Landscape of somatic mutations in gastric cancer assessed using next-generation sequencing analysis
Gastric cancer is a highly heterogeneous disease and the second leading cause of cancer-associated mortality. However, the genomic basis of gastric cancer is not completely understood and the underlying genetic heterogeneity has not been well studied. In the present study, 1,021 genes were sequenced...
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Veröffentlicht in: | Oncology letters 2018-10, Vol.16 (4), p.4863-4870 |
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description | Gastric cancer is a highly heterogeneous disease and the second leading cause of cancer-associated mortality. However, the genomic basis of gastric cancer is not completely understood and the underlying genetic heterogeneity has not been well studied. In the present study, 1,021 genes were sequenced and the somatic mutations of 45 formalin-fixed, paraffin-embedded gastric adenocarcinoma samples were assessed using next-generation sequencing technologies. In the present study, a median sequencing coverage depth of 708-fold was achieved. Somatic genomic alterations were detected in 37/45 patients (82.4%) and the most frequent genetic alterations identified were tumor protein P53 (TP53) gene mutations. Mutations in MLL4, ERBB3, FBXW7, MLL3, MTOR, NOTCH1, PIK3CA, KRAS, ERBB4 and EGFR were also detected. Patients with TP53 mutations had a higher number of somatic mutations, and the total number of somatic mutations was weakly correlated with patient age. These results provided data on the intratumoral heterogeneity of gastric cancer and may be used in order to develop personalized cancer therapy. |
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However, the genomic basis of gastric cancer is not completely understood and the underlying genetic heterogeneity has not been well studied. In the present study, 1,021 genes were sequenced and the somatic mutations of 45 formalin-fixed, paraffin-embedded gastric adenocarcinoma samples were assessed using next-generation sequencing technologies. In the present study, a median sequencing coverage depth of 708-fold was achieved. Somatic genomic alterations were detected in 37/45 patients (82.4%) and the most frequent genetic alterations identified were tumor protein P53 (TP53) gene mutations. Mutations in MLL4, ERBB3, FBXW7, MLL3, MTOR, NOTCH1, PIK3CA, KRAS, ERBB4 and EGFR were also detected. Patients with TP53 mutations had a higher number of somatic mutations, and the total number of somatic mutations was weakly correlated with patient age. These results provided data on the intratumoral heterogeneity of gastric cancer and may be used in order to develop personalized cancer therapy.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2018.9314</identifier><identifier>PMID: 30250552</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Cancer therapies ; Care and treatment ; Deoxyribonucleic acid ; Development and progression ; DNA ; Gastric cancer ; Gene mutation ; Genes ; Genetic aspects ; Genomes ; Growth factors ; Health aspects ; Histology ; Methods ; Mutation ; Oncology ; Patient outcomes ; Patients ; Precision medicine ; Proteins ; Stomach cancer ; Studies ; Tumor proteins</subject><ispartof>Oncology letters, 2018-10, Vol.16 (4), p.4863-4870</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Pan et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c510t-83d1063356205f4abe45c85a6aecf78cd3497355d612592ed087dcd5f2b88a6d3</citedby><cites>FETCH-LOGICAL-c510t-83d1063356205f4abe45c85a6aecf78cd3497355d612592ed087dcd5f2b88a6d3</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/PMC6144630/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6144630/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30250552$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Xuan</creatorcontrib><creatorcontrib>Ji, Xiaozhi</creatorcontrib><creatorcontrib>Zhang, Renmin</creatorcontrib><creatorcontrib>Zhou, Zhaofei</creatorcontrib><creatorcontrib>Zhong, Yuejiao</creatorcontrib><creatorcontrib>Peng, Wei</creatorcontrib><creatorcontrib>Sun, Ning</creatorcontrib><creatorcontrib>Xu, Xinyu</creatorcontrib><creatorcontrib>Xia, Lei</creatorcontrib><creatorcontrib>Li, Pansong</creatorcontrib><creatorcontrib>Lu, Jianwei</creatorcontrib><creatorcontrib>Tu, Jing</creatorcontrib><title>Landscape of somatic mutations in gastric cancer assessed using next-generation sequencing analysis</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Gastric cancer is a highly heterogeneous disease and the second leading cause of cancer-associated mortality. However, the genomic basis of gastric cancer is not completely understood and the underlying genetic heterogeneity has not been well studied. In the present study, 1,021 genes were sequenced and the somatic mutations of 45 formalin-fixed, paraffin-embedded gastric adenocarcinoma samples were assessed using next-generation sequencing technologies. In the present study, a median sequencing coverage depth of 708-fold was achieved. Somatic genomic alterations were detected in 37/45 patients (82.4%) and the most frequent genetic alterations identified were tumor protein P53 (TP53) gene mutations. Mutations in MLL4, ERBB3, FBXW7, MLL3, MTOR, NOTCH1, PIK3CA, KRAS, ERBB4 and EGFR were also detected. Patients with TP53 mutations had a higher number of somatic mutations, and the total number of somatic mutations was weakly correlated with patient age. These results provided data on the intratumoral heterogeneity of gastric cancer and may be used in order to develop personalized cancer therapy.</description><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>Gastric cancer</subject><subject>Gene mutation</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Growth factors</subject><subject>Health aspects</subject><subject>Histology</subject><subject>Methods</subject><subject>Mutation</subject><subject>Oncology</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Precision medicine</subject><subject>Proteins</subject><subject>Stomach cancer</subject><subject>Studies</subject><subject>Tumor proteins</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkt9rFDEQxxdRbKl981kWBPHBPfNjk82-CKWoLRz4os8hl8zepWSTM7Nb7H9vtq1nT0wCE2Y-M2Em36p6TcmKq559TGHFCFWrntP2WXVKu541lCj2_HDv2pPqHPGGlCUkVUq-rE44YYIIwU4ruzbRoTV7qNNQYxrN5G09zlOxKWLtY701OOXitCZayLVBhHJcPaOP2zrCr6nZQoR8n1Ej_Jwh2iVkogl36PFV9WIwAeH80Z5VP758_n551ay_fb2-vFg3VlAyNYo7SiTnQjIihtZsoBVWCSMN2KFT1vG277gQTlImegaOqM5ZJwa2UcpIx8-qTw919_NmBGchTtkEvc9-NPlOJ-P1cST6nd6mWy1p20pOSoH3jwVyKl3gpEePFkIwEdKMmlHKaF_m3hb07T_oTZpzaXihSE9kzzn7S21NAO3jkMq7dimqL4SQqqNE9IVa_Ycq28HobYow-OI_Snj3JGEHJkw7TGG-_7Jj8MMDaHNCzDAchkGJXgSkU9CLgPQioIK_eTrAA_xHLvw3CVDABQ</recordid><startdate>20181001</startdate><enddate>20181001</enddate><creator>Pan, Xuan</creator><creator>Ji, Xiaozhi</creator><creator>Zhang, Renmin</creator><creator>Zhou, Zhaofei</creator><creator>Zhong, Yuejiao</creator><creator>Peng, Wei</creator><creator>Sun, Ning</creator><creator>Xu, Xinyu</creator><creator>Xia, Lei</creator><creator>Li, Pansong</creator><creator>Lu, Jianwei</creator><creator>Tu, Jing</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. 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However, the genomic basis of gastric cancer is not completely understood and the underlying genetic heterogeneity has not been well studied. In the present study, 1,021 genes were sequenced and the somatic mutations of 45 formalin-fixed, paraffin-embedded gastric adenocarcinoma samples were assessed using next-generation sequencing technologies. In the present study, a median sequencing coverage depth of 708-fold was achieved. Somatic genomic alterations were detected in 37/45 patients (82.4%) and the most frequent genetic alterations identified were tumor protein P53 (TP53) gene mutations. Mutations in MLL4, ERBB3, FBXW7, MLL3, MTOR, NOTCH1, PIK3CA, KRAS, ERBB4 and EGFR were also detected. Patients with TP53 mutations had a higher number of somatic mutations, and the total number of somatic mutations was weakly correlated with patient age. These results provided data on the intratumoral heterogeneity of gastric cancer and may be used in order to develop personalized cancer therapy.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30250552</pmid><doi>10.3892/ol.2018.9314</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Cancer therapies Care and treatment Deoxyribonucleic acid Development and progression DNA Gastric cancer Gene mutation Genes Genetic aspects Genomes Growth factors Health aspects Histology Methods Mutation Oncology Patient outcomes Patients Precision medicine Proteins Stomach cancer Studies Tumor proteins |
title | Landscape of somatic mutations in gastric cancer assessed using next-generation sequencing analysis |
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