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Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease
Nonalcoholic fatty liver disease (NAFLD) is a risk factor for Hepatocellular carcinoma (HCC), but he transition from NAFLD to HCC is poorly understood. Feature selection algorithms in human and genetically modified mice NAFLD and HCC microarray data were applied to generate signatures of NAFLD progr...
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| Published in: | PloS one 2015-05, Vol.10 (5), p.e0124544-e0124544 |
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| creator | Frades, Itziar Andreasson, Erik Mato, Jose Maria Alexandersson, Erik Matthiesen, Rune Martínez-Chantar, Maria Luz |
| description | Nonalcoholic fatty liver disease (NAFLD) is a risk factor for Hepatocellular carcinoma (HCC), but he transition from NAFLD to HCC is poorly understood. Feature selection algorithms in human and genetically modified mice NAFLD and HCC microarray data were applied to generate signatures of NAFLD progression and HCC differential survival. These signatures were used to study the pathogenesis of NAFLD derived HCC and explore which subtypes of cancers that can be investigated using mouse models. Our findings show that: (I) HNF4 is a common potential transcription factor mediating the transcription of NAFLD progression genes (II) mice HCC derived from NAFLD co-cluster with a less aggressive human HCC subtype of differential prognosis and mixed etiology (III) the HCC survival signature is able to correctly classify 95% of the samples and gives Fgf20 and Tgfb1i1 as the most robust genes for prediction (IV) the expression values of genes composing the signature in an independent human HCC dataset revealed different HCC subtypes showing differences in survival time by a Logrank test. In summary, we present marker signatures for NAFLD derived HCC molecular pathogenesis both at the gene and pathway level. |
| doi_str_mv | 10.1371/journal.pone.0124544 |
| format | article |
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Feature selection algorithms in human and genetically modified mice NAFLD and HCC microarray data were applied to generate signatures of NAFLD progression and HCC differential survival. These signatures were used to study the pathogenesis of NAFLD derived HCC and explore which subtypes of cancers that can be investigated using mouse models. Our findings show that: (I) HNF4 is a common potential transcription factor mediating the transcription of NAFLD progression genes (II) mice HCC derived from NAFLD co-cluster with a less aggressive human HCC subtype of differential prognosis and mixed etiology (III) the HCC survival signature is able to correctly classify 95% of the samples and gives Fgf20 and Tgfb1i1 as the most robust genes for prediction (IV) the expression values of genes composing the signature in an independent human HCC dataset revealed different HCC subtypes showing differences in survival time by a Logrank test. In summary, we present marker signatures for NAFLD derived HCC molecular pathogenesis both at the gene and pathway level.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0124544</identifier><identifier>PMID: 25993042</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alcoholism ; Algorithms ; Analysis ; Animal models ; Animals ; Apoptosis ; Bioinformatics (Computational Biology) ; Bioinformatik (beräkningsbiologi) ; Biology ; Biomarkers ; Cancer genetics ; Carcinoma, Hepatocellular - genetics ; Composing ; Cytokines ; Development and progression ; Diabetes ; Disease Progression ; DNA microarrays ; Etiology ; Fatty liver ; Fibroblast growth factor 20 ; Fibroblast Growth Factors - genetics ; Gene expression ; Genes ; Genetic aspects ; Genetic modification ; Genetically modified organisms ; Health risks ; Hepatitis ; Hepatocellular carcinoma ; Hepatocyte Nuclear Factor 4 - genetics ; Homeostasis ; Humans ; Immune system ; Insulin resistance ; Insulin Resistance - physiology ; Intracellular Signaling Peptides and Proteins - genetics ; Kinases ; LIM Domain Proteins - genetics ; Lipids ; Liver ; Liver - pathology ; Liver cancer ; Liver diseases ; Liver Neoplasms - genetics ; Medical prognosis ; Medical research ; Metabolic syndrome ; Mice ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease - genetics ; Non-alcoholic Fatty Liver Disease - pathology ; Obesity ; Oxidative stress ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pathogenesis ; Risk Factors ; Rodents ; Signatures ; Survival</subject><ispartof>PloS one, 2015-05, Vol.10 (5), p.e0124544-e0124544</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Frades et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2015 Frades et al 2015 Frades et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c796t-5b1d6166cfdc1dd831f65af8cd01d7f7087c537255e469008fa66f73ff51a6383</citedby><cites>FETCH-LOGICAL-c796t-5b1d6166cfdc1dd831f65af8cd01d7f7087c537255e469008fa66f73ff51a6383</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1682209737/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1682209737?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25751,27922,27923,37010,37011,44588,53789,53791,74896</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25993042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://res.slu.se/id/publ/68330$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><contributor>Avila, Matias A</contributor><creatorcontrib>Frades, Itziar</creatorcontrib><creatorcontrib>Andreasson, Erik</creatorcontrib><creatorcontrib>Mato, Jose Maria</creatorcontrib><creatorcontrib>Alexandersson, Erik</creatorcontrib><creatorcontrib>Matthiesen, Rune</creatorcontrib><creatorcontrib>Martínez-Chantar, Maria Luz</creatorcontrib><creatorcontrib>Sveriges lantbruksuniversitet</creatorcontrib><title>Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Nonalcoholic fatty liver disease (NAFLD) is a risk factor for Hepatocellular carcinoma (HCC), but he transition from NAFLD to HCC is poorly understood. 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genetics</topic><topic>Composing</topic><topic>Cytokines</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Disease Progression</topic><topic>DNA microarrays</topic><topic>Etiology</topic><topic>Fatty liver</topic><topic>Fibroblast growth factor 20</topic><topic>Fibroblast Growth Factors - genetics</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic modification</topic><topic>Genetically modified organisms</topic><topic>Health risks</topic><topic>Hepatitis</topic><topic>Hepatocellular carcinoma</topic><topic>Hepatocyte Nuclear Factor 4 - genetics</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Immune system</topic><topic>Insulin resistance</topic><topic>Insulin Resistance - physiology</topic><topic>Intracellular Signaling Peptides and Proteins - genetics</topic><topic>Kinases</topic><topic>LIM Domain Proteins - genetics</topic><topic>Lipids</topic><topic>Liver</topic><topic>Liver - pathology</topic><topic>Liver cancer</topic><topic>Liver diseases</topic><topic>Liver Neoplasms - genetics</topic><topic>Medical prognosis</topic><topic>Medical research</topic><topic>Metabolic syndrome</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Non-alcoholic Fatty Liver Disease - genetics</topic><topic>Non-alcoholic Fatty Liver Disease - pathology</topic><topic>Obesity</topic><topic>Oxidative stress</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pathogenesis</topic><topic>Risk Factors</topic><topic>Rodents</topic><topic>Signatures</topic><topic>Survival</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Frades, Itziar</creatorcontrib><creatorcontrib>Andreasson, Erik</creatorcontrib><creatorcontrib>Mato, Jose Maria</creatorcontrib><creatorcontrib>Alexandersson, Erik</creatorcontrib><creatorcontrib>Matthiesen, Rune</creatorcontrib><creatorcontrib>Martínez-Chantar, Maria Luz</creatorcontrib><creatorcontrib>Sveriges lantbruksuniversitet</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale_Opposing Viewpoints In Context</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database (ProQuest)</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Complete (ProQuest Database)</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Database (1962 - 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Feature selection algorithms in human and genetically modified mice NAFLD and HCC microarray data were applied to generate signatures of NAFLD progression and HCC differential survival. These signatures were used to study the pathogenesis of NAFLD derived HCC and explore which subtypes of cancers that can be investigated using mouse models. Our findings show that: (I) HNF4 is a common potential transcription factor mediating the transcription of NAFLD progression genes (II) mice HCC derived from NAFLD co-cluster with a less aggressive human HCC subtype of differential prognosis and mixed etiology (III) the HCC survival signature is able to correctly classify 95% of the samples and gives Fgf20 and Tgfb1i1 as the most robust genes for prediction (IV) the expression values of genes composing the signature in an independent human HCC dataset revealed different HCC subtypes showing differences in survival time by a Logrank test. In summary, we present marker signatures for NAFLD derived HCC molecular pathogenesis both at the gene and pathway level.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25993042</pmid><doi>10.1371/journal.pone.0124544</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2015-05, Vol.10 (5), p.e0124544-e0124544 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1682209737 |
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| subjects | Alcoholism Algorithms Analysis Animal models Animals Apoptosis Bioinformatics (Computational Biology) Bioinformatik (beräkningsbiologi) Biology Biomarkers Cancer genetics Carcinoma, Hepatocellular - genetics Composing Cytokines Development and progression Diabetes Disease Progression DNA microarrays Etiology Fatty liver Fibroblast growth factor 20 Fibroblast Growth Factors - genetics Gene expression Genes Genetic aspects Genetic modification Genetically modified organisms Health risks Hepatitis Hepatocellular carcinoma Hepatocyte Nuclear Factor 4 - genetics Homeostasis Humans Immune system Insulin resistance Insulin Resistance - physiology Intracellular Signaling Peptides and Proteins - genetics Kinases LIM Domain Proteins - genetics Lipids Liver Liver - pathology Liver cancer Liver diseases Liver Neoplasms - genetics Medical prognosis Medical research Metabolic syndrome Mice Mice, Knockout Non-alcoholic Fatty Liver Disease - genetics Non-alcoholic Fatty Liver Disease - pathology Obesity Oxidative stress p38 Mitogen-Activated Protein Kinases - metabolism Pathogenesis Risk Factors Rodents Signatures Survival |
| title | Integrative genomic signatures of hepatocellular carcinoma derived from nonalcoholic Fatty liver disease |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T13%3A35%3A03IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Integrative%20genomic%20signatures%20of%20hepatocellular%20carcinoma%20derived%20from%20nonalcoholic%20Fatty%20liver%20disease&rft.jtitle=PloS%20one&rft.au=Frades,%20Itziar&rft.aucorp=Sveriges%20lantbruksuniversitet&rft.date=2015-05-20&rft.volume=10&rft.issue=5&rft.spage=e0124544&rft.epage=e0124544&rft.pages=e0124544-e0124544&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0124544&rft_dat=%3Cgale_plos_%3EA432295939%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c796t-5b1d6166cfdc1dd831f65af8cd01d7f7087c537255e469008fa66f73ff51a6383%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1682209737&rft_id=info:pmid/25993042&rft_galeid=A432295939&rfr_iscdi=true |