Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer
Purpose Cyclophosphamide is a commonly used cancer agent that is metabolically activated by polymorphic enzymes. This study aims to investigate the association between predicted activity of candidate pharmacogenes with severe toxicity during cyclophosphamide treatment. Methods Genome-wide genetic da...
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| Veröffentlicht in: | Supportive care in cancer 2022-09, Vol.30 (9), p.7355-7363 |
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| creator | Hwang, Mary Medley, Sarah Shakeel, Faisal Vanderwerff, Brett Zawistowski, Matthew Kidwell, Kelley M. Hertz, Daniel L. |
| description | Purpose
Cyclophosphamide is a commonly used cancer agent that is metabolically activated by polymorphic enzymes. This study aims to investigate the association between predicted activity of candidate pharmacogenes with severe toxicity during cyclophosphamide treatment.
Methods
Genome-wide genetic data was collected from an institutional genetic data repository for
CYP2B6
,
CYP3A4
,
CYP2C9
,
CYP2C19
,
GSTA1
,
GSTP1
,
ALDH1A1
,
ALDH3A1
,
ABCC1
,
ABCB1
, and
ERCC1
. Treatment and toxicity data were retrospectively collected from the patient’s medical record. The a priori selected primary hypothesis was that patients who have
CYP2B6
reduced metabolizer activity (poor or intermediate (PM/IM) vs. normal (NM) metabolizer) have lower risk of severe toxicity or cyclophosphamide treatment modification due to toxicity.
Results
In the primary analysis of 510 cyclophosphamide-treated patients with available genetic data, there was no difference in the odds of severe toxicity or treatment modification due to toxicity in
CYP2B6
PM/IM vs. NM (odds ratio = 0.97, 95% Confidence Interval: 0.62–1.50,
p
= 0.88). In an exploratory, statistically uncorrected secondary analysis, carriers of the
ALDH1A1
rs8187996 variant had a lower risk of the primary toxicity endpoint compared with wild-type homozygous patients (odds ratio = 0.31, 95% Confidence Interval: 0.09–0.78,
p
= 0.028). None of the other tested phenotypes or genotypes was associated with the primary or secondary endpoints in unadjusted analysis (all
p
> 0.05).
Conclusion
The finding that patients who carry
ALDH1A1
rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism. We found weak evidence that any of these candidate pharmacogenetic predictors of cyclophosphamide toxicity may be useful to personalize cyclophosphamide dosing to optimize therapeutic outcomes in patients with cancer. |
| doi_str_mv | 10.1007/s00520-022-07118-y |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_2668909386</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A714262735</galeid><sourcerecordid>A714262735</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-4603f4f57fccf980cdc87208bca0cd2764859fb2eddac8a626d9abcd6c3c98fd3</originalsourceid><addsrcrecordid>eNp9kUuPFCEUhYnROD2jf8CFqcSNmxp5VAG1HDs6mnSiC124IvQFuhmroAQ6Wv9e2p7xFWNYXLj3OyeXHISeEHxJMBYvMsY9xS2mtMWCENku99CKdIy1grHhPlrhoSNtx_r-DJ3nfIMxEaKnD9EZ6znmnZArZDcaPjfRNTrnCF4XH8Pxuf70nr7kzbzXadIQdzbY4iE3X33ZN7DAGOd9zHU8eWObEr958GVpfGjm6mFDuUN1AJseoQdOj9k-vq0X6OPrVx_Wb9rNu-u366tNC0zQ0nYcM9e5XjgAN0gMBqSgWG5B1zsVvJP94LbUGqNBak65GfQWDAcGg3SGXaDnJ985xS8Hm4uafAY7jjrYeMiKci4HPDDJK_rsL_QmHlKo2ykqMCOS0v43aqdHq3xwsSQNR1N1JUhHORWsr9TlP6h6jJ08xGCdr_0_BPQkgBRzTtapOflJp0URrI7ZqlO2qmarfmSrlip6ervxYTtZ81NyF2YF2AnIdRR2Nv360n9svwNel69d</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2703182256</pqid></control><display><type>article</type><title>Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer</title><source>Springer Nature - Complete Springer Journals</source><creator>Hwang, Mary ; Medley, Sarah ; Shakeel, Faisal ; Vanderwerff, Brett ; Zawistowski, Matthew ; Kidwell, Kelley M. ; Hertz, Daniel L.</creator><creatorcontrib>Hwang, Mary ; Medley, Sarah ; Shakeel, Faisal ; Vanderwerff, Brett ; Zawistowski, Matthew ; Kidwell, Kelley M. ; Hertz, Daniel L.</creatorcontrib><description>Purpose
Cyclophosphamide is a commonly used cancer agent that is metabolically activated by polymorphic enzymes. This study aims to investigate the association between predicted activity of candidate pharmacogenes with severe toxicity during cyclophosphamide treatment.
Methods
Genome-wide genetic data was collected from an institutional genetic data repository for
CYP2B6
,
CYP3A4
,
CYP2C9
,
CYP2C19
,
GSTA1
,
GSTP1
,
ALDH1A1
,
ALDH3A1
,
ABCC1
,
ABCB1
, and
ERCC1
. Treatment and toxicity data were retrospectively collected from the patient’s medical record. The a priori selected primary hypothesis was that patients who have
CYP2B6
reduced metabolizer activity (poor or intermediate (PM/IM) vs. normal (NM) metabolizer) have lower risk of severe toxicity or cyclophosphamide treatment modification due to toxicity.
Results
In the primary analysis of 510 cyclophosphamide-treated patients with available genetic data, there was no difference in the odds of severe toxicity or treatment modification due to toxicity in
CYP2B6
PM/IM vs. NM (odds ratio = 0.97, 95% Confidence Interval: 0.62–1.50,
p
= 0.88). In an exploratory, statistically uncorrected secondary analysis, carriers of the
ALDH1A1
rs8187996 variant had a lower risk of the primary toxicity endpoint compared with wild-type homozygous patients (odds ratio = 0.31, 95% Confidence Interval: 0.09–0.78,
p
= 0.028). None of the other tested phenotypes or genotypes was associated with the primary or secondary endpoints in unadjusted analysis (all
p
> 0.05).
Conclusion
The finding that patients who carry
ALDH1A1
rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism. We found weak evidence that any of these candidate pharmacogenetic predictors of cyclophosphamide toxicity may be useful to personalize cyclophosphamide dosing to optimize therapeutic outcomes in patients with cancer.</description><identifier>ISSN: 0941-4355</identifier><identifier>EISSN: 1433-7339</identifier><identifier>DOI: 10.1007/s00520-022-07118-y</identifier><identifier>PMID: 35606478</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Analysis ; Cancer ; Cancer patients ; Care and treatment ; Chemotherapy ; Clopidogrel ; Confidence intervals ; Cyclophosphamide ; Cytochrome P-450 ; Cytotoxicity ; Genomes ; Medical records ; Medicine ; Medicine & Public Health ; Nursing ; Nursing Research ; Oncology ; Oncology, Experimental ; Original Article ; Pain Medicine ; Pharmacogenetics ; Precision Oncology & Supportive Care ; Rehabilitation Medicine</subject><ispartof>Supportive care in cancer, 2022-09, Vol.30 (9), p.7355-7363</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022</rights><rights>2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><rights>COPYRIGHT 2022 Springer</rights><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2022.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-4603f4f57fccf980cdc87208bca0cd2764859fb2eddac8a626d9abcd6c3c98fd3</citedby><cites>FETCH-LOGICAL-c372t-4603f4f57fccf980cdc87208bca0cd2764859fb2eddac8a626d9abcd6c3c98fd3</cites><orcidid>0000-0003-0501-1035</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00520-022-07118-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00520-022-07118-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35606478$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hwang, Mary</creatorcontrib><creatorcontrib>Medley, Sarah</creatorcontrib><creatorcontrib>Shakeel, Faisal</creatorcontrib><creatorcontrib>Vanderwerff, Brett</creatorcontrib><creatorcontrib>Zawistowski, Matthew</creatorcontrib><creatorcontrib>Kidwell, Kelley M.</creatorcontrib><creatorcontrib>Hertz, Daniel L.</creatorcontrib><title>Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer</title><title>Supportive care in cancer</title><addtitle>Support Care Cancer</addtitle><addtitle>Support Care Cancer</addtitle><description>Purpose
Cyclophosphamide is a commonly used cancer agent that is metabolically activated by polymorphic enzymes. This study aims to investigate the association between predicted activity of candidate pharmacogenes with severe toxicity during cyclophosphamide treatment.
Methods
Genome-wide genetic data was collected from an institutional genetic data repository for
CYP2B6
,
CYP3A4
,
CYP2C9
,
CYP2C19
,
GSTA1
,
GSTP1
,
ALDH1A1
,
ALDH3A1
,
ABCC1
,
ABCB1
, and
ERCC1
. Treatment and toxicity data were retrospectively collected from the patient’s medical record. The a priori selected primary hypothesis was that patients who have
CYP2B6
reduced metabolizer activity (poor or intermediate (PM/IM) vs. normal (NM) metabolizer) have lower risk of severe toxicity or cyclophosphamide treatment modification due to toxicity.
Results
In the primary analysis of 510 cyclophosphamide-treated patients with available genetic data, there was no difference in the odds of severe toxicity or treatment modification due to toxicity in
CYP2B6
PM/IM vs. NM (odds ratio = 0.97, 95% Confidence Interval: 0.62–1.50,
p
= 0.88). In an exploratory, statistically uncorrected secondary analysis, carriers of the
ALDH1A1
rs8187996 variant had a lower risk of the primary toxicity endpoint compared with wild-type homozygous patients (odds ratio = 0.31, 95% Confidence Interval: 0.09–0.78,
p
= 0.028). None of the other tested phenotypes or genotypes was associated with the primary or secondary endpoints in unadjusted analysis (all
p
> 0.05).
Conclusion
The finding that patients who carry
ALDH1A1
rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism. We found weak evidence that any of these candidate pharmacogenetic predictors of cyclophosphamide toxicity may be useful to personalize cyclophosphamide dosing to optimize therapeutic outcomes in patients with cancer.</description><subject>Analysis</subject><subject>Cancer</subject><subject>Cancer patients</subject><subject>Care and treatment</subject><subject>Chemotherapy</subject><subject>Clopidogrel</subject><subject>Confidence intervals</subject><subject>Cyclophosphamide</subject><subject>Cytochrome P-450</subject><subject>Cytotoxicity</subject><subject>Genomes</subject><subject>Medical records</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Nursing</subject><subject>Nursing Research</subject><subject>Oncology</subject><subject>Oncology, Experimental</subject><subject>Original Article</subject><subject>Pain Medicine</subject><subject>Pharmacogenetics</subject><subject>Precision Oncology & Supportive Care</subject><subject>Rehabilitation Medicine</subject><issn>0941-4355</issn><issn>1433-7339</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kUuPFCEUhYnROD2jf8CFqcSNmxp5VAG1HDs6mnSiC124IvQFuhmroAQ6Wv9e2p7xFWNYXLj3OyeXHISeEHxJMBYvMsY9xS2mtMWCENku99CKdIy1grHhPlrhoSNtx_r-DJ3nfIMxEaKnD9EZ6znmnZArZDcaPjfRNTrnCF4XH8Pxuf70nr7kzbzXadIQdzbY4iE3X33ZN7DAGOd9zHU8eWObEr958GVpfGjm6mFDuUN1AJseoQdOj9k-vq0X6OPrVx_Wb9rNu-u366tNC0zQ0nYcM9e5XjgAN0gMBqSgWG5B1zsVvJP94LbUGqNBak65GfQWDAcGg3SGXaDnJ985xS8Hm4uafAY7jjrYeMiKci4HPDDJK_rsL_QmHlKo2ykqMCOS0v43aqdHq3xwsSQNR1N1JUhHORWsr9TlP6h6jJ08xGCdr_0_BPQkgBRzTtapOflJp0URrI7ZqlO2qmarfmSrlip6ervxYTtZ81NyF2YF2AnIdRR2Nv360n9svwNel69d</recordid><startdate>20220901</startdate><enddate>20220901</enddate><creator>Hwang, Mary</creator><creator>Medley, Sarah</creator><creator>Shakeel, Faisal</creator><creator>Vanderwerff, Brett</creator><creator>Zawistowski, Matthew</creator><creator>Kidwell, Kelley M.</creator><creator>Hertz, Daniel L.</creator><general>Springer Berlin Heidelberg</general><general>Springer</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88J</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HEHIP</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2R</scope><scope>M2S</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0501-1035</orcidid></search><sort><creationdate>20220901</creationdate><title>Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer</title><author>Hwang, Mary ; Medley, Sarah ; Shakeel, Faisal ; Vanderwerff, Brett ; Zawistowski, Matthew ; Kidwell, Kelley M. ; Hertz, Daniel L.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-4603f4f57fccf980cdc87208bca0cd2764859fb2eddac8a626d9abcd6c3c98fd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Analysis</topic><topic>Cancer</topic><topic>Cancer patients</topic><topic>Care and treatment</topic><topic>Chemotherapy</topic><topic>Clopidogrel</topic><topic>Confidence intervals</topic><topic>Cyclophosphamide</topic><topic>Cytochrome P-450</topic><topic>Cytotoxicity</topic><topic>Genomes</topic><topic>Medical records</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Nursing</topic><topic>Nursing Research</topic><topic>Oncology</topic><topic>Oncology, Experimental</topic><topic>Original Article</topic><topic>Pain Medicine</topic><topic>Pharmacogenetics</topic><topic>Precision Oncology & Supportive Care</topic><topic>Rehabilitation Medicine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hwang, Mary</creatorcontrib><creatorcontrib>Medley, Sarah</creatorcontrib><creatorcontrib>Shakeel, Faisal</creatorcontrib><creatorcontrib>Vanderwerff, Brett</creatorcontrib><creatorcontrib>Zawistowski, Matthew</creatorcontrib><creatorcontrib>Kidwell, Kelley M.</creatorcontrib><creatorcontrib>Hertz, Daniel L.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>ProQuest Pharma 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>Social Science Premium Collection</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>Sociology Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Social Science Database</collection><collection>Sociology Database (ProQuest)</collection><collection>Nursing & Allied Health Premium</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 Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Supportive care in cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hwang, Mary</au><au>Medley, Sarah</au><au>Shakeel, Faisal</au><au>Vanderwerff, Brett</au><au>Zawistowski, Matthew</au><au>Kidwell, Kelley M.</au><au>Hertz, Daniel L.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer</atitle><jtitle>Supportive care in cancer</jtitle><stitle>Support Care Cancer</stitle><addtitle>Support Care Cancer</addtitle><date>2022-09-01</date><risdate>2022</risdate><volume>30</volume><issue>9</issue><spage>7355</spage><epage>7363</epage><pages>7355-7363</pages><issn>0941-4355</issn><eissn>1433-7339</eissn><abstract>Purpose
Cyclophosphamide is a commonly used cancer agent that is metabolically activated by polymorphic enzymes. This study aims to investigate the association between predicted activity of candidate pharmacogenes with severe toxicity during cyclophosphamide treatment.
Methods
Genome-wide genetic data was collected from an institutional genetic data repository for
CYP2B6
,
CYP3A4
,
CYP2C9
,
CYP2C19
,
GSTA1
,
GSTP1
,
ALDH1A1
,
ALDH3A1
,
ABCC1
,
ABCB1
, and
ERCC1
. Treatment and toxicity data were retrospectively collected from the patient’s medical record. The a priori selected primary hypothesis was that patients who have
CYP2B6
reduced metabolizer activity (poor or intermediate (PM/IM) vs. normal (NM) metabolizer) have lower risk of severe toxicity or cyclophosphamide treatment modification due to toxicity.
Results
In the primary analysis of 510 cyclophosphamide-treated patients with available genetic data, there was no difference in the odds of severe toxicity or treatment modification due to toxicity in
CYP2B6
PM/IM vs. NM (odds ratio = 0.97, 95% Confidence Interval: 0.62–1.50,
p
= 0.88). In an exploratory, statistically uncorrected secondary analysis, carriers of the
ALDH1A1
rs8187996 variant had a lower risk of the primary toxicity endpoint compared with wild-type homozygous patients (odds ratio = 0.31, 95% Confidence Interval: 0.09–0.78,
p
= 0.028). None of the other tested phenotypes or genotypes was associated with the primary or secondary endpoints in unadjusted analysis (all
p
> 0.05).
Conclusion
The finding that patients who carry
ALDH1A1
rs8187996 may have a lower risk of cyclophosphamide toxicity than wild-type patients contradicts a prior finding for this variant and should be viewed with skepticism. We found weak evidence that any of these candidate pharmacogenetic predictors of cyclophosphamide toxicity may be useful to personalize cyclophosphamide dosing to optimize therapeutic outcomes in patients with cancer.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>35606478</pmid><doi>10.1007/s00520-022-07118-y</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-0501-1035</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0941-4355 |
| ispartof | Supportive care in cancer, 2022-09, Vol.30 (9), p.7355-7363 |
| issn | 0941-4355 1433-7339 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_2668909386 |
| source | Springer Nature - Complete Springer Journals |
| subjects | Analysis Cancer Cancer patients Care and treatment Chemotherapy Clopidogrel Confidence intervals Cyclophosphamide Cytochrome P-450 Cytotoxicity Genomes Medical records Medicine Medicine & Public Health Nursing Nursing Research Oncology Oncology, Experimental Original Article Pain Medicine Pharmacogenetics Precision Oncology & Supportive Care Rehabilitation Medicine |
| title | Lack of association of CYP2B6 pharmacogenetics with cyclophosphamide toxicity in patients with cancer |
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