Genomic landscape of gastric cancer: molecular classification and potential targets
Gastric cancer imposes a considerable health burden worldwide, and its mortality ranks as the second highest for all types of cancers. The limited knowledge of the molecular mechanisms underlying gastric cancer tumorigenesis hinders the development of therapeutic strategies. However, ongoing collabo...
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Veröffentlicht in: | Science China. Life sciences 2017-02, Vol.60 (2), p.126-137 |
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description | Gastric cancer imposes a considerable health burden worldwide, and its mortality ranks as the second highest for all types of cancers. The limited knowledge of the molecular mechanisms underlying gastric cancer tumorigenesis hinders the development of therapeutic strategies. However, ongoing collaborative sequencing efforts facilitate molecular classification and unveil the genomic landscape of gastric cancer. Several new drivers and tumorigenic pathways in gastric cancer, including chromatin remodeling genes, RhoA-related pathways, TP53 dysregulation, activation of receptor tyrosine kinases, stem cell pathways and abnormal DNA methylation, have been revealed. These newly identified genomic alterations await translation into clinical di- agnosis and targeted therapies. Considering that loss-of-function mutations are intractable, synthetic lethality could be em- ployed when discussing feasible therapeutic strategies. Although many challenges remain to be tackled, we are optimistic re- garding improvements in the prognosis and treatment of gastric cancer in the near future. |
doi_str_mv | 10.1007/s11427-016-0034-1 |
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The limited knowledge of the molecular mechanisms underlying gastric cancer tumorigenesis hinders the development of therapeutic strategies. However, ongoing collaborative sequencing efforts facilitate molecular classification and unveil the genomic landscape of gastric cancer. Several new drivers and tumorigenic pathways in gastric cancer, including chromatin remodeling genes, RhoA-related pathways, TP53 dysregulation, activation of receptor tyrosine kinases, stem cell pathways and abnormal DNA methylation, have been revealed. These newly identified genomic alterations await translation into clinical di- agnosis and targeted therapies. Considering that loss-of-function mutations are intractable, synthetic lethality could be em- ployed when discussing feasible therapeutic strategies. Although many challenges remain to be tackled, we are optimistic re- garding improvements in the prognosis and treatment of gastric cancer in the near future.</description><identifier>ISSN: 1674-7305</identifier><identifier>EISSN: 1869-1889</identifier><identifier>DOI: 10.1007/s11427-016-0034-1</identifier><identifier>PMID: 27460193</identifier><language>eng</language><publisher>Beijing: Science China Press</publisher><subject>Biomedical and Life Sciences ; Chromatin Assembly and Disassembly ; DNA Methylation ; DNA甲基化 ; Gene Expression Regulation, Neoplastic ; Genomics - methods ; Humans ; Life Sciences ; Mutation ; Receptor Protein-Tyrosine Kinases - genetics ; Review ; rhoA GTP-Binding Protein - genetics ; Stem Cells - cytology ; Stomach Neoplasms - genetics ; Tumor Suppressor Protein p53 - genetics ; 临床诊断 ; 分子分类 ; 受体酪氨酸激酶 ; 基因组图谱 ; 胃癌 ; 靶向治疗 ; 靶点</subject><ispartof>Science China. Life sciences, 2017-02, Vol.60 (2), p.126-137</ispartof><rights>The Author(s) 2016</rights><rights>Science China Life Sciences is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-bf6f372e662378d109ba2d2c25292a1b7eab95a99bbcddd0372cb3f24b9bcd443</citedby><cites>FETCH-LOGICAL-c475t-bf6f372e662378d109ba2d2c25292a1b7eab95a99bbcddd0372cb3f24b9bcd443</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/60112X/60112X.jpg</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11427-016-0034-1$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11427-016-0034-1$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>313,314,780,784,792,27921,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27460193$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Guo, Jiawei</creatorcontrib><creatorcontrib>Yu, Weiwei</creatorcontrib><creatorcontrib>Su, Hui</creatorcontrib><creatorcontrib>Pang, Xiufeng</creatorcontrib><title>Genomic landscape of gastric cancer: molecular classification and potential targets</title><title>Science China. Life sciences</title><addtitle>Sci. China Life Sci</addtitle><addtitle>Sci China Life Sci</addtitle><description>Gastric cancer imposes a considerable health burden worldwide, and its mortality ranks as the second highest for all types of cancers. The limited knowledge of the molecular mechanisms underlying gastric cancer tumorigenesis hinders the development of therapeutic strategies. However, ongoing collaborative sequencing efforts facilitate molecular classification and unveil the genomic landscape of gastric cancer. Several new drivers and tumorigenic pathways in gastric cancer, including chromatin remodeling genes, RhoA-related pathways, TP53 dysregulation, activation of receptor tyrosine kinases, stem cell pathways and abnormal DNA methylation, have been revealed. These newly identified genomic alterations await translation into clinical di- agnosis and targeted therapies. Considering that loss-of-function mutations are intractable, synthetic lethality could be em- ployed when discussing feasible therapeutic strategies. Although many challenges remain to be tackled, we are optimistic re- garding improvements in the prognosis and treatment of gastric cancer in the near future.</description><subject>Biomedical and Life Sciences</subject><subject>Chromatin Assembly and Disassembly</subject><subject>DNA Methylation</subject><subject>DNA甲基化</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Genomics - methods</subject><subject>Humans</subject><subject>Life Sciences</subject><subject>Mutation</subject><subject>Receptor Protein-Tyrosine Kinases - genetics</subject><subject>Review</subject><subject>rhoA GTP-Binding Protein - genetics</subject><subject>Stem Cells - cytology</subject><subject>Stomach Neoplasms - genetics</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>临床诊断</subject><subject>分子分类</subject><subject>受体酪氨酸激酶</subject><subject>基因组图谱</subject><subject>胃癌</subject><subject>靶向治疗</subject><subject>靶点</subject><issn>1674-7305</issn><issn>1869-1889</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNqNkT1OxDAQhS0EAgQcgAZF0NAExj-x1yVC_ElINFBbtuMsQUm82EnBVTgLd-IKDNoFIQqEG1vj773x-BGyT-GEAqjTTKlgqgQqSwAuSrpGtulM6pLOZnodz1KJUnGotshezk-Ai3NgSm2SLaaEBKr5Nnm4CkPsW190dqizt4tQxKaY2zwmLHo7-JDe316LPnbBT51Nhe9szm3Teju2cShQViziGIaxtV0x2jQPY94lG43tcthb7Tvk4fLi_vy6vL27ujk_uy29UNVYukY2XLEgJeNqVlPQzrKaeVYxzSx1KlinK6u1c76ua0DWO94w4TQWhOA75Hjpu0jxeQp5NH2bfehwmBCnbPArqKqkAP0PlEnFmRAM0aNf6FOc0oCDIIV2GrQEpOiS8inmnEJjFqntbXoxFMxnQmaZkMGEzGdChqLmYOU8uT7U34qvPBBgSyDj1TAP6UfrP1wPVy95jMP8GXXfxlIhDJQJ_gE6zqdp</recordid><startdate>20170201</startdate><enddate>20170201</enddate><creator>Guo, Jiawei</creator><creator>Yu, Weiwei</creator><creator>Su, Hui</creator><creator>Pang, Xiufeng</creator><general>Science China Press</general><general>Springer Nature B.V</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>~WA</scope><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>7QP</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20170201</creationdate><title>Genomic landscape of gastric cancer: molecular classification and potential targets</title><author>Guo, Jiawei ; 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subjects | Biomedical and Life Sciences Chromatin Assembly and Disassembly DNA Methylation DNA甲基化 Gene Expression Regulation, Neoplastic Genomics - methods Humans Life Sciences Mutation Receptor Protein-Tyrosine Kinases - genetics Review rhoA GTP-Binding Protein - genetics Stem Cells - cytology Stomach Neoplasms - genetics Tumor Suppressor Protein p53 - genetics 临床诊断 分子分类 受体酪氨酸激酶 基因组图谱 胃癌 靶向治疗 靶点 |
title | Genomic landscape of gastric cancer: molecular classification and potential targets |
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