Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma
Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via...
Gespeichert in:
| Veröffentlicht in: | Scientific reports 2016-02, Vol.6 (1), p.21678-21678, Article 21678 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 21678 |
|---|---|
| container_issue | 1 |
| container_start_page | 21678 |
| container_title | Scientific reports |
| container_volume | 6 |
| creator | Ritter, Cathrin Fan, Kaiji Paulson, Kelly G. Nghiem, Paul Schrama, David Becker, Jürgen C. |
| description | Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors
in situ
and are completely absent on MCC cell lines
in vitro
. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both
in vitro
and
in vivo
. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs. |
| doi_str_mv | 10.1038/srep21678 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4763224</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1767916405</sourcerecordid><originalsourceid>FETCH-LOGICAL-c438t-7fa118fb71490c314bbf02e27962f804c2fc61c6f178e09a0f3c4b532a97001f3</originalsourceid><addsrcrecordid>eNplkVFrFDEQx0NRbKl98AuUQF-qsJpkc8nmpdAeaguVQtHnkM1Ntml3kzXZPfDVT27Oq8epeUiGmR__mckfoTeUvKekbj7kBCOjQjYH6IgRvqhYzdiLvfgQneT8SMpZMMWpeoUOmVCEKaaO0M97WEPKpsfRYRh9BwEmb3H2PQTrQ7fJf7leYtubnPENtg_GhypBbyZY4THFCXzAl9iEFb7CfiiZNeQSDHMAnMDGLvjJx_BbCNIT9NhCXy6Tin4czGv00pk-w8nze4y-ffr4dXld3d59vlle3laW181USWcobVwrKVfE1pS3rSMMmFSCuYZwy5wV1ApHZQNEGeJqy9tFzYyShFBXH6OLre44twOsLIQpmV6PyQ8m_dDReP13JfgH3cW15lKUb-RF4PxZIMXvM-RJDz5vdjEB4pw1lUIqKjhZFPTsH_QxzimU9TRtVKOKIBGFerulbIq5-Oh2w1CiN-bqnbmFPd2ffkf-sbIA77ZALqXQQdpr-Z_aL13-rt4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1898963206</pqid></control><display><type>article</type><title>Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Nature Free</source><source>PubMed Central</source><source>Springer Nature OA/Free Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Ritter, Cathrin ; Fan, Kaiji ; Paulson, Kelly G. ; Nghiem, Paul ; Schrama, David ; Becker, Jürgen C.</creator><creatorcontrib>Ritter, Cathrin ; Fan, Kaiji ; Paulson, Kelly G. ; Nghiem, Paul ; Schrama, David ; Becker, Jürgen C.</creatorcontrib><description>Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors
in situ
and are completely absent on MCC cell lines
in vitro
. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both
in vitro
and
in vivo
. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/srep21678</identifier><identifier>PMID: 26902929</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>14/105 ; 38/39 ; 38/77 ; 631/250/251 ; 631/67/580/1884/2323 ; 64/60 ; 82/51 ; 82/80 ; 96/31 ; Acetylation ; Acetylation - drug effects ; Animals ; Carcinoma, Merkel Cell - drug therapy ; Carcinoma, Merkel Cell - genetics ; Carcinoma, Merkel Cell - immunology ; Carcinoma, Merkel Cell - pathology ; Cell Line, Tumor ; Cytotoxicity, Immunologic ; Epigenetics ; Gene Silencing - drug effects ; Gene Silencing - immunology ; Histocompatibility Antigens Class I - genetics ; Histocompatibility Antigens Class I - immunology ; Histone Deacetylase Inhibitors - pharmacology ; Histone Deacetylases - genetics ; Histone Deacetylases - immunology ; Histones - genetics ; Histones - immunology ; Humanities and Social Sciences ; Humans ; Hydroxamic Acids - pharmacology ; Immune system ; Immunogenicity ; Killer Cells, Lymphokine-Activated - cytology ; Killer Cells, Lymphokine-Activated - drug effects ; Killer Cells, Lymphokine-Activated - immunology ; Lysis ; Major histocompatibility complex ; Mice ; Mice, Inbred NOD ; multidisciplinary ; Natural killer cells ; NK Cell Lectin-Like Receptor Subfamily K - genetics ; NK Cell Lectin-Like Receptor Subfamily K - immunology ; Plicamycin - analogs & derivatives ; Plicamycin - pharmacology ; Promoter Regions, Genetic - drug effects ; Science ; Signal Transduction ; Skin cancer ; Skin Neoplasms - drug therapy ; Skin Neoplasms - genetics ; Skin Neoplasms - immunology ; Skin Neoplasms - pathology ; Tumors ; Xenograft Model Antitumor Assays</subject><ispartof>Scientific reports, 2016-02, Vol.6 (1), p.21678-21678, Article 21678</ispartof><rights>The Author(s) 2016</rights><rights>Copyright Nature Publishing Group Feb 2016</rights><rights>Copyright © 2016, Macmillan Publishers Limited 2016 Macmillan Publishers Limited</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c438t-7fa118fb71490c314bbf02e27962f804c2fc61c6f178e09a0f3c4b532a97001f3</citedby><cites>FETCH-LOGICAL-c438t-7fa118fb71490c314bbf02e27962f804c2fc61c6f178e09a0f3c4b532a97001f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763224/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4763224/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,27929,27930,41125,42194,51581,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26902929$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ritter, Cathrin</creatorcontrib><creatorcontrib>Fan, Kaiji</creatorcontrib><creatorcontrib>Paulson, Kelly G.</creatorcontrib><creatorcontrib>Nghiem, Paul</creatorcontrib><creatorcontrib>Schrama, David</creatorcontrib><creatorcontrib>Becker, Jürgen C.</creatorcontrib><title>Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors
in situ
and are completely absent on MCC cell lines
in vitro
. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both
in vitro
and
in vivo
. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.</description><subject>14/105</subject><subject>38/39</subject><subject>38/77</subject><subject>631/250/251</subject><subject>631/67/580/1884/2323</subject><subject>64/60</subject><subject>82/51</subject><subject>82/80</subject><subject>96/31</subject><subject>Acetylation</subject><subject>Acetylation - drug effects</subject><subject>Animals</subject><subject>Carcinoma, Merkel Cell - drug therapy</subject><subject>Carcinoma, Merkel Cell - genetics</subject><subject>Carcinoma, Merkel Cell - immunology</subject><subject>Carcinoma, Merkel Cell - pathology</subject><subject>Cell Line, Tumor</subject><subject>Cytotoxicity, Immunologic</subject><subject>Epigenetics</subject><subject>Gene Silencing - drug effects</subject><subject>Gene Silencing - immunology</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>Histocompatibility Antigens Class I - immunology</subject><subject>Histone Deacetylase Inhibitors - pharmacology</subject><subject>Histone Deacetylases - genetics</subject><subject>Histone Deacetylases - immunology</subject><subject>Histones - genetics</subject><subject>Histones - immunology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Immune system</subject><subject>Immunogenicity</subject><subject>Killer Cells, Lymphokine-Activated - cytology</subject><subject>Killer Cells, Lymphokine-Activated - drug effects</subject><subject>Killer Cells, Lymphokine-Activated - immunology</subject><subject>Lysis</subject><subject>Major histocompatibility complex</subject><subject>Mice</subject><subject>Mice, Inbred NOD</subject><subject>multidisciplinary</subject><subject>Natural killer cells</subject><subject>NK Cell Lectin-Like Receptor Subfamily K - genetics</subject><subject>NK Cell Lectin-Like Receptor Subfamily K - immunology</subject><subject>Plicamycin - analogs & derivatives</subject><subject>Plicamycin - pharmacology</subject><subject>Promoter Regions, Genetic - drug effects</subject><subject>Science</subject><subject>Signal Transduction</subject><subject>Skin cancer</subject><subject>Skin Neoplasms - drug therapy</subject><subject>Skin Neoplasms - genetics</subject><subject>Skin Neoplasms - immunology</subject><subject>Skin Neoplasms - pathology</subject><subject>Tumors</subject><subject>Xenograft Model Antitumor Assays</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNplkVFrFDEQx0NRbKl98AuUQF-qsJpkc8nmpdAeaguVQtHnkM1Ntml3kzXZPfDVT27Oq8epeUiGmR__mckfoTeUvKekbj7kBCOjQjYH6IgRvqhYzdiLvfgQneT8SMpZMMWpeoUOmVCEKaaO0M97WEPKpsfRYRh9BwEmb3H2PQTrQ7fJf7leYtubnPENtg_GhypBbyZY4THFCXzAl9iEFb7CfiiZNeQSDHMAnMDGLvjJx_BbCNIT9NhCXy6Tin4czGv00pk-w8nze4y-ffr4dXld3d59vlle3laW181USWcobVwrKVfE1pS3rSMMmFSCuYZwy5wV1ApHZQNEGeJqy9tFzYyShFBXH6OLre44twOsLIQpmV6PyQ8m_dDReP13JfgH3cW15lKUb-RF4PxZIMXvM-RJDz5vdjEB4pw1lUIqKjhZFPTsH_QxzimU9TRtVKOKIBGFerulbIq5-Oh2w1CiN-bqnbmFPd2ffkf-sbIA77ZALqXQQdpr-Z_aL13-rt4</recordid><startdate>20160223</startdate><enddate>20160223</enddate><creator>Ritter, Cathrin</creator><creator>Fan, Kaiji</creator><creator>Paulson, Kelly G.</creator><creator>Nghiem, Paul</creator><creator>Schrama, David</creator><creator>Becker, Jürgen C.</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20160223</creationdate><title>Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma</title><author>Ritter, Cathrin ; Fan, Kaiji ; Paulson, Kelly G. ; Nghiem, Paul ; Schrama, David ; Becker, Jürgen C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c438t-7fa118fb71490c314bbf02e27962f804c2fc61c6f178e09a0f3c4b532a97001f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>14/105</topic><topic>38/39</topic><topic>38/77</topic><topic>631/250/251</topic><topic>631/67/580/1884/2323</topic><topic>64/60</topic><topic>82/51</topic><topic>82/80</topic><topic>96/31</topic><topic>Acetylation</topic><topic>Acetylation - drug effects</topic><topic>Animals</topic><topic>Carcinoma, Merkel Cell - drug therapy</topic><topic>Carcinoma, Merkel Cell - genetics</topic><topic>Carcinoma, Merkel Cell - immunology</topic><topic>Carcinoma, Merkel Cell - pathology</topic><topic>Cell Line, Tumor</topic><topic>Cytotoxicity, Immunologic</topic><topic>Epigenetics</topic><topic>Gene Silencing - drug effects</topic><topic>Gene Silencing - immunology</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>Histocompatibility Antigens Class I - immunology</topic><topic>Histone Deacetylase Inhibitors - pharmacology</topic><topic>Histone Deacetylases - genetics</topic><topic>Histone Deacetylases - immunology</topic><topic>Histones - genetics</topic><topic>Histones - immunology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Immune system</topic><topic>Immunogenicity</topic><topic>Killer Cells, Lymphokine-Activated - cytology</topic><topic>Killer Cells, Lymphokine-Activated - drug effects</topic><topic>Killer Cells, Lymphokine-Activated - immunology</topic><topic>Lysis</topic><topic>Major histocompatibility complex</topic><topic>Mice</topic><topic>Mice, Inbred NOD</topic><topic>multidisciplinary</topic><topic>Natural killer cells</topic><topic>NK Cell Lectin-Like Receptor Subfamily K - genetics</topic><topic>NK Cell Lectin-Like Receptor Subfamily K - immunology</topic><topic>Plicamycin - analogs & derivatives</topic><topic>Plicamycin - pharmacology</topic><topic>Promoter Regions, Genetic - drug effects</topic><topic>Science</topic><topic>Signal Transduction</topic><topic>Skin cancer</topic><topic>Skin Neoplasms - drug therapy</topic><topic>Skin Neoplasms - genetics</topic><topic>Skin Neoplasms - immunology</topic><topic>Skin Neoplasms - pathology</topic><topic>Tumors</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ritter, Cathrin</creatorcontrib><creatorcontrib>Fan, Kaiji</creatorcontrib><creatorcontrib>Paulson, Kelly G.</creatorcontrib><creatorcontrib>Nghiem, Paul</creatorcontrib><creatorcontrib>Schrama, David</creatorcontrib><creatorcontrib>Becker, Jürgen C.</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ritter, Cathrin</au><au>Fan, Kaiji</au><au>Paulson, Kelly G.</au><au>Nghiem, Paul</au><au>Schrama, David</au><au>Becker, Jürgen C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2016-02-23</date><risdate>2016</risdate><volume>6</volume><issue>1</issue><spage>21678</spage><epage>21678</epage><pages>21678-21678</pages><artnum>21678</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Merkel cell carcinoma (MCC) is a virally associated cancer characterized by its aggressive behavior and strong immunogenicity. Both viral infection and malignant transformation induce expression of MHC class I chain-related protein (MIC) A and B, which signal stress to cells of the immune system via Natural Killer group 2D (NKG2D) resulting in elimination of target cells. However, despite transformation and the continued presence of virally-encoded proteins, MICs are only expressed in a minority of MCC tumors
in situ
and are completely absent on MCC cell lines
in vitro
. This lack of MIC expression was due to epigenetic silencing via MIC promoter hypo-acetylation; indeed, MIC expression was re-induced by pharmacological inhibition of histone deacetylases (HDACs) both
in vitro
and
in vivo
. This re-induction of MICs rendered MCC cells more sensitive to immune-mediated lysis. Thus, epigenetic silencing of MICs is an important immune escape mechanism of MCCs.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>26902929</pmid><doi>10.1038/srep21678</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2045-2322 |
| ispartof | Scientific reports, 2016-02, Vol.6 (1), p.21678-21678, Article 21678 |
| issn | 2045-2322 2045-2322 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4763224 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Nature Free; PubMed Central; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | 14/105 38/39 38/77 631/250/251 631/67/580/1884/2323 64/60 82/51 82/80 96/31 Acetylation Acetylation - drug effects Animals Carcinoma, Merkel Cell - drug therapy Carcinoma, Merkel Cell - genetics Carcinoma, Merkel Cell - immunology Carcinoma, Merkel Cell - pathology Cell Line, Tumor Cytotoxicity, Immunologic Epigenetics Gene Silencing - drug effects Gene Silencing - immunology Histocompatibility Antigens Class I - genetics Histocompatibility Antigens Class I - immunology Histone Deacetylase Inhibitors - pharmacology Histone Deacetylases - genetics Histone Deacetylases - immunology Histones - genetics Histones - immunology Humanities and Social Sciences Humans Hydroxamic Acids - pharmacology Immune system Immunogenicity Killer Cells, Lymphokine-Activated - cytology Killer Cells, Lymphokine-Activated - drug effects Killer Cells, Lymphokine-Activated - immunology Lysis Major histocompatibility complex Mice Mice, Inbred NOD multidisciplinary Natural killer cells NK Cell Lectin-Like Receptor Subfamily K - genetics NK Cell Lectin-Like Receptor Subfamily K - immunology Plicamycin - analogs & derivatives Plicamycin - pharmacology Promoter Regions, Genetic - drug effects Science Signal Transduction Skin cancer Skin Neoplasms - drug therapy Skin Neoplasms - genetics Skin Neoplasms - immunology Skin Neoplasms - pathology Tumors Xenograft Model Antitumor Assays |
| title | Reversal of epigenetic silencing of MHC class I chain-related protein A and B improves immune recognition of Merkel cell carcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-13T02%3A41%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Reversal%20of%20epigenetic%20silencing%20of%20MHC%20class%20I%20chain-related%20protein%20A%20and%20B%20improves%20immune%20recognition%20of%20Merkel%20cell%20carcinoma&rft.jtitle=Scientific%20reports&rft.au=Ritter,%20Cathrin&rft.date=2016-02-23&rft.volume=6&rft.issue=1&rft.spage=21678&rft.epage=21678&rft.pages=21678-21678&rft.artnum=21678&rft.issn=2045-2322&rft.eissn=2045-2322&rft_id=info:doi/10.1038/srep21678&rft_dat=%3Cproquest_pubme%3E1767916405%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1898963206&rft_id=info:pmid/26902929&rfr_iscdi=true |