usage thérapeutique), Lymphocytes TIL (effets des médicaments et des substances chimiques), Lymphocytes TIL (immunologie), Lymphocytes TIL (métabolisme), Mitogen-Activated Protein Kinases (métabolisme), Mutation (MeSH), Mélanome (anatomopathologie), Mélanome (immunologie), Mélanome (métabolisme), Mélanome (traitement médicamenteux), Prolifération cellulaire (effets des médicaments et des substances chimiques), Protéines proto-oncogènes B-raf (antagonistes et inhibiteurs), Protéines proto-oncogènes B-raf (génétique), Protéines proto-oncogènes B-raf (métabolisme), Thérapie moléculaire ciblée (MeSH), Transduction du signal (effets des médicaments et des substances chimiques).
- MESH :
- anatomopathologie : Mélanome.
- antagonistes et inhibiteurs : Protéines proto-oncogènes B-raf.
- effets des médicaments et des substances chimiques : Charge tumorale, Lymphocytes TIL, Prolifération cellulaire, Transduction du signal.
- génétique : Protéines proto-oncogènes B-raf.
- immunologie : Lymphocytes TIL, Mélanome.
- métabolisme : Lymphocytes TIL, Mitogen-Activated Protein Kinases, Mélanome, Protéines proto-oncogènes B-raf.
- méthodes : Immunothérapie.
- pharmacologie : Anticorps monoclonaux, Antinéoplasiques, Inhibiteurs de protéines kinases.
- traitement médicamenteux : Mélanome.
- usage thérapeutique : Anticorps monoclonaux, Antinéoplasiques, Inhibiteurs de protéines kinases.
- Humains, Mutation, Thérapie moléculaire ciblée.
English descriptors
- KwdEn :
- Antibodies, Monoclonal (pharmacology), Antibodies, Monoclonal (therapeutic use), Antineoplastic Agents (pharmacology), Antineoplastic Agents (therapeutic use), Cell Proliferation (drug effects), Humans (MeSH), Immunotherapy (methods), Lymphocytes, Tumor-Infiltrating (drug effects), Lymphocytes, Tumor-Infiltrating (immunology), Lymphocytes, Tumor-Infiltrating (metabolism), Melanoma (drug therapy), Melanoma (immunology), Melanoma (metabolism), Melanoma (pathology), Mitogen-Activated Protein Kinases (metabolism), Molecular Targeted Therapy (MeSH), Mutation (MeSH), Protein Kinase Inhibitors (pharmacology), Protein Kinase Inhibitors (therapeutic use), Proto-Oncogene Proteins B-raf (antagonists & inhibitors), Proto-Oncogene Proteins B-raf (genetics), Proto-Oncogene Proteins B-raf (metabolism), Signal Transduction (drug effects), Tumor Burden (drug effects).
- MESH :
- chemical , antagonists & inhibitors : Proto-Oncogene Proteins B-raf.
- chemical , genetics : Proto-Oncogene Proteins B-raf.
- chemical , metabolism : Mitogen-Activated Protein Kinases, Proto-Oncogene Proteins B-raf.
- chemical , pharmacology : Antibodies, Monoclonal, Antineoplastic Agents, Protein Kinase Inhibitors.
- chemical , therapeutic use : Antibodies, Monoclonal, Antineoplastic Agents, Protein Kinase Inhibitors.
- drug effects : Cell Proliferation, Lymphocytes, Tumor-Infiltrating, Signal Transduction, Tumor Burden.
- drug therapy : Melanoma.
- immunology : Lymphocytes, Tumor-Infiltrating, Melanoma.
- metabolism : Lymphocytes, Tumor-Infiltrating, Melanoma.
- methods : Immunotherapy.
- pathology : Melanoma.
- Humans, Molecular Targeted Therapy, Mutation.
Abstract
Therapies targeting the mitogen-activated protein kinase signaling pathway can induce profound tumor regression in patients with advanced BRAF-mutated melanoma. Most patients develop resistance after several months of treatment, which is typically followed by rapid disease progression and death. BRAF- and mitogen-activated protein kinase kinase (MEK)-targeted therapies were initially thought to exert their therapeutic effects through direct inhibition of signaling within the tumor cell, resulting in cell death. Recent evidence suggests that BRAF-targeted therapy also augments the host immune response to melanoma. This is characterized by enhanced expression of melanoma differentiation antigens, reduced levels of immunosuppressive cytokines in the micro environment, and a CD8 T-cell response and T-cell-mediated cytotoxicity. These changes are noted within days of starting therapy, correlate with tumor response, reverse with resistance, and occur in metastatic and advanced, operable disease. Enhanced PDL-1 expression by melanoma cells and increased markers of immune exhaustion, including PD-1 and TIM-1, have been identified, suggesting that the immune response is down-modulated before resistance occurs. These findings indicate that BRAF- and MEK-targeted therapies have multiple, complex, and interrelated mechanisms of action and validate the investigation of combination treatment strategies with targeted therapy and immune checkpoint inhibitors, as well as other therapies that modulate the immune microenvironment. They also lend support for clinical trials investigating preoperative and adjuvant BRAF-targeted therapy for high-risk, BRAF-mutated melanoma. Together, these studies will enhance our understanding of the mechanism of action of BRAF-targeted therapies and may identify additional opportunities to improve the outcome of patients with advanced melanoma.
DOI: 10.1615/CritRevOncog.2016017150
PubMed: 27481005
Affiliations:
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Most patients develop resistance after several months of treatment, which is typically followed by rapid disease progression and death. BRAF- and mitogen-activated protein kinase kinase (MEK)-targeted therapies were initially thought to exert their therapeutic effects through direct inhibition of signaling within the tumor cell, resulting in cell death. Recent evidence suggests that BRAF-targeted therapy also augments the host immune response to melanoma. This is characterized by enhanced expression of melanoma differentiation antigens, reduced levels of immunosuppressive cytokines in the micro environment, and a CD8 T-cell response and T-cell-mediated cytotoxicity. These changes are noted within days of starting therapy, correlate with tumor response, reverse with resistance, and occur in metastatic and advanced, operable disease. Enhanced PDL-1 expression by melanoma cells and increased markers of immune exhaustion, including PD-1 and TIM-1, have been identified, suggesting that the immune response is down-modulated before resistance occurs. These findings indicate that BRAF- and MEK-targeted therapies have multiple, complex, and interrelated mechanisms of action and validate the investigation of combination treatment strategies with targeted therapy and immune checkpoint inhibitors, as well as other therapies that modulate the immune microenvironment. They also lend support for clinical trials investigating preoperative and adjuvant BRAF-targeted therapy for high-risk, BRAF-mutated melanoma. Together, these studies will enhance our understanding of the mechanism of action of BRAF-targeted therapies and may identify additional opportunities to improve the outcome of patients with advanced melanoma.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27481005</PMID><DateCompleted><Year>2017</Year><Month>10</Month><Day>26</Day></DateCompleted><DateRevised><Year>2018</Year><Month>07</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0893-9675</ISSN><JournalIssue CitedMedium="Internet"><Volume>21</Volume><Issue>1-2</Issue><PubDate><Year>2016</Year></PubDate></JournalIssue><Title>Critical reviews in oncogenesis</Title><ISOAbbreviation>Crit Rev Oncog</ISOAbbreviation></Journal><ArticleTitle>Immune Responses to BRAF-Targeted Therapy in Melanoma: Is Targeted Therapy Immunotherapy?</ArticleTitle><Pagination><MedlinePgn>83-91</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1615/CritRevOncog.2016017150</ELocationID><Abstract><AbstractText>Therapies targeting the mitogen-activated protein kinase signaling pathway can induce profound tumor regression in patients with advanced BRAF-mutated melanoma. Most patients develop resistance after several months of treatment, which is typically followed by rapid disease progression and death. BRAF- and mitogen-activated protein kinase kinase (MEK)-targeted therapies were initially thought to exert their therapeutic effects through direct inhibition of signaling within the tumor cell, resulting in cell death. Recent evidence suggests that BRAF-targeted therapy also augments the host immune response to melanoma. This is characterized by enhanced expression of melanoma differentiation antigens, reduced levels of immunosuppressive cytokines in the micro environment, and a CD8 T-cell response and T-cell-mediated cytotoxicity. These changes are noted within days of starting therapy, correlate with tumor response, reverse with resistance, and occur in metastatic and advanced, operable disease. Enhanced PDL-1 expression by melanoma cells and increased markers of immune exhaustion, including PD-1 and TIM-1, have been identified, suggesting that the immune response is down-modulated before resistance occurs. These findings indicate that BRAF- and MEK-targeted therapies have multiple, complex, and interrelated mechanisms of action and validate the investigation of combination treatment strategies with targeted therapy and immune checkpoint inhibitors, as well as other therapies that modulate the immune microenvironment. They also lend support for clinical trials investigating preoperative and adjuvant BRAF-targeted therapy for high-risk, BRAF-mutated melanoma. Together, these studies will enhance our understanding of the mechanism of action of BRAF-targeted therapies and may identify additional opportunities to improve the outcome of patients with advanced melanoma.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kelley</LastName><ForeName>Mark C</ForeName><Initials>MC</Initials><AffiliationInfo><Affiliation>Innov8 Cancer Care LLC, 8199 Poplar Creek Road, Nashville, TN 37221.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D017418">Meta-Analysis</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Crit Rev 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MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000970" MajorTopicYN="N">Antineoplastic Agents</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D049109" MajorTopicYN="N">Cell Proliferation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007167" MajorTopicYN="N">Immunotherapy</DescriptorName><QualifierName UI="Q000379" MajorTopicYN="N">methods</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D016246" MajorTopicYN="N">Lymphocytes, Tumor-Infiltrating</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug 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UI="D047428" MajorTopicYN="N">Protein Kinase Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D048493" MajorTopicYN="N">Proto-Oncogene Proteins B-raf</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="Y">antagonists & inhibitors</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D047368" MajorTopicYN="N">Tumor Burden</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2016</Year><Month>8</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2016</Year><Month>8</Month><Day>3</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">27481005</ArticleId><ArticleId IdType="pii">3930394d2ef2dece,37d3e7c946ef14bc</ArticleId><ArticleId IdType="doi">10.1615/CritRevOncog.2016017150</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country><region><li>Tennessee</li></region></list><tree><country name="États-Unis"><region name="Tennessee"><name sortKey="Kelley, Mark C" sort="Kelley, Mark C" uniqKey="Kelley M" first="Mark C" last="Kelley">Mark C. 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