The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity
Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxi...
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| description | Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an
study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (
) and programmed cell death 1 (
) in blood exhibited significant and positive correlations with the severity of DICT. In an
study using cardiomyocyte H9c2 cells, knockdown of
or
by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of
and
in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for
and
mRNA expression in DICT. |
| doi_str_mv | 10.3892/mmr.2020.11752 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7723161</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A650119423</galeid><sourcerecordid>A650119423</sourcerecordid><originalsourceid>FETCH-LOGICAL-c485t-d92ece427a5d9921cdaeb71b5eae1e0a3451d87e0a992d1cb192193438b555853</originalsourceid><addsrcrecordid>eNptkc9qFTEUxoMotla3LiXg-l5zkslkshEuxT-FoqXUdcgkZ9qUO8k1mSm3u75CX9EnMW2vVaFkkZPz_c7HCR8hb4EtRaf5h3HMS844WwIoyZ-RfVAaFoKx5vmu5lqrPfKqlEvGWsmlfkn2hKgEk2qflLMLpOPptxXF7SZjKSFFmgZ6tG6pjZ6eeOeB2oy0qj64KVzhvbDJacKH52DdlHKhQ8rUp23Kcx9ciL9ubkP0s0NPnc0-pClta3-6fk1eDHZd8M3uPiA_Pn86O_y6OP7-5ehwdbxwTSenhdccHTZcWem15uC8xV5BL9EiILOikeA7VauqenA9VEiLRnS9lLKT4oB8fPDdzP2I3mGcsl2bTQ6jzdcm2WD-V2K4MOfpyijFBbRQDd7vDHL6OWOZzGWac6w7G94oBY1QLf9Lnds1mhCHVM3cGIozq1YyAN1wUanlE1Q9HsfgUsQh1P5TAy6nUjIOj4sDM3fZm5q9ucve3GdfB979-91H_E_Y4jfTGqvm</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2477143762</pqid></control><display><type>article</type><title>The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity</title><source>Spandidos Publications Journals</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Kanno, Syu-Ichi ; Hara, Akiyoshi</creator><creatorcontrib>Kanno, Syu-Ichi ; Hara, Akiyoshi</creatorcontrib><description>Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an
study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (
) and programmed cell death 1 (
) in blood exhibited significant and positive correlations with the severity of DICT. In an
study using cardiomyocyte H9c2 cells, knockdown of
or
by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of
and
in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for
and
mRNA expression in DICT.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2020.11752</identifier><identifier>PMID: 33300057</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Animals ; Anthracycline ; Apoptosis ; Aspartate aminotransferase ; Blood ; Calcium-binding protein ; Cancer ; Cardiomyocytes ; Cardiotoxicity ; Cardiotoxicity - metabolism ; Cardiotoxicity - pathology ; Cell death ; Cell Line ; Chemotherapy ; Complications and side effects ; Congestive heart failure ; Creatine ; Creatine kinase ; Dehydrogenases ; Doxorubicin ; Doxorubicin - pharmacology ; Drug dosages ; Drug therapy ; Drugs ; Experiments ; Gene expression ; Gene Expression Regulation - drug effects ; Genes ; Genetic aspects ; Health aspects ; Heart diseases ; Heart failure ; Hematology ; Interleukin 6 ; Interleukin-6 - biosynthesis ; Kinases ; L-Lactate dehydrogenase ; Laboratories ; Lactic acid ; Male ; Messenger RNA ; Mice ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; PD-1 protein ; Physiological aspects ; Prognosis ; Programmed Cell Death 1 Receptor - biosynthesis ; Risk factors ; RNA, Messenger - biosynthesis ; Serum levels ; siRNA ; Transcription ; Troponin ; Troponin T</subject><ispartof>Molecular medicine reports, 2021-02, Vol.23 (2), Article 113</ispartof><rights>COPYRIGHT 2021 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2021</rights><rights>Copyright: © Kanno et al. 2020</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c485t-d92ece427a5d9921cdaeb71b5eae1e0a3451d87e0a992d1cb192193438b555853</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,778,782,883,27911,27912</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33300057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kanno, Syu-Ichi</creatorcontrib><creatorcontrib>Hara, Akiyoshi</creatorcontrib><title>The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an
study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (
) and programmed cell death 1 (
) in blood exhibited significant and positive correlations with the severity of DICT. In an
study using cardiomyocyte H9c2 cells, knockdown of
or
by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of
and
in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for
and
mRNA expression in DICT.</description><subject>Animals</subject><subject>Anthracycline</subject><subject>Apoptosis</subject><subject>Aspartate aminotransferase</subject><subject>Blood</subject><subject>Calcium-binding protein</subject><subject>Cancer</subject><subject>Cardiomyocytes</subject><subject>Cardiotoxicity</subject><subject>Cardiotoxicity - metabolism</subject><subject>Cardiotoxicity - pathology</subject><subject>Cell death</subject><subject>Cell Line</subject><subject>Chemotherapy</subject><subject>Complications and side effects</subject><subject>Congestive heart failure</subject><subject>Creatine</subject><subject>Creatine kinase</subject><subject>Dehydrogenases</subject><subject>Doxorubicin</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug dosages</subject><subject>Drug therapy</subject><subject>Drugs</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Hematology</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - biosynthesis</subject><subject>Kinases</subject><subject>L-Lactate dehydrogenase</subject><subject>Laboratories</subject><subject>Lactic acid</subject><subject>Male</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>PD-1 protein</subject><subject>Physiological aspects</subject><subject>Prognosis</subject><subject>Programmed Cell Death 1 Receptor - biosynthesis</subject><subject>Risk factors</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Serum levels</subject><subject>siRNA</subject><subject>Transcription</subject><subject>Troponin</subject><subject>Troponin T</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc9qFTEUxoMotla3LiXg-l5zkslkshEuxT-FoqXUdcgkZ9qUO8k1mSm3u75CX9EnMW2vVaFkkZPz_c7HCR8hb4EtRaf5h3HMS844WwIoyZ-RfVAaFoKx5vmu5lqrPfKqlEvGWsmlfkn2hKgEk2qflLMLpOPptxXF7SZjKSFFmgZ6tG6pjZ6eeOeB2oy0qj64KVzhvbDJacKH52DdlHKhQ8rUp23Kcx9ciL9ubkP0s0NPnc0-pClta3-6fk1eDHZd8M3uPiA_Pn86O_y6OP7-5ehwdbxwTSenhdccHTZcWem15uC8xV5BL9EiILOikeA7VauqenA9VEiLRnS9lLKT4oB8fPDdzP2I3mGcsl2bTQ6jzdcm2WD-V2K4MOfpyijFBbRQDd7vDHL6OWOZzGWac6w7G94oBY1QLf9Lnds1mhCHVM3cGIozq1YyAN1wUanlE1Q9HsfgUsQh1P5TAy6nUjIOj4sDM3fZm5q9ucve3GdfB979-91H_E_Y4jfTGqvm</recordid><startdate>20210201</startdate><enddate>20210201</enddate><creator>Kanno, Syu-Ichi</creator><creator>Hara, Akiyoshi</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><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>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20210201</creationdate><title>The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity</title><author>Kanno, Syu-Ichi ; Hara, Akiyoshi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c485t-d92ece427a5d9921cdaeb71b5eae1e0a3451d87e0a992d1cb192193438b555853</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Anthracycline</topic><topic>Apoptosis</topic><topic>Aspartate aminotransferase</topic><topic>Blood</topic><topic>Calcium-binding protein</topic><topic>Cancer</topic><topic>Cardiomyocytes</topic><topic>Cardiotoxicity</topic><topic>Cardiotoxicity - metabolism</topic><topic>Cardiotoxicity - pathology</topic><topic>Cell death</topic><topic>Cell Line</topic><topic>Chemotherapy</topic><topic>Complications and side effects</topic><topic>Congestive heart failure</topic><topic>Creatine</topic><topic>Creatine kinase</topic><topic>Dehydrogenases</topic><topic>Doxorubicin</topic><topic>Doxorubicin - pharmacology</topic><topic>Drug dosages</topic><topic>Drug therapy</topic><topic>Drugs</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Hematology</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - biosynthesis</topic><topic>Kinases</topic><topic>L-Lactate dehydrogenase</topic><topic>Laboratories</topic><topic>Lactic acid</topic><topic>Male</topic><topic>Messenger RNA</topic><topic>Mice</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>PD-1 protein</topic><topic>Physiological aspects</topic><topic>Prognosis</topic><topic>Programmed Cell Death 1 Receptor - biosynthesis</topic><topic>Risk factors</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Serum levels</topic><topic>siRNA</topic><topic>Transcription</topic><topic>Troponin</topic><topic>Troponin T</topic><toplevel>online_resources</toplevel><creatorcontrib>Kanno, Syu-Ichi</creatorcontrib><creatorcontrib>Hara, Akiyoshi</creatorcontrib><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>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</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>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science 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>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kanno, Syu-Ichi</au><au>Hara, Akiyoshi</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2021-02-01</date><risdate>2021</risdate><volume>23</volume><issue>2</issue><artnum>113</artnum><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Anthracyclines, such as doxorubicin (DOX), have been widely used in the treatment of a number of different solid and hematological malignancies. However, these drugs can inflict cumulative dose‑dependent and irreversible damage to the heart, and can occasionally lead to heart failure. The cardiotoxic susceptibility varies among patients treated with anthracycline, and delays in the recognition of cardiotoxicity can result in poor prognoses. Accordingly, if the risk of cardiotoxicity could be predicted prior to drug administration, it would aid in safer and more effective chemotherapy treatment. The present study was carried out to identify genes that can predict DOX‑induced cardiotoxicity (DICT). In an
study, mice cumulatively treated with DOX demonstrated increases in serum levels of cardiac enzymes (aspartate aminotransferase, lactate dehydrogenase, creatine kinase MB isoenzyme and troponin T), in addition to decreases in body and heart weights. These changes were indicative of DICT, but the severity of these effects varied among individual mice. In the current study, the correlation in these mice between the extent of DICT and circulating blood concentrations of relevant transcripts before DOX administration was analyzed. Among various candidate genes, the plasma mRNA levels of the genes encoding interleukin 6 (
) and programmed cell death 1 (
) in blood exhibited significant and positive correlations with the severity of DICT. In an
study using cardiomyocyte H9c2 cells, knockdown of
or
by small interfering RNA was revealed to enhance DOX‑induced apoptosis, as determined by luminescent assays. These results suggested that the levels of transcription of
and
in cardiomyocytes serve a protective role against DICT, and that the accumulation of these gene transcripts in blood is a predictive marker for DICT. To the best of our knowledge, this is the first report to demonstrate a role for
and
mRNA expression in DICT.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>33300057</pmid><doi>10.3892/mmr.2020.11752</doi><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Anthracycline Apoptosis Aspartate aminotransferase Blood Calcium-binding protein Cancer Cardiomyocytes Cardiotoxicity Cardiotoxicity - metabolism Cardiotoxicity - pathology Cell death Cell Line Chemotherapy Complications and side effects Congestive heart failure Creatine Creatine kinase Dehydrogenases Doxorubicin Doxorubicin - pharmacology Drug dosages Drug therapy Drugs Experiments Gene expression Gene Expression Regulation - drug effects Genes Genetic aspects Health aspects Heart diseases Heart failure Hematology Interleukin 6 Interleukin-6 - biosynthesis Kinases L-Lactate dehydrogenase Laboratories Lactic acid Male Messenger RNA Mice Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology PD-1 protein Physiological aspects Prognosis Programmed Cell Death 1 Receptor - biosynthesis Risk factors RNA, Messenger - biosynthesis Serum levels siRNA Transcription Troponin Troponin T |
| title | The mRNA expression of Il6 and Pdcd1 are predictive and protective factors for doxorubicin‑induced cardiotoxicity |
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