Emerging role for R-loop formation in hepatocellular carcinoma
Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minim...
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| Autor*in: |
Baek, Hyojin [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2023 |
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| Schlagwörter: |
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© The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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| Übergeordnetes Werk: |
Enthalten in: Genes & Genomics - The Genetics Society of Korea, 2010, 45(2023), 5 vom: 12. Jan., Seite 543-551 |
|---|---|
| Übergeordnetes Werk: |
volume:45 ; year:2023 ; number:5 ; day:12 ; month:01 ; pages:543-551 |
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10.1007/s13258-022-01360-8 |
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| 520 | |a Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. | ||
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10.1007/s13258-022-01360-8 doi (DE-627)SPR050098810 (SPR)s13258-022-01360-8-e DE-627 ger DE-627 rakwb eng Baek, Hyojin verfasserin aut Emerging role for R-loop formation in hepatocellular carcinoma 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. R-loop (dpeaa)DE-He213 Hepatocellular carcinoma (dpeaa)DE-He213 Genome integrity (dpeaa)DE-He213 DNA damage and repair (dpeaa)DE-He213 Park, Sang-Uk aut Kim, Jeongkyu (orcid)0000-0002-8550-6654 aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2023), 5 vom: 12. Jan., Seite 543-551 (DE-627)SPR031096425 nnns volume:45 year:2023 number:5 day:12 month:01 pages:543-551 https://dx.doi.org/10.1007/s13258-022-01360-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 45 2023 5 12 01 543-551 |
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10.1007/s13258-022-01360-8 doi (DE-627)SPR050098810 (SPR)s13258-022-01360-8-e DE-627 ger DE-627 rakwb eng Baek, Hyojin verfasserin aut Emerging role for R-loop formation in hepatocellular carcinoma 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. R-loop (dpeaa)DE-He213 Hepatocellular carcinoma (dpeaa)DE-He213 Genome integrity (dpeaa)DE-He213 DNA damage and repair (dpeaa)DE-He213 Park, Sang-Uk aut Kim, Jeongkyu (orcid)0000-0002-8550-6654 aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2023), 5 vom: 12. Jan., Seite 543-551 (DE-627)SPR031096425 nnns volume:45 year:2023 number:5 day:12 month:01 pages:543-551 https://dx.doi.org/10.1007/s13258-022-01360-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 45 2023 5 12 01 543-551 |
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10.1007/s13258-022-01360-8 doi (DE-627)SPR050098810 (SPR)s13258-022-01360-8-e DE-627 ger DE-627 rakwb eng Baek, Hyojin verfasserin aut Emerging role for R-loop formation in hepatocellular carcinoma 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. R-loop (dpeaa)DE-He213 Hepatocellular carcinoma (dpeaa)DE-He213 Genome integrity (dpeaa)DE-He213 DNA damage and repair (dpeaa)DE-He213 Park, Sang-Uk aut Kim, Jeongkyu (orcid)0000-0002-8550-6654 aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2023), 5 vom: 12. Jan., Seite 543-551 (DE-627)SPR031096425 nnns volume:45 year:2023 number:5 day:12 month:01 pages:543-551 https://dx.doi.org/10.1007/s13258-022-01360-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 45 2023 5 12 01 543-551 |
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10.1007/s13258-022-01360-8 doi (DE-627)SPR050098810 (SPR)s13258-022-01360-8-e DE-627 ger DE-627 rakwb eng Baek, Hyojin verfasserin aut Emerging role for R-loop formation in hepatocellular carcinoma 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. R-loop (dpeaa)DE-He213 Hepatocellular carcinoma (dpeaa)DE-He213 Genome integrity (dpeaa)DE-He213 DNA damage and repair (dpeaa)DE-He213 Park, Sang-Uk aut Kim, Jeongkyu (orcid)0000-0002-8550-6654 aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2023), 5 vom: 12. Jan., Seite 543-551 (DE-627)SPR031096425 nnns volume:45 year:2023 number:5 day:12 month:01 pages:543-551 https://dx.doi.org/10.1007/s13258-022-01360-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 45 2023 5 12 01 543-551 |
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10.1007/s13258-022-01360-8 doi (DE-627)SPR050098810 (SPR)s13258-022-01360-8-e DE-627 ger DE-627 rakwb eng Baek, Hyojin verfasserin aut Emerging role for R-loop formation in hepatocellular carcinoma 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. R-loop (dpeaa)DE-He213 Hepatocellular carcinoma (dpeaa)DE-He213 Genome integrity (dpeaa)DE-He213 DNA damage and repair (dpeaa)DE-He213 Park, Sang-Uk aut Kim, Jeongkyu (orcid)0000-0002-8550-6654 aut Enthalten in Genes & Genomics The Genetics Society of Korea, 2010 45(2023), 5 vom: 12. Jan., Seite 543-551 (DE-627)SPR031096425 nnns volume:45 year:2023 number:5 day:12 month:01 pages:543-551 https://dx.doi.org/10.1007/s13258-022-01360-8 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER AR 45 2023 5 12 01 543-551 |
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Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Abstract The pathophysiological characteristics of hepatocellular carcinoma (HCC) is closely associated with genomic instability. Genomic instability has long been considered to be a hallmark of both human genetic disease and cancers. It is now well accepted that regulating R-loop formation to minimized levels is one of critical modulation to maintain genome integrity, and that improper regulation of R-loop metabolism causes genomic instability via DNA breakage, ultimately resulting in replicative senescence and even tumorigenesis. Given that R-loop is natural by-product formed during normal transcription condition, and that several types of cancer have defense mechanism against the genomic instability resulted from R-loop formation, modulating functional implication of proteins involved in the intrinsic and specific mechanisms of abnormal R-loop formation in cancers therefore could play an important part in appropriated therapeutic strategies for HCC cohorts. In this review, we highlight the latest understanding on how R-loops promote genomic instability and address how alterations in these pathways link to human HCC. © The Author(s) under exclusive licence to The Genetics Society of Korea 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Emerging role for R-loop formation in hepatocellular carcinoma |
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Park, Sang-Uk Kim, Jeongkyu |
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