Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma
Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma. Hepatotoxicity and bone marrow suppression often limit its use, however. The objective of this study was to determine the genetic polymorphisms associated with the hepatotoxicity and el...
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| Veröffentlicht in: | Journal of human genetics 2007-02, Vol.52 (2), p.166-171 |
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| creator | Imanishi, Hiroyuki Okamura, Noboru Yagi, Mariko Noro, Yukari Moriya, Yuka Nakamura, Tsutomu Hayakawa, Akira Takeshima, Yasuhiro Sakaeda, Toshiyuki Matsuo, Masafumi Okumura, Katsuhiko |
| description | Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma. Hepatotoxicity and bone marrow suppression often limit its use, however. The objective of this study was to determine the genetic polymorphisms associated with the hepatotoxicity and elimination of methotrexate. Genetic polymorphisms of glutathione S-transferase (GST) genes including
GSTT1
positive/null,
GSTM1
positive/null, and
GSTP1
A313G, and genes for reduced folate carrier 1 G80A (
RFC1
G80A), methylenetetrahydrofolate reductase C677T (
MTHFR
C677T), and breast cancer resistant protein C421A (
BCRP
C421A) were determined for 26 patients by the polymerase chain reaction (PCR) method or by direct sequencing. A high frequency of hepatotoxicity (
P
= 0.035) was observed for patients with
GSTM1
positive and
RFC1
AA
80
, and serum concentrations of methotrexate 48 h after the start of infusion were higher for patients with the TT
677
genotype of
MTHFR
(
P
= 0.028). In conclusion,
GSTM1
positive/null and
RFC1
G80A polymorphisms could be predictors for hepatotoxicity, and the
MTHFR
C677T polymorphism is associated with elimination of methotrexate. |
| doi_str_mv | 10.1007/s10038-006-0096-z |
| format | Article |
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GSTT1
positive/null,
GSTM1
positive/null, and
GSTP1
A313G, and genes for reduced folate carrier 1 G80A (
RFC1
G80A), methylenetetrahydrofolate reductase C677T (
MTHFR
C677T), and breast cancer resistant protein C421A (
BCRP
C421A) were determined for 26 patients by the polymerase chain reaction (PCR) method or by direct sequencing. A high frequency of hepatotoxicity (
P
= 0.035) was observed for patients with
GSTM1
positive and
RFC1
AA
80
, and serum concentrations of methotrexate 48 h after the start of infusion were higher for patients with the TT
677
genotype of
MTHFR
(
P
= 0.028). In conclusion,
GSTM1
positive/null and
RFC1
G80A polymorphisms could be predictors for hepatotoxicity, and the
MTHFR
C677T polymorphism is associated with elimination of methotrexate.</description><identifier>ISSN: 1434-5161</identifier><identifier>EISSN: 1435-232X</identifier><identifier>DOI: 10.1007/s10038-006-0096-z</identifier><identifier>PMID: 17180579</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Acute lymphoblastic leukemia ; Adolescent ; Antimetabolites, Antineoplastic - therapeutic use ; Biomedicine ; Bone marrow ; Breast cancer ; Child ; Child, Preschool ; Childhood ; Children ; Female ; Folic acid ; Gene Expression ; Gene Function ; Gene polymorphism ; Gene Therapy ; Genetic Predisposition to Disease ; Genotype ; Glutathione S-Transferase pi - genetics ; Glutathione transferase ; Glutathione Transferase - genetics ; GSTM1 protein ; GSTT1 protein ; Hepatotoxicity ; Human Genetics ; Humans ; Infant ; Leukemia ; Liver Diseases - genetics ; Lymphatic leukemia ; Lymphoma ; Lymphoma - drug therapy ; Lymphoma - genetics ; Male ; Methotrexate ; Methotrexate - therapeutic use ; Methylenetetrahydrofolate reductase ; Methylenetetrahydrofolate Reductase (NADPH2) - genetics ; Molecular Medicine ; Myelosuppression ; Original Article ; Polymerase chain reaction ; Polymorphism, Genetic ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy ; Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics ; Risk Factors</subject><ispartof>Journal of human genetics, 2007-02, Vol.52 (2), p.166-171</ispartof><rights>The Japan Society of Human Genetics and Springer 2006</rights><rights>The Japan Society of Human Genetics and Springer 2006.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c461t-d58da4d87233f7d572e4d247476ba4539bf5e3e2d1a9227ef5a21ab484447b563</citedby><cites>FETCH-LOGICAL-c461t-d58da4d87233f7d572e4d247476ba4539bf5e3e2d1a9227ef5a21ab484447b563</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10038-006-0096-z$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10038-006-0096-z$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17180579$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Imanishi, Hiroyuki</creatorcontrib><creatorcontrib>Okamura, Noboru</creatorcontrib><creatorcontrib>Yagi, Mariko</creatorcontrib><creatorcontrib>Noro, Yukari</creatorcontrib><creatorcontrib>Moriya, Yuka</creatorcontrib><creatorcontrib>Nakamura, Tsutomu</creatorcontrib><creatorcontrib>Hayakawa, Akira</creatorcontrib><creatorcontrib>Takeshima, Yasuhiro</creatorcontrib><creatorcontrib>Sakaeda, Toshiyuki</creatorcontrib><creatorcontrib>Matsuo, Masafumi</creatorcontrib><creatorcontrib>Okumura, Katsuhiko</creatorcontrib><title>Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma</title><title>Journal of human genetics</title><addtitle>J Hum Genet</addtitle><addtitle>J Hum Genet</addtitle><description>Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma. Hepatotoxicity and bone marrow suppression often limit its use, however. The objective of this study was to determine the genetic polymorphisms associated with the hepatotoxicity and elimination of methotrexate. Genetic polymorphisms of glutathione S-transferase (GST) genes including
GSTT1
positive/null,
GSTM1
positive/null, and
GSTP1
A313G, and genes for reduced folate carrier 1 G80A (
RFC1
G80A), methylenetetrahydrofolate reductase C677T (
MTHFR
C677T), and breast cancer resistant protein C421A (
BCRP
C421A) were determined for 26 patients by the polymerase chain reaction (PCR) method or by direct sequencing. A high frequency of hepatotoxicity (
P
= 0.035) was observed for patients with
GSTM1
positive and
RFC1
AA
80
, and serum concentrations of methotrexate 48 h after the start of infusion were higher for patients with the TT
677
genotype of
MTHFR
(
P
= 0.028). In conclusion,
GSTM1
positive/null and
RFC1
G80A polymorphisms could be predictors for hepatotoxicity, and the
MTHFR
C677T polymorphism is associated with elimination of methotrexate.</description><subject>Acute lymphoblastic leukemia</subject><subject>Adolescent</subject><subject>Antimetabolites, Antineoplastic - therapeutic use</subject><subject>Biomedicine</subject><subject>Bone marrow</subject><subject>Breast cancer</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Childhood</subject><subject>Children</subject><subject>Female</subject><subject>Folic acid</subject><subject>Gene Expression</subject><subject>Gene Function</subject><subject>Gene polymorphism</subject><subject>Gene Therapy</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Glutathione S-Transferase pi - genetics</subject><subject>Glutathione transferase</subject><subject>Glutathione Transferase - genetics</subject><subject>GSTM1 protein</subject><subject>GSTT1 protein</subject><subject>Hepatotoxicity</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Infant</subject><subject>Leukemia</subject><subject>Liver Diseases - genetics</subject><subject>Lymphatic leukemia</subject><subject>Lymphoma</subject><subject>Lymphoma - drug therapy</subject><subject>Lymphoma - genetics</subject><subject>Male</subject><subject>Methotrexate</subject><subject>Methotrexate - therapeutic use</subject><subject>Methylenetetrahydrofolate reductase</subject><subject>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</subject><subject>Molecular Medicine</subject><subject>Myelosuppression</subject><subject>Original Article</subject><subject>Polymerase chain reaction</subject><subject>Polymorphism, Genetic</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy</subject><subject>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</subject><subject>Risk Factors</subject><issn>1434-5161</issn><issn>1435-232X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</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>eNp9kc1u1DAUhS1URH_gAdhQS6wD8V-cWVYVlEqV2IDEznLim4mH2E5tZ6B9D94XTzOiOxa2r3zP-a50D0JvSf2B1LX8mMrN2qqum3I2TfX4Ap0RzkRFGf1x8lTzSpCGnKLzlHZ1UVNJX6FTIklbC7k5Q39uwEO2PZ7D9OBCnEebXMI6pdBbncHgXzaPWJs9xAQY9uBzaXuDYbLOep1t8DgM2EEeQ47wu5iw9bgf7WTGEAzW_VK-Cn0eQzfpdJg2wfITnNVPJKcnu_Xa56PI6dfo5aCnBG-O7wX6_vnTt-sv1d3Xm9vrq7uq5w3JlRGt0dy0kjI2SCMkBW4ol1w2neaCbbpBAANqiN5QKmEQmhLd8ZZzLjvRsAv0fuXOMdwvkLLahSX6MlJRTkVDeCvboiKrqo8hpQiDmqN1Oj4oUqtDEGoNQpUg1CEI9Vg8747kpXNgnh3HzRcBXQWptPwW4vPo_1EvV1PZ-xLhH3U3bmlxUMr-AnDwoqE</recordid><startdate>20070201</startdate><enddate>20070201</enddate><creator>Imanishi, Hiroyuki</creator><creator>Okamura, Noboru</creator><creator>Yagi, Mariko</creator><creator>Noro, Yukari</creator><creator>Moriya, Yuka</creator><creator>Nakamura, Tsutomu</creator><creator>Hayakawa, Akira</creator><creator>Takeshima, Yasuhiro</creator><creator>Sakaeda, Toshiyuki</creator><creator>Matsuo, Masafumi</creator><creator>Okumura, Katsuhiko</creator><general>Springer Japan</general><general>Nature Publishing Group</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>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>RC3</scope></search><sort><creationdate>20070201</creationdate><title>Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma</title><author>Imanishi, Hiroyuki ; Okamura, Noboru ; Yagi, Mariko ; Noro, Yukari ; Moriya, Yuka ; Nakamura, Tsutomu ; Hayakawa, Akira ; Takeshima, Yasuhiro ; Sakaeda, Toshiyuki ; Matsuo, Masafumi ; Okumura, Katsuhiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c461t-d58da4d87233f7d572e4d247476ba4539bf5e3e2d1a9227ef5a21ab484447b563</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acute lymphoblastic leukemia</topic><topic>Adolescent</topic><topic>Antimetabolites, Antineoplastic - therapeutic use</topic><topic>Biomedicine</topic><topic>Bone marrow</topic><topic>Breast cancer</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Childhood</topic><topic>Children</topic><topic>Female</topic><topic>Folic acid</topic><topic>Gene Expression</topic><topic>Gene Function</topic><topic>Gene polymorphism</topic><topic>Gene Therapy</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Glutathione S-Transferase pi - genetics</topic><topic>Glutathione transferase</topic><topic>Glutathione Transferase - genetics</topic><topic>GSTM1 protein</topic><topic>GSTT1 protein</topic><topic>Hepatotoxicity</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Infant</topic><topic>Leukemia</topic><topic>Liver Diseases - genetics</topic><topic>Lymphatic leukemia</topic><topic>Lymphoma</topic><topic>Lymphoma - drug therapy</topic><topic>Lymphoma - genetics</topic><topic>Male</topic><topic>Methotrexate</topic><topic>Methotrexate - therapeutic use</topic><topic>Methylenetetrahydrofolate reductase</topic><topic>Methylenetetrahydrofolate Reductase (NADPH2) - genetics</topic><topic>Molecular Medicine</topic><topic>Myelosuppression</topic><topic>Original Article</topic><topic>Polymerase chain reaction</topic><topic>Polymorphism, Genetic</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy</topic><topic>Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Imanishi, Hiroyuki</creatorcontrib><creatorcontrib>Okamura, Noboru</creatorcontrib><creatorcontrib>Yagi, Mariko</creatorcontrib><creatorcontrib>Noro, Yukari</creatorcontrib><creatorcontrib>Moriya, Yuka</creatorcontrib><creatorcontrib>Nakamura, Tsutomu</creatorcontrib><creatorcontrib>Hayakawa, Akira</creatorcontrib><creatorcontrib>Takeshima, Yasuhiro</creatorcontrib><creatorcontrib>Sakaeda, Toshiyuki</creatorcontrib><creatorcontrib>Matsuo, Masafumi</creatorcontrib><creatorcontrib>Okumura, Katsuhiko</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>Technology Research Database</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>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>Engineering Research Database</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>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><jtitle>Journal of human genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Imanishi, Hiroyuki</au><au>Okamura, Noboru</au><au>Yagi, Mariko</au><au>Noro, Yukari</au><au>Moriya, Yuka</au><au>Nakamura, Tsutomu</au><au>Hayakawa, Akira</au><au>Takeshima, Yasuhiro</au><au>Sakaeda, Toshiyuki</au><au>Matsuo, Masafumi</au><au>Okumura, Katsuhiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma</atitle><jtitle>Journal of human genetics</jtitle><stitle>J Hum Genet</stitle><addtitle>J Hum Genet</addtitle><date>2007-02-01</date><risdate>2007</risdate><volume>52</volume><issue>2</issue><spage>166</spage><epage>171</epage><pages>166-171</pages><issn>1434-5161</issn><eissn>1435-232X</eissn><abstract>Methotrexate is administered in high doses to treat childhood acute lymphoblastic leukemia and malignant lymphoma. Hepatotoxicity and bone marrow suppression often limit its use, however. The objective of this study was to determine the genetic polymorphisms associated with the hepatotoxicity and elimination of methotrexate. Genetic polymorphisms of glutathione S-transferase (GST) genes including
GSTT1
positive/null,
GSTM1
positive/null, and
GSTP1
A313G, and genes for reduced folate carrier 1 G80A (
RFC1
G80A), methylenetetrahydrofolate reductase C677T (
MTHFR
C677T), and breast cancer resistant protein C421A (
BCRP
C421A) were determined for 26 patients by the polymerase chain reaction (PCR) method or by direct sequencing. A high frequency of hepatotoxicity (
P
= 0.035) was observed for patients with
GSTM1
positive and
RFC1
AA
80
, and serum concentrations of methotrexate 48 h after the start of infusion were higher for patients with the TT
677
genotype of
MTHFR
(
P
= 0.028). In conclusion,
GSTM1
positive/null and
RFC1
G80A polymorphisms could be predictors for hepatotoxicity, and the
MTHFR
C677T polymorphism is associated with elimination of methotrexate.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>17180579</pmid><doi>10.1007/s10038-006-0096-z</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| ispartof | Journal of human genetics, 2007-02, Vol.52 (2), p.166-171 |
| issn | 1434-5161 1435-232X |
| language | eng |
| recordid | cdi_proquest_journals_2425614878 |
| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; SpringerLink Journals - AutoHoldings |
| subjects | Acute lymphoblastic leukemia Adolescent Antimetabolites, Antineoplastic - therapeutic use Biomedicine Bone marrow Breast cancer Child Child, Preschool Childhood Children Female Folic acid Gene Expression Gene Function Gene polymorphism Gene Therapy Genetic Predisposition to Disease Genotype Glutathione S-Transferase pi - genetics Glutathione transferase Glutathione Transferase - genetics GSTM1 protein GSTT1 protein Hepatotoxicity Human Genetics Humans Infant Leukemia Liver Diseases - genetics Lymphatic leukemia Lymphoma Lymphoma - drug therapy Lymphoma - genetics Male Methotrexate Methotrexate - therapeutic use Methylenetetrahydrofolate reductase Methylenetetrahydrofolate Reductase (NADPH2) - genetics Molecular Medicine Myelosuppression Original Article Polymerase chain reaction Polymorphism, Genetic Precursor Cell Lymphoblastic Leukemia-Lymphoma - drug therapy Precursor Cell Lymphoblastic Leukemia-Lymphoma - genetics Risk Factors |
| title | Genetic polymorphisms associated with adverse events and elimination of methotrexate in childhood acute lymphoblastic leukemia and malignant lymphoma |
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