Fusobacterium Nucleatum-Induced Tumor Mutation Burden Predicts Poor Survival of Gastric Cancer Patients
Co-infection of and is a microbial biomarker for poor prognosis of gastric cancer patients. is associated with microsatellite instability and the accumulation of mutations in colorectal cancer. Here, we investigated the mutation landscape of -positive resected gastric cancer tissues using Illumina T...
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| Veröffentlicht in: | Cancers 2022-12, Vol.15 (1), p.269 |
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| creator | Hsieh, Yung-Yu Kuo, Wen-Lin Hsu, Wan-Ting Tung, Shui-Yi Li, Chin |
| description | Co-infection of
and
is a microbial biomarker for poor prognosis of gastric cancer patients.
is associated with microsatellite instability and the accumulation of mutations in colorectal cancer. Here, we investigated the mutation landscape of
-positive resected gastric cancer tissues using Illumina TruSight Oncology 500 comprehensive panel. Sequencing data were processed to identify the small nucleotide variants, small insertions and deletions, and unstable microsatellite sites. The bioinformatic algorithm also calculated copy number gains of preselected genes and tumor mutation burden. The recurrent genetic aberrations were identified in this study cohort. For gene amplification events, ERBB2, cell cycle regulators, and specific FGF ligands and receptors were the most frequently amplified genes. Pathogenic activation mutations of ERBB2, ERBB3, and PIK3CA, as well as loss-of-function of TP53, were identified in multiple patients. Furthermore,
infection is positively correlated with a higher tumor mutation burden. Survival analysis showed that the combination of
infection and high tumor mutation burden formed an extremely effective biomarker to predict poor prognosis. Our results indicated that the ERBB2-PIK3-AKT-mTOR pathway is frequently activated in gastric cancer and that
and high mutation burden are strong biomarkers of poor prognosis for gastric cancer patients. |
| doi_str_mv | 10.3390/cancers15010269 |
| format | Article |
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and
is a microbial biomarker for poor prognosis of gastric cancer patients.
is associated with microsatellite instability and the accumulation of mutations in colorectal cancer. Here, we investigated the mutation landscape of
-positive resected gastric cancer tissues using Illumina TruSight Oncology 500 comprehensive panel. Sequencing data were processed to identify the small nucleotide variants, small insertions and deletions, and unstable microsatellite sites. The bioinformatic algorithm also calculated copy number gains of preselected genes and tumor mutation burden. The recurrent genetic aberrations were identified in this study cohort. For gene amplification events, ERBB2, cell cycle regulators, and specific FGF ligands and receptors were the most frequently amplified genes. Pathogenic activation mutations of ERBB2, ERBB3, and PIK3CA, as well as loss-of-function of TP53, were identified in multiple patients. Furthermore,
infection is positively correlated with a higher tumor mutation burden. Survival analysis showed that the combination of
infection and high tumor mutation burden formed an extremely effective biomarker to predict poor prognosis. Our results indicated that the ERBB2-PIK3-AKT-mTOR pathway is frequently activated in gastric cancer and that
and high mutation burden are strong biomarkers of poor prognosis for gastric cancer patients.</description><identifier>ISSN: 2072-6694</identifier><identifier>EISSN: 2072-6694</identifier><identifier>DOI: 10.3390/cancers15010269</identifier><identifier>PMID: 36612265</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>AKT protein ; Biomarkers ; Capillary electrophoresis ; Cell cycle ; Colorectal cancer ; Colorectal carcinoma ; Copy number ; DNA damage ; ErbB-2 protein ; ErbB-3 protein ; Fibroblast growth factors ; Fusobacterium nucleatum ; Gastric cancer ; Gastrointestinal tract ; Gene amplification ; Genetic aspects ; Genomes ; Gram-negative bacteria ; Health aspects ; Helicobacter pylori ; Infections ; Medical prognosis ; Microbiota ; Microsatellite instability ; Mutation ; Mutation (Biology) ; Oncology ; p53 Protein ; Prognosis ; Review boards ; Risk factors ; Statistical analysis ; Stomach cancer ; TOR protein ; Transcription activation ; Tumors</subject><ispartof>Cancers, 2022-12, Vol.15 (1), p.269</ispartof><rights>COPYRIGHT 2022 MDPI AG</rights><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c488t-734dc11033684c8b713930db7597a468a4f93fdec27d45fbb8e557320e38c6263</citedby><cites>FETCH-LOGICAL-c488t-734dc11033684c8b713930db7597a468a4f93fdec27d45fbb8e557320e38c6263</cites><orcidid>0000-0001-8465-5204 ; 0000-0002-5457-9623</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/PMC9818776/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9818776/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36612265$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hsieh, Yung-Yu</creatorcontrib><creatorcontrib>Kuo, Wen-Lin</creatorcontrib><creatorcontrib>Hsu, Wan-Ting</creatorcontrib><creatorcontrib>Tung, Shui-Yi</creatorcontrib><creatorcontrib>Li, Chin</creatorcontrib><title>Fusobacterium Nucleatum-Induced Tumor Mutation Burden Predicts Poor Survival of Gastric Cancer Patients</title><title>Cancers</title><addtitle>Cancers (Basel)</addtitle><description>Co-infection of
and
is a microbial biomarker for poor prognosis of gastric cancer patients.
is associated with microsatellite instability and the accumulation of mutations in colorectal cancer. Here, we investigated the mutation landscape of
-positive resected gastric cancer tissues using Illumina TruSight Oncology 500 comprehensive panel. Sequencing data were processed to identify the small nucleotide variants, small insertions and deletions, and unstable microsatellite sites. The bioinformatic algorithm also calculated copy number gains of preselected genes and tumor mutation burden. The recurrent genetic aberrations were identified in this study cohort. For gene amplification events, ERBB2, cell cycle regulators, and specific FGF ligands and receptors were the most frequently amplified genes. Pathogenic activation mutations of ERBB2, ERBB3, and PIK3CA, as well as loss-of-function of TP53, were identified in multiple patients. Furthermore,
infection is positively correlated with a higher tumor mutation burden. Survival analysis showed that the combination of
infection and high tumor mutation burden formed an extremely effective biomarker to predict poor prognosis. Our results indicated that the ERBB2-PIK3-AKT-mTOR pathway is frequently activated in gastric cancer and that
and high mutation burden are strong biomarkers of poor prognosis for gastric cancer patients.</description><subject>AKT protein</subject><subject>Biomarkers</subject><subject>Capillary electrophoresis</subject><subject>Cell cycle</subject><subject>Colorectal cancer</subject><subject>Colorectal carcinoma</subject><subject>Copy number</subject><subject>DNA damage</subject><subject>ErbB-2 protein</subject><subject>ErbB-3 protein</subject><subject>Fibroblast growth factors</subject><subject>Fusobacterium nucleatum</subject><subject>Gastric cancer</subject><subject>Gastrointestinal tract</subject><subject>Gene amplification</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Gram-negative bacteria</subject><subject>Health aspects</subject><subject>Helicobacter pylori</subject><subject>Infections</subject><subject>Medical prognosis</subject><subject>Microbiota</subject><subject>Microsatellite instability</subject><subject>Mutation</subject><subject>Mutation (Biology)</subject><subject>Oncology</subject><subject>p53 Protein</subject><subject>Prognosis</subject><subject>Review boards</subject><subject>Risk factors</subject><subject>Statistical analysis</subject><subject>Stomach cancer</subject><subject>TOR protein</subject><subject>Transcription activation</subject><subject>Tumors</subject><issn>2072-6694</issn><issn>2072-6694</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNptks9vFSEQx4nR2Kb27M2QePGyLT92gb2Y1Je2Nqn6EuuZsDD7pNmFCstL_O_ltbW2jXCAMJ_vd2bIIPSWkiPOe3JsTbCQMu0IJUz0L9A-I5I1QvTty0f3PXSY8zWpi3MqhXyN9rgQlDHR7aPNWclxMHaB5MuMvxY7gVnK3FwEVyw4fFXmmPCXspjFx4A_leQg4HUC5-2S8TrW6PeStn5rJhxHfG7ykrzFq9vi8LrKICz5DXo1minD4f15gH6cnV6tPjeX384vVieXjW2VWhrJW2cprZUK1Vo1SMp7Ttwgu16aVijTjj0fHVgmXduNw6Cg6yRnBLiyggl-gD7e-d6UYQZna-5kJn2T_GzSbx2N108jwf_Um7jVvaJKyp3Bh3uDFH8VyIuefbYwTSZALFkzKWhfQdVW9P0z9DqWFGp7txTpFePsH7UxE2gfxljz2p2pPpFtxyTvGKnU0X-ouh3M3sYAo6_vTwTHdwKbYs4JxoceKdG78dDPxqMq3j3-mgf-7zDwP28GtlI</recordid><startdate>20221230</startdate><enddate>20221230</enddate><creator>Hsieh, Yung-Yu</creator><creator>Kuo, Wen-Lin</creator><creator>Hsu, Wan-Ting</creator><creator>Tung, Shui-Yi</creator><creator>Li, Chin</creator><general>MDPI AG</general><general>MDPI</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>LK8</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-8465-5204</orcidid><orcidid>https://orcid.org/0000-0002-5457-9623</orcidid></search><sort><creationdate>20221230</creationdate><title>Fusobacterium Nucleatum-Induced Tumor Mutation Burden Predicts Poor Survival of Gastric Cancer Patients</title><author>Hsieh, Yung-Yu ; 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and
is a microbial biomarker for poor prognosis of gastric cancer patients.
is associated with microsatellite instability and the accumulation of mutations in colorectal cancer. Here, we investigated the mutation landscape of
-positive resected gastric cancer tissues using Illumina TruSight Oncology 500 comprehensive panel. Sequencing data were processed to identify the small nucleotide variants, small insertions and deletions, and unstable microsatellite sites. The bioinformatic algorithm also calculated copy number gains of preselected genes and tumor mutation burden. The recurrent genetic aberrations were identified in this study cohort. For gene amplification events, ERBB2, cell cycle regulators, and specific FGF ligands and receptors were the most frequently amplified genes. Pathogenic activation mutations of ERBB2, ERBB3, and PIK3CA, as well as loss-of-function of TP53, were identified in multiple patients. Furthermore,
infection is positively correlated with a higher tumor mutation burden. Survival analysis showed that the combination of
infection and high tumor mutation burden formed an extremely effective biomarker to predict poor prognosis. Our results indicated that the ERBB2-PIK3-AKT-mTOR pathway is frequently activated in gastric cancer and that
and high mutation burden are strong biomarkers of poor prognosis for gastric cancer patients.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>36612265</pmid><doi>10.3390/cancers15010269</doi><orcidid>https://orcid.org/0000-0001-8465-5204</orcidid><orcidid>https://orcid.org/0000-0002-5457-9623</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancers, 2022-12, Vol.15 (1), p.269 |
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| source | MDPI - Multidisciplinary Digital Publishing Institute; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; PubMed Central Open Access |
| subjects | AKT protein Biomarkers Capillary electrophoresis Cell cycle Colorectal cancer Colorectal carcinoma Copy number DNA damage ErbB-2 protein ErbB-3 protein Fibroblast growth factors Fusobacterium nucleatum Gastric cancer Gastrointestinal tract Gene amplification Genetic aspects Genomes Gram-negative bacteria Health aspects Helicobacter pylori Infections Medical prognosis Microbiota Microsatellite instability Mutation Mutation (Biology) Oncology p53 Protein Prognosis Review boards Risk factors Statistical analysis Stomach cancer TOR protein Transcription activation Tumors |
| title | Fusobacterium Nucleatum-Induced Tumor Mutation Burden Predicts Poor Survival of Gastric Cancer Patients |
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