HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity
HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tis...
Gespeichert in:
Veröffentlicht in: | Oncology reports 2010-01, Vol.23 (1), p.263-269 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 269 |
---|---|
container_issue | 1 |
container_start_page | 263 |
container_title | Oncology reports |
container_volume | 23 |
creator | PURRUCKER, Jan C FRICKE, Andreas MEI FANG ONG RÜBE, Christian RÜBE, Claudia E MAHLKNECHT, Ulrich |
description | HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tissue cells. We studied the effect of suberoylanilide hydroxamic acid (SAHA), MS275, sodium-butyrate and valproic acid in healthy human fibroblasts and found HDACi-treatment to go along with increased radiosensitivity and reduced DSB repair capacity. In view of the potential genotoxic effects of HDACi-treatment, particularly when being administered long-term for chronic disease or when given to children, to women of childbearing age or their partners or in combination with radiotherapy, an extensive education of patients and prescribing physicians as well as a stringent definition of clinical indications is urgently required. |
doi_str_mv | 10.3892/or_00000632 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_755143174</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>755143174</sourcerecordid><originalsourceid>FETCH-LOGICAL-c317t-77efccf76266f73a704e83ddccad8f208193405838a86cede32bd39c98e4906c3</originalsourceid><addsrcrecordid>eNpNkMtLxDAQh4Movk_eJRfxINU82iY5Lru-QPSi4K2kyZSN9rFm2oP-9WZxUecyM_w-huEj5ISzS6mNuBpixdZVSrFF9rkyPBO55NtpZoJnUhave-QA8Y0xoVhpdskeN6YoteH7pLtbzOY09MtQhzEMPY3WhwGhx7R-AdLl1Nme9kPsbEvHgDgBddC2SG3vaQQ_uUQtHmfUD1PdQoZjXCd1BPue8pUNkTq7si6Mn0dkp7EtwvGmH5KXm-vn-V328HR7P589ZE5yNWZKQeNco0pRlo2SVrEctPTeOet1I5jmRuas0FJbXTrwIEXtpXFGQ25Y6eQhOf-5u4rDxwQ4Vl3A9de2h2HCShUFT4pUnsiLH9LFATFCU61i6Gz8rDir1nqrf3oTfbq5O9Ud-D924zMBZxvAorNtk1S4gL-cEDkvcl3Ibwoig8c</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>755143174</pqid></control><display><type>article</type><title>HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>PURRUCKER, Jan C ; FRICKE, Andreas ; MEI FANG ONG ; RÜBE, Christian ; RÜBE, Claudia E ; MAHLKNECHT, Ulrich</creator><creatorcontrib>PURRUCKER, Jan C ; FRICKE, Andreas ; MEI FANG ONG ; RÜBE, Christian ; RÜBE, Claudia E ; MAHLKNECHT, Ulrich</creatorcontrib><description>HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tissue cells. We studied the effect of suberoylanilide hydroxamic acid (SAHA), MS275, sodium-butyrate and valproic acid in healthy human fibroblasts and found HDACi-treatment to go along with increased radiosensitivity and reduced DSB repair capacity. In view of the potential genotoxic effects of HDACi-treatment, particularly when being administered long-term for chronic disease or when given to children, to women of childbearing age or their partners or in combination with radiotherapy, an extensive education of patients and prescribing physicians as well as a stringent definition of clinical indications is urgently required.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or_00000632</identifier><identifier>PMID: 19956891</identifier><language>eng</language><publisher>Athens: Spandidos</publisher><subject>Benzamides - pharmacology ; Biological and medical sciences ; Cell Proliferation ; DNA Breaks, Double-Stranded ; DNA Repair ; Dose-Response Relationship, Radiation ; Fibroblasts - cytology ; Fibroblasts - drug effects ; Histone Deacetylases - metabolism ; Humans ; Hydroxamic Acids - pharmacology ; Medical sciences ; Microscopy, Fluorescence - methods ; Pyridines - pharmacology ; Signal Transduction ; Sodium Oxybate - pharmacology ; Time Factors ; Tumors ; Valproic Acid - pharmacology</subject><ispartof>Oncology reports, 2010-01, Vol.23 (1), p.263-269</ispartof><rights>2015 INIST-CNRS</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c317t-77efccf76266f73a704e83ddccad8f208193405838a86cede32bd39c98e4906c3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22415485$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19956891$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>PURRUCKER, Jan C</creatorcontrib><creatorcontrib>FRICKE, Andreas</creatorcontrib><creatorcontrib>MEI FANG ONG</creatorcontrib><creatorcontrib>RÜBE, Christian</creatorcontrib><creatorcontrib>RÜBE, Claudia E</creatorcontrib><creatorcontrib>MAHLKNECHT, Ulrich</creatorcontrib><title>HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tissue cells. We studied the effect of suberoylanilide hydroxamic acid (SAHA), MS275, sodium-butyrate and valproic acid in healthy human fibroblasts and found HDACi-treatment to go along with increased radiosensitivity and reduced DSB repair capacity. In view of the potential genotoxic effects of HDACi-treatment, particularly when being administered long-term for chronic disease or when given to children, to women of childbearing age or their partners or in combination with radiotherapy, an extensive education of patients and prescribing physicians as well as a stringent definition of clinical indications is urgently required.</description><subject>Benzamides - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cell Proliferation</subject><subject>DNA Breaks, Double-Stranded</subject><subject>DNA Repair</subject><subject>Dose-Response Relationship, Radiation</subject><subject>Fibroblasts - cytology</subject><subject>Fibroblasts - drug effects</subject><subject>Histone Deacetylases - metabolism</subject><subject>Humans</subject><subject>Hydroxamic Acids - pharmacology</subject><subject>Medical sciences</subject><subject>Microscopy, Fluorescence - methods</subject><subject>Pyridines - pharmacology</subject><subject>Signal Transduction</subject><subject>Sodium Oxybate - pharmacology</subject><subject>Time Factors</subject><subject>Tumors</subject><subject>Valproic Acid - pharmacology</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkMtLxDAQh4Movk_eJRfxINU82iY5Lru-QPSi4K2kyZSN9rFm2oP-9WZxUecyM_w-huEj5ISzS6mNuBpixdZVSrFF9rkyPBO55NtpZoJnUhave-QA8Y0xoVhpdskeN6YoteH7pLtbzOY09MtQhzEMPY3WhwGhx7R-AdLl1Nme9kPsbEvHgDgBddC2SG3vaQQ_uUQtHmfUD1PdQoZjXCd1BPue8pUNkTq7si6Mn0dkp7EtwvGmH5KXm-vn-V328HR7P589ZE5yNWZKQeNco0pRlo2SVrEctPTeOet1I5jmRuas0FJbXTrwIEXtpXFGQ25Y6eQhOf-5u4rDxwQ4Vl3A9de2h2HCShUFT4pUnsiLH9LFATFCU61i6Gz8rDir1nqrf3oTfbq5O9Ud-D924zMBZxvAorNtk1S4gL-cEDkvcl3Ibwoig8c</recordid><startdate>20100101</startdate><enddate>20100101</enddate><creator>PURRUCKER, Jan C</creator><creator>FRICKE, Andreas</creator><creator>MEI FANG ONG</creator><creator>RÜBE, Christian</creator><creator>RÜBE, Claudia E</creator><creator>MAHLKNECHT, Ulrich</creator><general>Spandidos</general><scope>IQODW</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>7TM</scope></search><sort><creationdate>20100101</creationdate><title>HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity</title><author>PURRUCKER, Jan C ; FRICKE, Andreas ; MEI FANG ONG ; RÜBE, Christian ; RÜBE, Claudia E ; MAHLKNECHT, Ulrich</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c317t-77efccf76266f73a704e83ddccad8f208193405838a86cede32bd39c98e4906c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Benzamides - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cell Proliferation</topic><topic>DNA Breaks, Double-Stranded</topic><topic>DNA Repair</topic><topic>Dose-Response Relationship, Radiation</topic><topic>Fibroblasts - cytology</topic><topic>Fibroblasts - drug effects</topic><topic>Histone Deacetylases - metabolism</topic><topic>Humans</topic><topic>Hydroxamic Acids - pharmacology</topic><topic>Medical sciences</topic><topic>Microscopy, Fluorescence - methods</topic><topic>Pyridines - pharmacology</topic><topic>Signal Transduction</topic><topic>Sodium Oxybate - pharmacology</topic><topic>Time Factors</topic><topic>Tumors</topic><topic>Valproic Acid - pharmacology</topic><toplevel>online_resources</toplevel><creatorcontrib>PURRUCKER, Jan C</creatorcontrib><creatorcontrib>FRICKE, Andreas</creatorcontrib><creatorcontrib>MEI FANG ONG</creatorcontrib><creatorcontrib>RÜBE, Christian</creatorcontrib><creatorcontrib>RÜBE, Claudia E</creatorcontrib><creatorcontrib>MAHLKNECHT, Ulrich</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Nucleic Acids Abstracts</collection><jtitle>Oncology reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>PURRUCKER, Jan C</au><au>FRICKE, Andreas</au><au>MEI FANG ONG</au><au>RÜBE, Christian</au><au>RÜBE, Claudia E</au><au>MAHLKNECHT, Ulrich</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity</atitle><jtitle>Oncology reports</jtitle><addtitle>Oncol Rep</addtitle><date>2010-01-01</date><risdate>2010</risdate><volume>23</volume><issue>1</issue><spage>263</spage><epage>269</epage><pages>263-269</pages><issn>1021-335X</issn><eissn>1791-2431</eissn><abstract>HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tissue cells. We studied the effect of suberoylanilide hydroxamic acid (SAHA), MS275, sodium-butyrate and valproic acid in healthy human fibroblasts and found HDACi-treatment to go along with increased radiosensitivity and reduced DSB repair capacity. In view of the potential genotoxic effects of HDACi-treatment, particularly when being administered long-term for chronic disease or when given to children, to women of childbearing age or their partners or in combination with radiotherapy, an extensive education of patients and prescribing physicians as well as a stringent definition of clinical indications is urgently required.</abstract><cop>Athens</cop><pub>Spandidos</pub><pmid>19956891</pmid><doi>10.3892/or_00000632</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1021-335X |
ispartof | Oncology reports, 2010-01, Vol.23 (1), p.263-269 |
issn | 1021-335X 1791-2431 |
language | eng |
recordid | cdi_proquest_miscellaneous_755143174 |
source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
subjects | Benzamides - pharmacology Biological and medical sciences Cell Proliferation DNA Breaks, Double-Stranded DNA Repair Dose-Response Relationship, Radiation Fibroblasts - cytology Fibroblasts - drug effects Histone Deacetylases - metabolism Humans Hydroxamic Acids - pharmacology Medical sciences Microscopy, Fluorescence - methods Pyridines - pharmacology Signal Transduction Sodium Oxybate - pharmacology Time Factors Tumors Valproic Acid - pharmacology |
title | HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T07%3A26%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=HDAC%20inhibition%20radiosensitizes%20human%20normal%20tissue%20cells%20and%20reduces%20DNA%20double-strand%20break%20repair%20capacity&rft.jtitle=Oncology%20reports&rft.au=PURRUCKER,%20Jan%20C&rft.date=2010-01-01&rft.volume=23&rft.issue=1&rft.spage=263&rft.epage=269&rft.pages=263-269&rft.issn=1021-335X&rft.eissn=1791-2431&rft_id=info:doi/10.3892/or_00000632&rft_dat=%3Cproquest_cross%3E755143174%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=755143174&rft_id=info:pmid/19956891&rfr_iscdi=true |