Clinical and genetic associations for carboplatin‐related ototoxicity in children treated for retinoblastoma: A retrospective noncomparative single‐institute experience
Background Children with retinoblastoma treated with carboplatin chemotherapy risk moderate to severe, irreversible hearing loss. Based on published evidence, we hypothesized that ototoxicity risk is associated with clinical parameters and variants in candidate genes in drug metabolism pathways (met...
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| creator | Soliman, Sameh E. D'Silva, Crystal N. Dimaras, Helen Dzneladze, Irakli Chan, Helen Gallie, Brenda L. |
| description | Background
Children with retinoblastoma treated with carboplatin chemotherapy risk moderate to severe, irreversible hearing loss. Based on published evidence, we hypothesized that ototoxicity risk is associated with clinical parameters and variants in candidate genes in drug metabolism pathways (methyltransferases [thiopurine S‐methyltransferase, TPMT] and [catechol‐O‐methyltransferase, COMT], and drug transporter ABCC3).
Procedure
We retrospectively reviewed clinical records of patients with retinoblastoma treated with carboplatin chemotherapy regarding age (at diagnosis and chemotherapy initiation), chemotherapy sessions (cycles number, drug doses, and cumulative carboplatin dose), and hearing loss (defined as ototoxicity ≥grade 2 by at least one classification system). Blood samples were genotyped for genetic variants in TPMT (rs12201199, rs1800460), COMT (rs4646316, rs9332377), and ABCC3 (rs1051640) by quantitative PCR and confirmed by allele‐specific PCR. Univariate statistical tests, receiver‐operating characteristic analysis, and Kaplan–Meier curves were used to examine the association between hearing loss, clinical factors, and variants in candidate genes.
Results
Audiometric data and stored DNA were available for 71 patients with retinoblastoma (88% carried an RB1 pathogenic variant allele). Median carboplatin cumulative dose was 1,400 mg/m2 (260–5,148 mg/m2). Ototoxicity occurred in 18 patients (25%), strongly associated with age at diagnosis (P = 0.01) and age at chemotherapy initiation (OR = 4.99, P = 0.008). The highest likelihood ratio of hearing loss was associated with chemotherapy initiation |
| doi_str_mv | 10.1002/pbc.26931 |
| format | Article |
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Children with retinoblastoma treated with carboplatin chemotherapy risk moderate to severe, irreversible hearing loss. Based on published evidence, we hypothesized that ototoxicity risk is associated with clinical parameters and variants in candidate genes in drug metabolism pathways (methyltransferases [thiopurine S‐methyltransferase, TPMT] and [catechol‐O‐methyltransferase, COMT], and drug transporter ABCC3).
Procedure
We retrospectively reviewed clinical records of patients with retinoblastoma treated with carboplatin chemotherapy regarding age (at diagnosis and chemotherapy initiation), chemotherapy sessions (cycles number, drug doses, and cumulative carboplatin dose), and hearing loss (defined as ototoxicity ≥grade 2 by at least one classification system). Blood samples were genotyped for genetic variants in TPMT (rs12201199, rs1800460), COMT (rs4646316, rs9332377), and ABCC3 (rs1051640) by quantitative PCR and confirmed by allele‐specific PCR. Univariate statistical tests, receiver‐operating characteristic analysis, and Kaplan–Meier curves were used to examine the association between hearing loss, clinical factors, and variants in candidate genes.
Results
Audiometric data and stored DNA were available for 71 patients with retinoblastoma (88% carried an RB1 pathogenic variant allele). Median carboplatin cumulative dose was 1,400 mg/m2 (260–5,148 mg/m2). Ototoxicity occurred in 18 patients (25%), strongly associated with age at diagnosis (P = 0.01) and age at chemotherapy initiation (OR = 4.99, P = 0.008). The highest likelihood ratio of hearing loss was associated with chemotherapy initiation <4.25 months of age. Ototoxicity was not associated with any tested genetic variants.
Conclusions
We observed a 25% prevalence of ototoxicity in patients with retinoblastoma treated with carboplatin, higher than previously published. Age at chemotherapy initiation was associated with carboplatin‐induced ototoxicity, with children <4.25 months of age at highest risk.</description><identifier>ISSN: 1545-5009</identifier><identifier>EISSN: 1545-5017</identifier><identifier>DOI: 10.1002/pbc.26931</identifier><identifier>PMID: 29350448</identifier><language>eng</language><publisher>United States: Wiley Subscription Services, Inc</publisher><subject>Age ; Alleles ; Antineoplastic Agents - adverse effects ; Cancer ; Carboplatin ; Carboplatin - adverse effects ; Catechol ; Catechol O-methyltransferase ; Catechol O-Methyltransferase - genetics ; Chemotherapy ; Child ; Child, Preschool ; Children ; Deoxyribonucleic acid ; Diagnosis ; DNA ; Drug dosages ; Drug metabolism ; Female ; Follow-Up Studies ; Genetic diversity ; Genetic Markers ; Genetic variance ; genetics ; Hearing loss ; Hearing Loss - chemically induced ; Hearing Loss - diagnosis ; Hearing Loss - genetics ; Hematology ; Humans ; Infant ; Likelihood ratio ; Male ; Methyltransferase ; Methyltransferases - genetics ; Multidrug Resistance-Associated Proteins - genetics ; Oncology ; Ototoxicity ; Pediatrics ; Polymerase chain reaction ; Polymorphism, Single Nucleotide ; Prognosis ; Retina ; Retinal Neoplasms - drug therapy ; Retinal Neoplasms - pathology ; Retinoblastoma ; Retinoblastoma - drug therapy ; Retinoblastoma - pathology ; Retrospective Studies ; Statistical analysis ; Tumors</subject><ispartof>Pediatric blood & cancer, 2018-05, Vol.65 (5), p.e26931-n/a</ispartof><rights>2018 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3531-f528c2772b1fec6e300903d6ad080231e523667352080d6a6ad0b2d9966ca8fc3</citedby><cites>FETCH-LOGICAL-c3531-f528c2772b1fec6e300903d6ad080231e523667352080d6a6ad0b2d9966ca8fc3</cites><orcidid>0000-0001-8926-0252</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fpbc.26931$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fpbc.26931$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,777,781,1412,27905,27906,45555,45556</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29350448$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Soliman, Sameh E.</creatorcontrib><creatorcontrib>D'Silva, Crystal N.</creatorcontrib><creatorcontrib>Dimaras, Helen</creatorcontrib><creatorcontrib>Dzneladze, Irakli</creatorcontrib><creatorcontrib>Chan, Helen</creatorcontrib><creatorcontrib>Gallie, Brenda L.</creatorcontrib><title>Clinical and genetic associations for carboplatin‐related ototoxicity in children treated for retinoblastoma: A retrospective noncomparative single‐institute experience</title><title>Pediatric blood & cancer</title><addtitle>Pediatr Blood Cancer</addtitle><description>Background
Children with retinoblastoma treated with carboplatin chemotherapy risk moderate to severe, irreversible hearing loss. Based on published evidence, we hypothesized that ototoxicity risk is associated with clinical parameters and variants in candidate genes in drug metabolism pathways (methyltransferases [thiopurine S‐methyltransferase, TPMT] and [catechol‐O‐methyltransferase, COMT], and drug transporter ABCC3).
Procedure
We retrospectively reviewed clinical records of patients with retinoblastoma treated with carboplatin chemotherapy regarding age (at diagnosis and chemotherapy initiation), chemotherapy sessions (cycles number, drug doses, and cumulative carboplatin dose), and hearing loss (defined as ototoxicity ≥grade 2 by at least one classification system). Blood samples were genotyped for genetic variants in TPMT (rs12201199, rs1800460), COMT (rs4646316, rs9332377), and ABCC3 (rs1051640) by quantitative PCR and confirmed by allele‐specific PCR. Univariate statistical tests, receiver‐operating characteristic analysis, and Kaplan–Meier curves were used to examine the association between hearing loss, clinical factors, and variants in candidate genes.
Results
Audiometric data and stored DNA were available for 71 patients with retinoblastoma (88% carried an RB1 pathogenic variant allele). Median carboplatin cumulative dose was 1,400 mg/m2 (260–5,148 mg/m2). Ototoxicity occurred in 18 patients (25%), strongly associated with age at diagnosis (P = 0.01) and age at chemotherapy initiation (OR = 4.99, P = 0.008). The highest likelihood ratio of hearing loss was associated with chemotherapy initiation <4.25 months of age. Ototoxicity was not associated with any tested genetic variants.
Conclusions
We observed a 25% prevalence of ototoxicity in patients with retinoblastoma treated with carboplatin, higher than previously published. Age at chemotherapy initiation was associated with carboplatin‐induced ototoxicity, with children <4.25 months of age at highest risk.</description><subject>Age</subject><subject>Alleles</subject><subject>Antineoplastic Agents - adverse effects</subject><subject>Cancer</subject><subject>Carboplatin</subject><subject>Carboplatin - adverse effects</subject><subject>Catechol</subject><subject>Catechol O-methyltransferase</subject><subject>Catechol O-Methyltransferase - genetics</subject><subject>Chemotherapy</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Children</subject><subject>Deoxyribonucleic acid</subject><subject>Diagnosis</subject><subject>DNA</subject><subject>Drug dosages</subject><subject>Drug metabolism</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Genetic diversity</subject><subject>Genetic Markers</subject><subject>Genetic variance</subject><subject>genetics</subject><subject>Hearing loss</subject><subject>Hearing Loss - chemically induced</subject><subject>Hearing Loss - diagnosis</subject><subject>Hearing Loss - genetics</subject><subject>Hematology</subject><subject>Humans</subject><subject>Infant</subject><subject>Likelihood ratio</subject><subject>Male</subject><subject>Methyltransferase</subject><subject>Methyltransferases - genetics</subject><subject>Multidrug Resistance-Associated Proteins - genetics</subject><subject>Oncology</subject><subject>Ototoxicity</subject><subject>Pediatrics</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prognosis</subject><subject>Retina</subject><subject>Retinal Neoplasms - drug therapy</subject><subject>Retinal Neoplasms - pathology</subject><subject>Retinoblastoma</subject><subject>Retinoblastoma - drug therapy</subject><subject>Retinoblastoma - pathology</subject><subject>Retrospective Studies</subject><subject>Statistical analysis</subject><subject>Tumors</subject><issn>1545-5009</issn><issn>1545-5017</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kbtOHDEUhq0oKMCGIi-ALKWBYsGXtXcmHaxIgoSUFKG2PJ4zxMhjD7YH2I5H4EHyVHmSeHYJRaTIhc_lO78vP0IfKDmhhLDToTEnTNacvkF7VCzEXBC6fPsak3oX7ad0W1BJRPUO7bKaC7JYVHvo18pZb412WPsW34CHbA3WKQVjdbbBJ9yFiI2OTRhcqfjfT88RSgQtDrmsR2tsXmPrsflpXRvB4xxh058mYxH0oXE65dDrT_hsqsSQBjDZ3gP2wZvQDzrqTZqsv3FQzrA-ZZvHDBgeB4gWvIH3aKfTLsHByz5D158vfqy-zq--fblcnV3NDReczjvBKsOWS9bQDowEXn6A8FbqllSEcQqCcSmXXLCSl_LUaFhb11IaXXWGz9DRVneI4W6ElFVvkwHntIcwJkXrqpZkMYnN0Md_0NswRl9up1gxQVac8KpQx1vKlJenCJ0aou11XCtK1GShKhaqjYWFPXxRHJse2lfyr2cFON0CD9bB-v9K6vv5aiv5B8bFq40</recordid><startdate>201805</startdate><enddate>201805</enddate><creator>Soliman, Sameh E.</creator><creator>D'Silva, Crystal N.</creator><creator>Dimaras, Helen</creator><creator>Dzneladze, Irakli</creator><creator>Chan, Helen</creator><creator>Gallie, Brenda L.</creator><general>Wiley Subscription Services, Inc</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>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-8926-0252</orcidid></search><sort><creationdate>201805</creationdate><title>Clinical and genetic associations for carboplatin‐related ototoxicity in children treated for retinoblastoma: A retrospective noncomparative single‐institute experience</title><author>Soliman, Sameh E. ; D'Silva, Crystal N. ; Dimaras, Helen ; Dzneladze, Irakli ; Chan, Helen ; Gallie, Brenda L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3531-f528c2772b1fec6e300903d6ad080231e523667352080d6a6ad0b2d9966ca8fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Age</topic><topic>Alleles</topic><topic>Antineoplastic Agents - adverse effects</topic><topic>Cancer</topic><topic>Carboplatin</topic><topic>Carboplatin - adverse effects</topic><topic>Catechol</topic><topic>Catechol O-methyltransferase</topic><topic>Catechol O-Methyltransferase - genetics</topic><topic>Chemotherapy</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Children</topic><topic>Deoxyribonucleic acid</topic><topic>Diagnosis</topic><topic>DNA</topic><topic>Drug dosages</topic><topic>Drug metabolism</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Genetic diversity</topic><topic>Genetic Markers</topic><topic>Genetic variance</topic><topic>genetics</topic><topic>Hearing loss</topic><topic>Hearing Loss - chemically induced</topic><topic>Hearing Loss - diagnosis</topic><topic>Hearing Loss - genetics</topic><topic>Hematology</topic><topic>Humans</topic><topic>Infant</topic><topic>Likelihood ratio</topic><topic>Male</topic><topic>Methyltransferase</topic><topic>Methyltransferases - genetics</topic><topic>Multidrug Resistance-Associated Proteins - genetics</topic><topic>Oncology</topic><topic>Ototoxicity</topic><topic>Pediatrics</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prognosis</topic><topic>Retina</topic><topic>Retinal Neoplasms - drug therapy</topic><topic>Retinal Neoplasms - pathology</topic><topic>Retinoblastoma</topic><topic>Retinoblastoma - drug therapy</topic><topic>Retinoblastoma - pathology</topic><topic>Retrospective Studies</topic><topic>Statistical analysis</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Soliman, Sameh E.</creatorcontrib><creatorcontrib>D'Silva, Crystal N.</creatorcontrib><creatorcontrib>Dimaras, Helen</creatorcontrib><creatorcontrib>Dzneladze, Irakli</creatorcontrib><creatorcontrib>Chan, Helen</creatorcontrib><creatorcontrib>Gallie, Brenda L.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Neurosciences 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>MEDLINE - Academic</collection><jtitle>Pediatric blood & cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Soliman, Sameh E.</au><au>D'Silva, Crystal N.</au><au>Dimaras, Helen</au><au>Dzneladze, Irakli</au><au>Chan, Helen</au><au>Gallie, Brenda L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical and genetic associations for carboplatin‐related ototoxicity in children treated for retinoblastoma: A retrospective noncomparative single‐institute experience</atitle><jtitle>Pediatric blood & cancer</jtitle><addtitle>Pediatr Blood Cancer</addtitle><date>2018-05</date><risdate>2018</risdate><volume>65</volume><issue>5</issue><spage>e26931</spage><epage>n/a</epage><pages>e26931-n/a</pages><issn>1545-5009</issn><eissn>1545-5017</eissn><abstract>Background
Children with retinoblastoma treated with carboplatin chemotherapy risk moderate to severe, irreversible hearing loss. Based on published evidence, we hypothesized that ototoxicity risk is associated with clinical parameters and variants in candidate genes in drug metabolism pathways (methyltransferases [thiopurine S‐methyltransferase, TPMT] and [catechol‐O‐methyltransferase, COMT], and drug transporter ABCC3).
Procedure
We retrospectively reviewed clinical records of patients with retinoblastoma treated with carboplatin chemotherapy regarding age (at diagnosis and chemotherapy initiation), chemotherapy sessions (cycles number, drug doses, and cumulative carboplatin dose), and hearing loss (defined as ototoxicity ≥grade 2 by at least one classification system). Blood samples were genotyped for genetic variants in TPMT (rs12201199, rs1800460), COMT (rs4646316, rs9332377), and ABCC3 (rs1051640) by quantitative PCR and confirmed by allele‐specific PCR. Univariate statistical tests, receiver‐operating characteristic analysis, and Kaplan–Meier curves were used to examine the association between hearing loss, clinical factors, and variants in candidate genes.
Results
Audiometric data and stored DNA were available for 71 patients with retinoblastoma (88% carried an RB1 pathogenic variant allele). Median carboplatin cumulative dose was 1,400 mg/m2 (260–5,148 mg/m2). Ototoxicity occurred in 18 patients (25%), strongly associated with age at diagnosis (P = 0.01) and age at chemotherapy initiation (OR = 4.99, P = 0.008). The highest likelihood ratio of hearing loss was associated with chemotherapy initiation <4.25 months of age. Ototoxicity was not associated with any tested genetic variants.
Conclusions
We observed a 25% prevalence of ototoxicity in patients with retinoblastoma treated with carboplatin, higher than previously published. Age at chemotherapy initiation was associated with carboplatin‐induced ototoxicity, with children <4.25 months of age at highest risk.</abstract><cop>United States</cop><pub>Wiley Subscription Services, Inc</pub><pmid>29350448</pmid><doi>10.1002/pbc.26931</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-8926-0252</orcidid></addata></record> |
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| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | Age Alleles Antineoplastic Agents - adverse effects Cancer Carboplatin Carboplatin - adverse effects Catechol Catechol O-methyltransferase Catechol O-Methyltransferase - genetics Chemotherapy Child Child, Preschool Children Deoxyribonucleic acid Diagnosis DNA Drug dosages Drug metabolism Female Follow-Up Studies Genetic diversity Genetic Markers Genetic variance genetics Hearing loss Hearing Loss - chemically induced Hearing Loss - diagnosis Hearing Loss - genetics Hematology Humans Infant Likelihood ratio Male Methyltransferase Methyltransferases - genetics Multidrug Resistance-Associated Proteins - genetics Oncology Ototoxicity Pediatrics Polymerase chain reaction Polymorphism, Single Nucleotide Prognosis Retina Retinal Neoplasms - drug therapy Retinal Neoplasms - pathology Retinoblastoma Retinoblastoma - drug therapy Retinoblastoma - pathology Retrospective Studies Statistical analysis Tumors |
| title | Clinical and genetic associations for carboplatin‐related ototoxicity in children treated for retinoblastoma: A retrospective noncomparative single‐institute experience |
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