Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction
Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linki...
Gespeichert in:
| Veröffentlicht in: | Oxidative medicine and cellular longevity 2016-01, Vol.2016 (2016), p.1-7 |
|---|---|
| Hauptverfasser: | , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 7 |
|---|---|
| container_issue | 2016 |
| container_start_page | 1 |
| container_title | Oxidative medicine and cellular longevity |
| container_volume | 2016 |
| creator | Longini, M. Guidoni, Elisa Geronzi, Ursula Lotti, Federica Perrone, Serafina Buonocore, Giuseppe |
| description | Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients. |
| doi_str_mv | 10.1155/2016/4782426 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4863121</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A515125466</galeid><sourcerecordid>A515125466</sourcerecordid><originalsourceid>FETCH-LOGICAL-c499t-c92d66369663bb4240a16634a2d3c32424fd2c61422b482bfdc7bc25b6a64bbd3</originalsourceid><addsrcrecordid>eNqN0c9vFCEUB3BiNLZdvXk2JF5M6lh-DTN4MNlstZrUtNF6Jgy82aWZhQoz1f73su66VU9egMAnX97LQ-gZJa8presTRqg8EU3LBJMP0CFVglVEKfFwfybkAB3lfE2I5EzQx-iANYwrVtND5C9-eGdGfwv4y5ggZ-wDXphgIVWXKQbAZxBg9Baf-gwmwy9wCc6bMZXb-RLe4KsV4M9xABx7_MmP0a5icMmbAZ_e5X4KdvQxPEGPejNkeLrbZ-jr-3dXiw_V-cXZx8X8vLJCqbGyijkpuVRl6TrBBDG0HIVhjttSPhO9Y1ZSwVgnWtb1zjadZXUnjRRd5_gMvd3m3kzdGpyFMCYz6Jvk1ybd6Wi8_vsl-JVexlstWskpoyXg5S4gxW8T5FGvfbYwDCZAnLKmjeKFCdoW-uIfeh2nFEp7RbWNqDkhzb1amgG0D30s_9pNqJ7XtKasFqXDGXq1VTbFnBP0-5Ip0ZtJ682k9W7ShT__s809_j3aAo63YOWDM9_9f8ZBMdCbe00pV5Lyn0rGuOo</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1787453007</pqid></control><display><type>article</type><title>Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>Wiley-Blackwell Open Access Titles</source><source>PubMed Central</source><source>Alma/SFX Local Collection</source><creator>Longini, M. ; Guidoni, Elisa ; Geronzi, Ursula ; Lotti, Federica ; Perrone, Serafina ; Buonocore, Giuseppe</creator><contributor>Saretzki, Gabriele</contributor><creatorcontrib>Longini, M. ; Guidoni, Elisa ; Geronzi, Ursula ; Lotti, Federica ; Perrone, Serafina ; Buonocore, Giuseppe ; Saretzki, Gabriele</creatorcontrib><description>Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2016/4782426</identifier><identifier>PMID: 27239251</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Age ; Age Factors ; Aging ; Animals ; Anticarcinogenic Agents - therapeutic use ; Antioxidants ; Antioxidants - therapeutic use ; Apoptosis ; Beckwith-Wiedemann Syndrome - complications ; Beckwith-Wiedemann Syndrome - drug therapy ; Beckwith-Wiedemann Syndrome - genetics ; Beckwith-Wiedemann Syndrome - metabolism ; Bioenergetics ; Biomarkers ; Cancer ; Cell cycle ; Cell Transformation, Neoplastic - genetics ; Cell Transformation, Neoplastic - metabolism ; Children ; Clinical trials ; Deoxyribonucleic acid ; Diseases ; DNA ; DNA damage ; DNA methylation ; Down syndrome ; Fanconi's anemia ; Free radicals ; Gene expression ; Genetic aspects ; Genetic disorders ; Genetic Predisposition to Disease ; Health aspects ; Humans ; Injuries ; Ionizing radiation ; Metabolism ; Mitochondria ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondrial Diseases - drug therapy ; Mitochondrial Diseases - genetics ; Mitochondrial Diseases - metabolism ; Mitochondrial DNA ; Neoplasms - genetics ; Neoplasms - metabolism ; Neoplasms - prevention & control ; Oxidative stress ; Oxidative Stress - drug effects ; Pathogenesis ; Patients ; Pediatrics ; Physiology ; Potassium ; Prader-Willi Syndrome - complications ; Prader-Willi Syndrome - drug therapy ; Prader-Willi Syndrome - genetics ; Prader-Willi Syndrome - metabolism ; Proteins ; Risk Factors ; Type 2 diabetes ; Vitamin C</subject><ispartof>Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-7</ispartof><rights>Copyright © 2016 Serafina Perrone et al.</rights><rights>COPYRIGHT 2016 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Serafina Perrone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2016 Serafina Perrone et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-c92d66369663bb4240a16634a2d3c32424fd2c61422b482bfdc7bc25b6a64bbd3</citedby><cites>FETCH-LOGICAL-c499t-c92d66369663bb4240a16634a2d3c32424fd2c61422b482bfdc7bc25b6a64bbd3</cites><orcidid>0000-0002-0878-5346 ; 0000-0001-5478-5657 ; 0000-0002-0395-7524 ; 0000-0002-7500-8686</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/PMC4863121/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4863121/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27239251$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Saretzki, Gabriele</contributor><creatorcontrib>Longini, M.</creatorcontrib><creatorcontrib>Guidoni, Elisa</creatorcontrib><creatorcontrib>Geronzi, Ursula</creatorcontrib><creatorcontrib>Lotti, Federica</creatorcontrib><creatorcontrib>Perrone, Serafina</creatorcontrib><creatorcontrib>Buonocore, Giuseppe</creatorcontrib><title>Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients.</description><subject>Age</subject><subject>Age Factors</subject><subject>Aging</subject><subject>Animals</subject><subject>Anticarcinogenic Agents - therapeutic use</subject><subject>Antioxidants</subject><subject>Antioxidants - therapeutic use</subject><subject>Apoptosis</subject><subject>Beckwith-Wiedemann Syndrome - complications</subject><subject>Beckwith-Wiedemann Syndrome - drug therapy</subject><subject>Beckwith-Wiedemann Syndrome - genetics</subject><subject>Beckwith-Wiedemann Syndrome - metabolism</subject><subject>Bioenergetics</subject><subject>Biomarkers</subject><subject>Cancer</subject><subject>Cell cycle</subject><subject>Cell Transformation, Neoplastic - genetics</subject><subject>Cell Transformation, Neoplastic - metabolism</subject><subject>Children</subject><subject>Clinical trials</subject><subject>Deoxyribonucleic acid</subject><subject>Diseases</subject><subject>DNA</subject><subject>DNA damage</subject><subject>DNA methylation</subject><subject>Down syndrome</subject><subject>Fanconi's anemia</subject><subject>Free radicals</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genetic disorders</subject><subject>Genetic Predisposition to Disease</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Injuries</subject><subject>Ionizing radiation</subject><subject>Metabolism</subject><subject>Mitochondria</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondrial Diseases - drug therapy</subject><subject>Mitochondrial Diseases - genetics</subject><subject>Mitochondrial Diseases - metabolism</subject><subject>Mitochondrial DNA</subject><subject>Neoplasms - genetics</subject><subject>Neoplasms - metabolism</subject><subject>Neoplasms - prevention & control</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Pediatrics</subject><subject>Physiology</subject><subject>Potassium</subject><subject>Prader-Willi Syndrome - complications</subject><subject>Prader-Willi Syndrome - drug therapy</subject><subject>Prader-Willi Syndrome - genetics</subject><subject>Prader-Willi Syndrome - metabolism</subject><subject>Proteins</subject><subject>Risk Factors</subject><subject>Type 2 diabetes</subject><subject>Vitamin C</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqN0c9vFCEUB3BiNLZdvXk2JF5M6lh-DTN4MNlstZrUtNF6Jgy82aWZhQoz1f73su66VU9egMAnX97LQ-gZJa8presTRqg8EU3LBJMP0CFVglVEKfFwfybkAB3lfE2I5EzQx-iANYwrVtND5C9-eGdGfwv4y5ggZ-wDXphgIVWXKQbAZxBg9Baf-gwmwy9wCc6bMZXb-RLe4KsV4M9xABx7_MmP0a5icMmbAZ_e5X4KdvQxPEGPejNkeLrbZ-jr-3dXiw_V-cXZx8X8vLJCqbGyijkpuVRl6TrBBDG0HIVhjttSPhO9Y1ZSwVgnWtb1zjadZXUnjRRd5_gMvd3m3kzdGpyFMCYz6Jvk1ybd6Wi8_vsl-JVexlstWskpoyXg5S4gxW8T5FGvfbYwDCZAnLKmjeKFCdoW-uIfeh2nFEp7RbWNqDkhzb1amgG0D30s_9pNqJ7XtKasFqXDGXq1VTbFnBP0-5Ip0ZtJ682k9W7ShT__s809_j3aAo63YOWDM9_9f8ZBMdCbe00pV5Lyn0rGuOo</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Longini, M.</creator><creator>Guidoni, Elisa</creator><creator>Geronzi, Ursula</creator><creator>Lotti, Federica</creator><creator>Perrone, Serafina</creator><creator>Buonocore, Giuseppe</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-0878-5346</orcidid><orcidid>https://orcid.org/0000-0001-5478-5657</orcidid><orcidid>https://orcid.org/0000-0002-0395-7524</orcidid><orcidid>https://orcid.org/0000-0002-7500-8686</orcidid></search><sort><creationdate>20160101</creationdate><title>Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction</title><author>Longini, M. ; Guidoni, Elisa ; Geronzi, Ursula ; Lotti, Federica ; Perrone, Serafina ; Buonocore, Giuseppe</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-c92d66369663bb4240a16634a2d3c32424fd2c61422b482bfdc7bc25b6a64bbd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Age</topic><topic>Age Factors</topic><topic>Aging</topic><topic>Animals</topic><topic>Anticarcinogenic Agents - therapeutic use</topic><topic>Antioxidants</topic><topic>Antioxidants - therapeutic use</topic><topic>Apoptosis</topic><topic>Beckwith-Wiedemann Syndrome - complications</topic><topic>Beckwith-Wiedemann Syndrome - drug therapy</topic><topic>Beckwith-Wiedemann Syndrome - genetics</topic><topic>Beckwith-Wiedemann Syndrome - metabolism</topic><topic>Bioenergetics</topic><topic>Biomarkers</topic><topic>Cancer</topic><topic>Cell cycle</topic><topic>Cell Transformation, Neoplastic - genetics</topic><topic>Cell Transformation, Neoplastic - metabolism</topic><topic>Children</topic><topic>Clinical trials</topic><topic>Deoxyribonucleic acid</topic><topic>Diseases</topic><topic>DNA</topic><topic>DNA damage</topic><topic>DNA methylation</topic><topic>Down syndrome</topic><topic>Fanconi's anemia</topic><topic>Free radicals</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genetic disorders</topic><topic>Genetic Predisposition to Disease</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Injuries</topic><topic>Ionizing radiation</topic><topic>Metabolism</topic><topic>Mitochondria</topic><topic>Mitochondria - drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondrial Diseases - drug therapy</topic><topic>Mitochondrial Diseases - genetics</topic><topic>Mitochondrial Diseases - metabolism</topic><topic>Mitochondrial DNA</topic><topic>Neoplasms - genetics</topic><topic>Neoplasms - metabolism</topic><topic>Neoplasms - prevention & control</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Pediatrics</topic><topic>Physiology</topic><topic>Potassium</topic><topic>Prader-Willi Syndrome - complications</topic><topic>Prader-Willi Syndrome - drug therapy</topic><topic>Prader-Willi Syndrome - genetics</topic><topic>Prader-Willi Syndrome - metabolism</topic><topic>Proteins</topic><topic>Risk Factors</topic><topic>Type 2 diabetes</topic><topic>Vitamin C</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Longini, M.</creatorcontrib><creatorcontrib>Guidoni, Elisa</creatorcontrib><creatorcontrib>Geronzi, Ursula</creatorcontrib><creatorcontrib>Lotti, Federica</creatorcontrib><creatorcontrib>Perrone, Serafina</creatorcontrib><creatorcontrib>Buonocore, Giuseppe</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Longini, M.</au><au>Guidoni, Elisa</au><au>Geronzi, Ursula</au><au>Lotti, Federica</au><au>Perrone, Serafina</au><au>Buonocore, Giuseppe</au><au>Saretzki, Gabriele</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>2016</volume><issue>2016</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Oxidative stress is a distinctive sign in several genetic disorders characterized by cancer predisposition, such as Ataxia-Telangiectasia, Fanconi Anemia, Down syndrome, progeroid syndromes, Beckwith-Wiedemann syndrome, and Costello syndrome. Recent literature unveiled new molecular mechanisms linking oxidative stress to the pathogenesis of these conditions, with particular regard to mitochondrial dysfunction. Since mitochondria are one of the major sites of ROS production as well as one of the major targets of their action, this dysfunction is thought to be the cause of the prooxidant status. Deeper insight of the pathogenesis of the syndromes raises the possibility to identify new possible therapeutic targets. In particular, the use of mitochondrial-targeted agents seems to be an appropriate clinical strategy in order to improve the quality of life and the life span of the patients.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>27239251</pmid><doi>10.1155/2016/4782426</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0002-0878-5346</orcidid><orcidid>https://orcid.org/0000-0001-5478-5657</orcidid><orcidid>https://orcid.org/0000-0002-0395-7524</orcidid><orcidid>https://orcid.org/0000-0002-7500-8686</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1942-0900 |
| ispartof | Oxidative medicine and cellular longevity, 2016-01, Vol.2016 (2016), p.1-7 |
| issn | 1942-0900 1942-0994 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4863121 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley-Blackwell Open Access Titles; PubMed Central; Alma/SFX Local Collection |
| subjects | Age Age Factors Aging Animals Anticarcinogenic Agents - therapeutic use Antioxidants Antioxidants - therapeutic use Apoptosis Beckwith-Wiedemann Syndrome - complications Beckwith-Wiedemann Syndrome - drug therapy Beckwith-Wiedemann Syndrome - genetics Beckwith-Wiedemann Syndrome - metabolism Bioenergetics Biomarkers Cancer Cell cycle Cell Transformation, Neoplastic - genetics Cell Transformation, Neoplastic - metabolism Children Clinical trials Deoxyribonucleic acid Diseases DNA DNA damage DNA methylation Down syndrome Fanconi's anemia Free radicals Gene expression Genetic aspects Genetic disorders Genetic Predisposition to Disease Health aspects Humans Injuries Ionizing radiation Metabolism Mitochondria Mitochondria - drug effects Mitochondria - metabolism Mitochondrial Diseases - drug therapy Mitochondrial Diseases - genetics Mitochondrial Diseases - metabolism Mitochondrial DNA Neoplasms - genetics Neoplasms - metabolism Neoplasms - prevention & control Oxidative stress Oxidative Stress - drug effects Pathogenesis Patients Pediatrics Physiology Potassium Prader-Willi Syndrome - complications Prader-Willi Syndrome - drug therapy Prader-Willi Syndrome - genetics Prader-Willi Syndrome - metabolism Proteins Risk Factors Type 2 diabetes Vitamin C |
| title | Oxidative Stress in Cancer-Prone Genetic Diseases in Pediatric Age: The Role of Mitochondrial Dysfunction |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-18T12%3A22%3A29IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Oxidative%20Stress%20in%20Cancer-Prone%20Genetic%20Diseases%20in%20Pediatric%20Age:%20The%20Role%20of%20Mitochondrial%20Dysfunction&rft.jtitle=Oxidative%20medicine%20and%20cellular%20longevity&rft.au=Longini,%20M.&rft.date=2016-01-01&rft.volume=2016&rft.issue=2016&rft.spage=1&rft.epage=7&rft.pages=1-7&rft.issn=1942-0900&rft.eissn=1942-0994&rft_id=info:doi/10.1155/2016/4782426&rft_dat=%3Cgale_pubme%3EA515125466%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1787453007&rft_id=info:pmid/27239251&rft_galeid=A515125466&rfr_iscdi=true |