Promyelocytic leukaemia protein links DNA damage response and repair to hepatitis B virus-related hepatocarcinogenesis
DNA damage response and repair pathways are important barriers to carcinogenesis. Here, we show that promyelocytic leukaemia (PML, also known as TRIM19), involved in sensing DNA damage and executing homologous recombination repair, is down‐regulated in non‐tumour liver cells surrounding hepatitis B...
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| Veröffentlicht in: | The Journal of pathology 2013-08, Vol.230 (4), p.377-387 |
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| description | DNA damage response and repair pathways are important barriers to carcinogenesis. Here, we show that promyelocytic leukaemia (PML, also known as TRIM19), involved in sensing DNA damage and executing homologous recombination repair, is down‐regulated in non‐tumour liver cells surrounding hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC). No PML mutation or deletion was found in HBV‐infected liver or HCC cells. Immunohistochemical analysis of liver biopsies from patients with breast or liver cancer and HBV reactivation after chemotherapy revealed PML up‐regulation and HBV exacerbation in normal liver tissue in response to DNA damage (functional PML), PML down‐regulation in HCC peritumour cells associated with high HBsAg accumulation and low HBV replication activity (suppressive PML), and heterogeneous nuclear PML expression in HCC cells that lost HBV DNA and HBsAg and were non‐reactive to DNA damage (dysregulated PML). Loss of PML in HBsAg‐transgenic mice promoted chromosome breaks in liver cells and accelerated the accumulation of body and liver fat and the development of a liver steatosis–dysplasia–adenoma–carcinoma sequence in an inflammation‐independent and male‐predominant manner, compared to PML knock‐out or HBsAg‐transgenic mice during the same time period. These results indicate that PML deficiency facilitates genomic instability and promotes HBsAg‐related hepatocarcinogenesis, which also involves androgen and lipid metabolism. These findings uncover a novel PML link between HBV‐related tumourigenesis, DNA repair, and metabolism. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd. |
| doi_str_mv | 10.1002/path.4195 |
| format | Article |
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Here, we show that promyelocytic leukaemia (PML, also known as TRIM19), involved in sensing DNA damage and executing homologous recombination repair, is down‐regulated in non‐tumour liver cells surrounding hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC). No PML mutation or deletion was found in HBV‐infected liver or HCC cells. Immunohistochemical analysis of liver biopsies from patients with breast or liver cancer and HBV reactivation after chemotherapy revealed PML up‐regulation and HBV exacerbation in normal liver tissue in response to DNA damage (functional PML), PML down‐regulation in HCC peritumour cells associated with high HBsAg accumulation and low HBV replication activity (suppressive PML), and heterogeneous nuclear PML expression in HCC cells that lost HBV DNA and HBsAg and were non‐reactive to DNA damage (dysregulated PML). Loss of PML in HBsAg‐transgenic mice promoted chromosome breaks in liver cells and accelerated the accumulation of body and liver fat and the development of a liver steatosis–dysplasia–adenoma–carcinoma sequence in an inflammation‐independent and male‐predominant manner, compared to PML knock‐out or HBsAg‐transgenic mice during the same time period. These results indicate that PML deficiency facilitates genomic instability and promotes HBsAg‐related hepatocarcinogenesis, which also involves androgen and lipid metabolism. These findings uncover a novel PML link between HBV‐related tumourigenesis, DNA repair, and metabolism. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><identifier>ISSN: 0022-3417</identifier><identifier>EISSN: 1096-9896</identifier><identifier>DOI: 10.1002/path.4195</identifier><identifier>PMID: 23620081</identifier><language>eng</language><publisher>Chichester, UK: John Wiley & Sons, Ltd</publisher><subject>Adiposity ; Androgens ; Animals ; Antibiotics, Antineoplastic - therapeutic use ; Biomarkers - blood ; Biopsy ; Carcinoma, Hepatocellular - chemically induced ; Carcinoma, Hepatocellular - drug therapy ; Carcinoma, Hepatocellular - genetics ; Carcinoma, Hepatocellular - metabolism ; Carcinoma, Hepatocellular - pathology ; Carcinoma, Hepatocellular - virology ; Cell Transformation, Viral ; Diethylnitrosamine ; Disease Models, Animal ; DNA Damage ; DNA damage response and repair ; DNA Repair ; Doxorubicin - therapeutic use ; Fatty Liver - metabolism ; Fatty Liver - pathology ; Fatty Liver - virology ; Female ; Genomic Instability ; Hepatitis B - complications ; Hepatitis B - diagnosis ; Hepatitis B - genetics ; Hepatitis B Surface Antigens - blood ; Hepatitis B Surface Antigens - genetics ; Hepatitis B virus ; Hepatitis B virus - genetics ; Hepatitis B virus - growth & development ; Hepatitis B virus - immunology ; Hepatitis B virus - pathogenicity ; hepatitis B virus surface antigen ; hepatocellular carcinoma ; Humans ; Immunohistochemistry ; Liver Neoplasms - chemically induced ; Liver Neoplasms - drug therapy ; Liver Neoplasms - genetics ; Liver Neoplasms - metabolism ; Liver Neoplasms - pathology ; Liver Neoplasms - virology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Nuclear Proteins - deficiency ; Nuclear Proteins - genetics ; Nuclear Proteins - metabolism ; promyelocytic leukaemia protein ; Promyelocytic Leukemia Protein ; Sex Factors ; Time Factors ; Transcription Factors - deficiency ; Transcription Factors - genetics ; Transcription Factors - metabolism ; Tumor Suppressor Proteins - deficiency ; Tumor Suppressor Proteins - genetics ; Tumor Suppressor Proteins - metabolism ; Up-Regulation ; Virus Activation ; Virus Replication</subject><ispartof>The Journal of pathology, 2013-08, Vol.230 (4), p.377-387</ispartof><rights>Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</rights><rights>Copyright © 2013 Pathological Society of Great Britain and Ireland</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4245-49cf06aa76329369adeb29fda832d459d22c85286b71a95589d7b439cb3bce3d3</citedby><cites>FETCH-LOGICAL-c4245-49cf06aa76329369adeb29fda832d459d22c85286b71a95589d7b439cb3bce3d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpath.4195$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpath.4195$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23620081$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chung, Yih-Lin</creatorcontrib><creatorcontrib>Wu, Mei-Ling</creatorcontrib><title>Promyelocytic leukaemia protein links DNA damage response and repair to hepatitis B virus-related hepatocarcinogenesis</title><title>The Journal of pathology</title><addtitle>J. Pathol</addtitle><description>DNA damage response and repair pathways are important barriers to carcinogenesis. Here, we show that promyelocytic leukaemia (PML, also known as TRIM19), involved in sensing DNA damage and executing homologous recombination repair, is down‐regulated in non‐tumour liver cells surrounding hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC). No PML mutation or deletion was found in HBV‐infected liver or HCC cells. Immunohistochemical analysis of liver biopsies from patients with breast or liver cancer and HBV reactivation after chemotherapy revealed PML up‐regulation and HBV exacerbation in normal liver tissue in response to DNA damage (functional PML), PML down‐regulation in HCC peritumour cells associated with high HBsAg accumulation and low HBV replication activity (suppressive PML), and heterogeneous nuclear PML expression in HCC cells that lost HBV DNA and HBsAg and were non‐reactive to DNA damage (dysregulated PML). Loss of PML in HBsAg‐transgenic mice promoted chromosome breaks in liver cells and accelerated the accumulation of body and liver fat and the development of a liver steatosis–dysplasia–adenoma–carcinoma sequence in an inflammation‐independent and male‐predominant manner, compared to PML knock‐out or HBsAg‐transgenic mice during the same time period. These results indicate that PML deficiency facilitates genomic instability and promotes HBsAg‐related hepatocarcinogenesis, which also involves androgen and lipid metabolism. These findings uncover a novel PML link between HBV‐related tumourigenesis, DNA repair, and metabolism. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</description><subject>Adiposity</subject><subject>Androgens</subject><subject>Animals</subject><subject>Antibiotics, Antineoplastic - therapeutic use</subject><subject>Biomarkers - blood</subject><subject>Biopsy</subject><subject>Carcinoma, Hepatocellular - chemically induced</subject><subject>Carcinoma, Hepatocellular - drug therapy</subject><subject>Carcinoma, Hepatocellular - genetics</subject><subject>Carcinoma, Hepatocellular - metabolism</subject><subject>Carcinoma, Hepatocellular - pathology</subject><subject>Carcinoma, Hepatocellular - virology</subject><subject>Cell Transformation, Viral</subject><subject>Diethylnitrosamine</subject><subject>Disease Models, Animal</subject><subject>DNA Damage</subject><subject>DNA damage response and repair</subject><subject>DNA Repair</subject><subject>Doxorubicin - therapeutic use</subject><subject>Fatty Liver - metabolism</subject><subject>Fatty Liver - pathology</subject><subject>Fatty Liver - virology</subject><subject>Female</subject><subject>Genomic Instability</subject><subject>Hepatitis B - complications</subject><subject>Hepatitis B - diagnosis</subject><subject>Hepatitis B - genetics</subject><subject>Hepatitis B Surface Antigens - blood</subject><subject>Hepatitis B Surface Antigens - genetics</subject><subject>Hepatitis B virus</subject><subject>Hepatitis B virus - genetics</subject><subject>Hepatitis B virus - growth & development</subject><subject>Hepatitis B virus - immunology</subject><subject>Hepatitis B virus - pathogenicity</subject><subject>hepatitis B virus surface antigen</subject><subject>hepatocellular carcinoma</subject><subject>Humans</subject><subject>Immunohistochemistry</subject><subject>Liver Neoplasms - chemically induced</subject><subject>Liver Neoplasms - drug therapy</subject><subject>Liver Neoplasms - genetics</subject><subject>Liver Neoplasms - metabolism</subject><subject>Liver Neoplasms - pathology</subject><subject>Liver Neoplasms - virology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Nuclear Proteins - deficiency</subject><subject>Nuclear Proteins - genetics</subject><subject>Nuclear Proteins - metabolism</subject><subject>promyelocytic leukaemia protein</subject><subject>Promyelocytic Leukemia Protein</subject><subject>Sex Factors</subject><subject>Time Factors</subject><subject>Transcription Factors - deficiency</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><subject>Tumor Suppressor Proteins - deficiency</subject><subject>Tumor Suppressor Proteins - genetics</subject><subject>Tumor Suppressor Proteins - metabolism</subject><subject>Up-Regulation</subject><subject>Virus Activation</subject><subject>Virus Replication</subject><issn>0022-3417</issn><issn>1096-9896</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kU1vEzEQhi0EomnhwB9AlrjQw7b-Wu_6mLbQIEUlhyCOlteetG5211t7t5B_j6OEHpA4zYzmmVcz8yL0gZILSgi7HMz4cCGoKl-hGSVKFqpW8jWa5R4ruKDVCTpN6ZEQolRZvkUnjEtGSE1n6HkVQ7eDNtjd6C1uYdoa6LzBQwwj-B63vt8mfHM3x8505h5whDSEPgE2vcvFYHzEY8APORv96BO-ws8-TqmI0JoR3KETrInW9-Eeekg-vUNvNqZN8P4Yz9CPr1_W14ti-f322_V8WVjBRFkIZTdEGlNJzhSXyjhomNo4U3PmRKkcY7YuWS2bipp8Wq1c1QiubMMbC9zxM_T5oJvPeZogjbrzyULbmh7ClDQVomaM04pn9NM_6GOYYp-305SrWgrJZJmp8wNlY0gpwkYP0Xcm7jQlem-G3puh92Zk9uNRcWo6cC_k3-9n4PIA_PIt7P6vpFfz9eIoWRwmfBrh98uEiVstK16V-ufdrV7fLJZXakW14n8AR2KkYA</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Chung, Yih-Lin</creator><creator>Wu, Mei-Ling</creator><general>John Wiley & Sons, Ltd</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7U9</scope></search><sort><creationdate>201308</creationdate><title>Promyelocytic leukaemia protein links DNA damage response and repair to hepatitis B virus-related hepatocarcinogenesis</title><author>Chung, Yih-Lin ; Wu, Mei-Ling</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4245-49cf06aa76329369adeb29fda832d459d22c85286b71a95589d7b439cb3bce3d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adiposity</topic><topic>Androgens</topic><topic>Animals</topic><topic>Antibiotics, Antineoplastic - therapeutic use</topic><topic>Biomarkers - blood</topic><topic>Biopsy</topic><topic>Carcinoma, Hepatocellular - chemically induced</topic><topic>Carcinoma, Hepatocellular - drug therapy</topic><topic>Carcinoma, Hepatocellular - genetics</topic><topic>Carcinoma, Hepatocellular - metabolism</topic><topic>Carcinoma, Hepatocellular - pathology</topic><topic>Carcinoma, Hepatocellular - virology</topic><topic>Cell Transformation, Viral</topic><topic>Diethylnitrosamine</topic><topic>Disease Models, Animal</topic><topic>DNA Damage</topic><topic>DNA damage response and repair</topic><topic>DNA Repair</topic><topic>Doxorubicin - therapeutic use</topic><topic>Fatty Liver - metabolism</topic><topic>Fatty Liver - pathology</topic><topic>Fatty Liver - virology</topic><topic>Female</topic><topic>Genomic Instability</topic><topic>Hepatitis B - complications</topic><topic>Hepatitis B - diagnosis</topic><topic>Hepatitis B - genetics</topic><topic>Hepatitis B Surface Antigens - blood</topic><topic>Hepatitis B Surface Antigens - genetics</topic><topic>Hepatitis B virus</topic><topic>Hepatitis B virus - genetics</topic><topic>Hepatitis B virus - growth & development</topic><topic>Hepatitis B virus - immunology</topic><topic>Hepatitis B virus - pathogenicity</topic><topic>hepatitis B virus surface antigen</topic><topic>hepatocellular carcinoma</topic><topic>Humans</topic><topic>Immunohistochemistry</topic><topic>Liver Neoplasms - chemically induced</topic><topic>Liver Neoplasms - drug therapy</topic><topic>Liver Neoplasms - genetics</topic><topic>Liver Neoplasms - metabolism</topic><topic>Liver Neoplasms - pathology</topic><topic>Liver Neoplasms - virology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mice, Transgenic</topic><topic>Nuclear Proteins - deficiency</topic><topic>Nuclear Proteins - genetics</topic><topic>Nuclear Proteins - metabolism</topic><topic>promyelocytic leukaemia protein</topic><topic>Promyelocytic Leukemia Protein</topic><topic>Sex Factors</topic><topic>Time Factors</topic><topic>Transcription Factors - deficiency</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><topic>Tumor Suppressor Proteins - deficiency</topic><topic>Tumor Suppressor Proteins - genetics</topic><topic>Tumor Suppressor Proteins - metabolism</topic><topic>Up-Regulation</topic><topic>Virus Activation</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chung, Yih-Lin</creatorcontrib><creatorcontrib>Wu, Mei-Ling</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>Virology and AIDS Abstracts</collection><jtitle>The Journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chung, Yih-Lin</au><au>Wu, Mei-Ling</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Promyelocytic leukaemia protein links DNA damage response and repair to hepatitis B virus-related hepatocarcinogenesis</atitle><jtitle>The Journal of pathology</jtitle><addtitle>J. Pathol</addtitle><date>2013-08</date><risdate>2013</risdate><volume>230</volume><issue>4</issue><spage>377</spage><epage>387</epage><pages>377-387</pages><issn>0022-3417</issn><eissn>1096-9896</eissn><abstract>DNA damage response and repair pathways are important barriers to carcinogenesis. Here, we show that promyelocytic leukaemia (PML, also known as TRIM19), involved in sensing DNA damage and executing homologous recombination repair, is down‐regulated in non‐tumour liver cells surrounding hepatitis B virus (HBV)‐related hepatocellular carcinoma (HCC). No PML mutation or deletion was found in HBV‐infected liver or HCC cells. Immunohistochemical analysis of liver biopsies from patients with breast or liver cancer and HBV reactivation after chemotherapy revealed PML up‐regulation and HBV exacerbation in normal liver tissue in response to DNA damage (functional PML), PML down‐regulation in HCC peritumour cells associated with high HBsAg accumulation and low HBV replication activity (suppressive PML), and heterogeneous nuclear PML expression in HCC cells that lost HBV DNA and HBsAg and were non‐reactive to DNA damage (dysregulated PML). Loss of PML in HBsAg‐transgenic mice promoted chromosome breaks in liver cells and accelerated the accumulation of body and liver fat and the development of a liver steatosis–dysplasia–adenoma–carcinoma sequence in an inflammation‐independent and male‐predominant manner, compared to PML knock‐out or HBsAg‐transgenic mice during the same time period. These results indicate that PML deficiency facilitates genomic instability and promotes HBsAg‐related hepatocarcinogenesis, which also involves androgen and lipid metabolism. These findings uncover a novel PML link between HBV‐related tumourigenesis, DNA repair, and metabolism. Copyright © 2013 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.</abstract><cop>Chichester, UK</cop><pub>John Wiley & Sons, Ltd</pub><pmid>23620081</pmid><doi>10.1002/path.4195</doi><tpages>11</tpages></addata></record> |
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| ispartof | The Journal of pathology, 2013-08, Vol.230 (4), p.377-387 |
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| subjects | Adiposity Androgens Animals Antibiotics, Antineoplastic - therapeutic use Biomarkers - blood Biopsy Carcinoma, Hepatocellular - chemically induced Carcinoma, Hepatocellular - drug therapy Carcinoma, Hepatocellular - genetics Carcinoma, Hepatocellular - metabolism Carcinoma, Hepatocellular - pathology Carcinoma, Hepatocellular - virology Cell Transformation, Viral Diethylnitrosamine Disease Models, Animal DNA Damage DNA damage response and repair DNA Repair Doxorubicin - therapeutic use Fatty Liver - metabolism Fatty Liver - pathology Fatty Liver - virology Female Genomic Instability Hepatitis B - complications Hepatitis B - diagnosis Hepatitis B - genetics Hepatitis B Surface Antigens - blood Hepatitis B Surface Antigens - genetics Hepatitis B virus Hepatitis B virus - genetics Hepatitis B virus - growth & development Hepatitis B virus - immunology Hepatitis B virus - pathogenicity hepatitis B virus surface antigen hepatocellular carcinoma Humans Immunohistochemistry Liver Neoplasms - chemically induced Liver Neoplasms - drug therapy Liver Neoplasms - genetics Liver Neoplasms - metabolism Liver Neoplasms - pathology Liver Neoplasms - virology Male Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Nuclear Proteins - deficiency Nuclear Proteins - genetics Nuclear Proteins - metabolism promyelocytic leukaemia protein Promyelocytic Leukemia Protein Sex Factors Time Factors Transcription Factors - deficiency Transcription Factors - genetics Transcription Factors - metabolism Tumor Suppressor Proteins - deficiency Tumor Suppressor Proteins - genetics Tumor Suppressor Proteins - metabolism Up-Regulation Virus Activation Virus Replication |
| title | Promyelocytic leukaemia protein links DNA damage response and repair to hepatitis B virus-related hepatocarcinogenesis |
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