Identification of Potential Immune Checkpoint Inhibitor Targets in Gliomas via Bioinformatic Analyses
Background. Glioma is a common tumor originating from the glial cells of the brain. Immune checkpoint inhibitors can potentially be used to treat gliomas, although no drug is currently approved. Methods. The expression levels of the immune checkpoint genes in glioma and normal tissues, and their cor...
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| description | Background. Glioma is a common tumor originating from the glial cells of the brain. Immune checkpoint inhibitors can potentially be used to treat gliomas, although no drug is currently approved. Methods. The expression levels of the immune checkpoint genes in glioma and normal tissues, and their correlation with the IDH mutation status and complete 1p/19q codeletion, were analyzed using The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Survival analyses were conducted using the CGGA database. Protein-protein interaction and functional enrichment analyses were performed via the STRING database using GO, KEGG, and Reactome pathways. The correlation between the immune checkpoints and the immune cell infiltration was determined using the TISIDB and TIMER databases. Results. HAVCR2 was overexpressed in the gliomas compared to normal brain tissues, as well as in the high-grade glioma patients and significantly downregulated in IDH mutant or 1p/19q codeletion patients. Overexpression of HAVCR2 was associated with poor survival in tumor grades II, III, and IV and was the most correlated with immune infiltration of B and T cells. Conclusion. HAVCR2 can be a potential therapeutic target for cancer immunotherapy for glioma patients. |
| doi_str_mv | 10.1155/2022/1734847 |
| format | Article |
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Glioma is a common tumor originating from the glial cells of the brain. Immune checkpoint inhibitors can potentially be used to treat gliomas, although no drug is currently approved. Methods. The expression levels of the immune checkpoint genes in glioma and normal tissues, and their correlation with the IDH mutation status and complete 1p/19q codeletion, were analyzed using The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Survival analyses were conducted using the CGGA database. Protein-protein interaction and functional enrichment analyses were performed via the STRING database using GO, KEGG, and Reactome pathways. The correlation between the immune checkpoints and the immune cell infiltration was determined using the TISIDB and TIMER databases. Results. HAVCR2 was overexpressed in the gliomas compared to normal brain tissues, as well as in the high-grade glioma patients and significantly downregulated in IDH mutant or 1p/19q codeletion patients. Overexpression of HAVCR2 was associated with poor survival in tumor grades II, III, and IV and was the most correlated with immune infiltration of B and T cells. Conclusion. HAVCR2 can be a potential therapeutic target for cancer immunotherapy for glioma patients.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2022/1734847</identifier><identifier>PMID: 35198632</identifier><language>eng</language><publisher>United States: Hindawi</publisher><subject>Brain ; Brain cancer ; Brain Neoplasms - drug therapy ; Brain Neoplasms - genetics ; Brain tumors ; Cancer ; Cancer immunotherapy ; Cancer therapies ; Care and treatment ; Chromosomes ; Computational Biology ; Correlation ; Databases, Genetic ; Datasets ; Gender ; Gene expression ; Genetic aspects ; Genomes ; Glial cells ; Glioma ; Glioma - drug therapy ; Glioma - genetics ; Gliomas ; Hepatitis A Virus Cellular Receptor 2 ; Humans ; Immune checkpoint ; Immune checkpoint inhibitors ; Immune Checkpoint Inhibitors - pharmacology ; Immune system ; Immunotherapy ; Infiltration ; Lymphocytes ; Lymphocytes T ; Medical prognosis ; Metastases ; Monoclonal antibodies ; Mutation ; Oncology, Experimental ; Protein interaction ; Protein Interaction Maps ; Proteins ; Survival ; Survival Analysis ; Therapeutic targets ; Tumors</subject><ispartof>BioMed research international, 2022, Vol.2022 (1), p.1734847-1734847</ispartof><rights>Copyright © 2022 Mengmeng Ding et al.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>Copyright © 2022 Mengmeng Ding et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2022 Mengmeng Ding et al. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c476t-c9723ca75916a531ff11a41b2b6aa638b6e78863890a1a553d296edc7ac299d3</citedby><cites>FETCH-LOGICAL-c476t-c9723ca75916a531ff11a41b2b6aa638b6e78863890a1a553d296edc7ac299d3</cites><orcidid>0000-0002-4102-4012</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8860561/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8860561/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,4010,27900,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35198632$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Aziz, Aziz ur Rehman</contributor><creatorcontrib>Ding, Mengmeng</creatorcontrib><creatorcontrib>Li, Yong-an</creatorcontrib><creatorcontrib>Lu, Zhimin</creatorcontrib><creatorcontrib>Hou, Guoxin</creatorcontrib><title>Identification of Potential Immune Checkpoint Inhibitor Targets in Gliomas via Bioinformatic Analyses</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Background. Glioma is a common tumor originating from the glial cells of the brain. Immune checkpoint inhibitors can potentially be used to treat gliomas, although no drug is currently approved. Methods. The expression levels of the immune checkpoint genes in glioma and normal tissues, and their correlation with the IDH mutation status and complete 1p/19q codeletion, were analyzed using The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Survival analyses were conducted using the CGGA database. Protein-protein interaction and functional enrichment analyses were performed via the STRING database using GO, KEGG, and Reactome pathways. The correlation between the immune checkpoints and the immune cell infiltration was determined using the TISIDB and TIMER databases. Results. HAVCR2 was overexpressed in the gliomas compared to normal brain tissues, as well as in the high-grade glioma patients and significantly downregulated in IDH mutant or 1p/19q codeletion patients. Overexpression of HAVCR2 was associated with poor survival in tumor grades II, III, and IV and was the most correlated with immune infiltration of B and T cells. Conclusion. HAVCR2 can be a potential therapeutic target for cancer immunotherapy for glioma patients.</description><subject>Brain</subject><subject>Brain cancer</subject><subject>Brain Neoplasms - drug therapy</subject><subject>Brain Neoplasms - genetics</subject><subject>Brain tumors</subject><subject>Cancer</subject><subject>Cancer immunotherapy</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Chromosomes</subject><subject>Computational Biology</subject><subject>Correlation</subject><subject>Databases, Genetic</subject><subject>Datasets</subject><subject>Gender</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Glial cells</subject><subject>Glioma</subject><subject>Glioma - drug therapy</subject><subject>Glioma - genetics</subject><subject>Gliomas</subject><subject>Hepatitis A Virus Cellular Receptor 2</subject><subject>Humans</subject><subject>Immune checkpoint</subject><subject>Immune checkpoint inhibitors</subject><subject>Immune Checkpoint Inhibitors - pharmacology</subject><subject>Immune system</subject><subject>Immunotherapy</subject><subject>Infiltration</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Medical prognosis</subject><subject>Metastases</subject><subject>Monoclonal antibodies</subject><subject>Mutation</subject><subject>Oncology, Experimental</subject><subject>Protein interaction</subject><subject>Protein Interaction Maps</subject><subject>Proteins</subject><subject>Survival</subject><subject>Survival Analysis</subject><subject>Therapeutic targets</subject><subject>Tumors</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUuP0zAUhS0EYkZldqyRJTZIUMaP-JENUqlgqDQSLLq3bhyn9ZDYxU4Gzb_HoaU8Fnhj6_rTuffcg9BzSt5SKsQ1I4xdU8UrXalH6JJxWi0lrejj85vzC3SV8x0pR1NJavkUXXBBay05u0Ru07ow-s5bGH0MOHb4SxznEvR4MwxTcHi9d_brIfow4k3Y-8aPMeEtpJ0bM_YB3_Q-DpDxvQf83heui2kochavAvQP2eVn6EkHfXZXp3uBth8_bNeflrefbzbr1e3SVkqOS1srxi0oUVMJgtOuoxQq2rBGAkiuG-mULnPrmgAFIXjLaulaq8Cyum75Ar07yh6mZij1YiNBbw7JD5AeTARv_v4Jfm928d4UUSLKrhbo1UkgxW-Ty6MZfLau7yG4OGXDys40YYqRgr78B72LUyp-f1JcSKGk_E3toHdm3kzpa2dRs5K1khWXWhfqzZGyKeacXHcemRIz52zmnM0p54K_-NPmGf6VagFeH4G9Dy189_-X-wHnqa8g</recordid><startdate>2022</startdate><enddate>2022</enddate><creator>Ding, Mengmeng</creator><creator>Li, Yong-an</creator><creator>Lu, Zhimin</creator><creator>Hou, Guoxin</creator><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-4102-4012</orcidid></search><sort><creationdate>2022</creationdate><title>Identification of Potential Immune Checkpoint Inhibitor Targets in Gliomas via Bioinformatic Analyses</title><author>Ding, Mengmeng ; Li, Yong-an ; Lu, Zhimin ; Hou, Guoxin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-c9723ca75916a531ff11a41b2b6aa638b6e78863890a1a553d296edc7ac299d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Brain</topic><topic>Brain cancer</topic><topic>Brain Neoplasms - drug therapy</topic><topic>Brain Neoplasms - genetics</topic><topic>Brain tumors</topic><topic>Cancer</topic><topic>Cancer immunotherapy</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Chromosomes</topic><topic>Computational Biology</topic><topic>Correlation</topic><topic>Databases, Genetic</topic><topic>Datasets</topic><topic>Gender</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Glial cells</topic><topic>Glioma</topic><topic>Glioma - drug therapy</topic><topic>Glioma - genetics</topic><topic>Gliomas</topic><topic>Hepatitis A Virus Cellular Receptor 2</topic><topic>Humans</topic><topic>Immune checkpoint</topic><topic>Immune checkpoint inhibitors</topic><topic>Immune Checkpoint Inhibitors - pharmacology</topic><topic>Immune system</topic><topic>Immunotherapy</topic><topic>Infiltration</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Medical prognosis</topic><topic>Metastases</topic><topic>Monoclonal antibodies</topic><topic>Mutation</topic><topic>Oncology, Experimental</topic><topic>Protein interaction</topic><topic>Protein Interaction Maps</topic><topic>Proteins</topic><topic>Survival</topic><topic>Survival Analysis</topic><topic>Therapeutic targets</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ding, Mengmeng</creatorcontrib><creatorcontrib>Li, Yong-an</creatorcontrib><creatorcontrib>Lu, Zhimin</creatorcontrib><creatorcontrib>Hou, Guoxin</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</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>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Middle East & Africa Database</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Publicly Available Content Database</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 China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ding, Mengmeng</au><au>Li, Yong-an</au><au>Lu, Zhimin</au><au>Hou, Guoxin</au><au>Aziz, Aziz ur Rehman</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Identification of Potential Immune Checkpoint Inhibitor Targets in Gliomas via Bioinformatic Analyses</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2022</date><risdate>2022</risdate><volume>2022</volume><issue>1</issue><spage>1734847</spage><epage>1734847</epage><pages>1734847-1734847</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Background. Glioma is a common tumor originating from the glial cells of the brain. Immune checkpoint inhibitors can potentially be used to treat gliomas, although no drug is currently approved. Methods. The expression levels of the immune checkpoint genes in glioma and normal tissues, and their correlation with the IDH mutation status and complete 1p/19q codeletion, were analyzed using The Cancer Genome Atlas (TCGA) and the Chinese Glioma Genome Atlas (CGGA) databases. Survival analyses were conducted using the CGGA database. Protein-protein interaction and functional enrichment analyses were performed via the STRING database using GO, KEGG, and Reactome pathways. The correlation between the immune checkpoints and the immune cell infiltration was determined using the TISIDB and TIMER databases. Results. HAVCR2 was overexpressed in the gliomas compared to normal brain tissues, as well as in the high-grade glioma patients and significantly downregulated in IDH mutant or 1p/19q codeletion patients. Overexpression of HAVCR2 was associated with poor survival in tumor grades II, III, and IV and was the most correlated with immune infiltration of B and T cells. Conclusion. HAVCR2 can be a potential therapeutic target for cancer immunotherapy for glioma patients.</abstract><cop>United States</cop><pub>Hindawi</pub><pmid>35198632</pmid><doi>10.1155/2022/1734847</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-4102-4012</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Brain Brain cancer Brain Neoplasms - drug therapy Brain Neoplasms - genetics Brain tumors Cancer Cancer immunotherapy Cancer therapies Care and treatment Chromosomes Computational Biology Correlation Databases, Genetic Datasets Gender Gene expression Genetic aspects Genomes Glial cells Glioma Glioma - drug therapy Glioma - genetics Gliomas Hepatitis A Virus Cellular Receptor 2 Humans Immune checkpoint Immune checkpoint inhibitors Immune Checkpoint Inhibitors - pharmacology Immune system Immunotherapy Infiltration Lymphocytes Lymphocytes T Medical prognosis Metastases Monoclonal antibodies Mutation Oncology, Experimental Protein interaction Protein Interaction Maps Proteins Survival Survival Analysis Therapeutic targets Tumors |
| title | Identification of Potential Immune Checkpoint Inhibitor Targets in Gliomas via Bioinformatic Analyses |
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