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Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias
DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) (n = 63) or t(8;21) (n = 47) was screened for mutations in the c‐KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(...
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| Published in: | British journal of haematology 2003-06, Vol.121 (5), p.775-777 |
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| container_title | British journal of haematology |
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| creator | Care, Rory S. Valk, Peter J. M. Goodeve, Anne C. Abu‐Duhier, Faisel M. Geertsma‐Kleinekoort, Wendy M. C. Wilson, Giu A. Gari, Mamdooh A. Peake, Ian R. Löwenberg, Bob Reilly, John T. |
| description | DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) (n = 63) or t(8;21) (n = 47) was screened for mutations in the c‐KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(8;21) patients. c‐KIT Asp816 mutations were present in 5/63 (7·9%) inv(16) AML and 5/47 (10·6%) t(8;21) AML. FLT3 mutations were identified in five patients (7·9%) with inv(16) and three patients (5·6%) with t(8;21) AML. All mutations were mutually exclusive; 40% of inv(16) AML patients possessed either a c‐KIT or FLT3 mutation. c‐KIT exon 8 mutations were shown to be a significant factor adversely affecting relapse rate. |
| doi_str_mv | 10.1046/j.1365-2141.2003.04362.x |
| format | article |
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M. ; Goodeve, Anne C. ; Abu‐Duhier, Faisel M. ; Geertsma‐Kleinekoort, Wendy M. C. ; Wilson, Giu A. ; Gari, Mamdooh A. ; Peake, Ian R. ; Löwenberg, Bob ; Reilly, John T.</creator><creatorcontrib>Care, Rory S. ; Valk, Peter J. M. ; Goodeve, Anne C. ; Abu‐Duhier, Faisel M. ; Geertsma‐Kleinekoort, Wendy M. C. ; Wilson, Giu A. ; Gari, Mamdooh A. ; Peake, Ian R. ; Löwenberg, Bob ; Reilly, John T.</creatorcontrib><description>DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) (n = 63) or t(8;21) (n = 47) was screened for mutations in the c‐KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(8;21) patients. c‐KIT Asp816 mutations were present in 5/63 (7·9%) inv(16) AML and 5/47 (10·6%) t(8;21) AML. FLT3 mutations were identified in five patients (7·9%) with inv(16) and three patients (5·6%) with t(8;21) AML. All mutations were mutually exclusive; 40% of inv(16) AML patients possessed either a c‐KIT or FLT3 mutation. c‐KIT exon 8 mutations were shown to be a significant factor adversely affecting relapse rate.</description><identifier>ISSN: 0007-1048</identifier><identifier>EISSN: 1365-2141</identifier><identifier>DOI: 10.1046/j.1365-2141.2003.04362.x</identifier><identifier>PMID: 12780793</identifier><identifier>CODEN: BJHEAL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Acute Disease ; Adolescent ; Adult ; Aged ; Aged, 80 and over ; AML ; Biological and medical sciences ; CBF ; c‐KIT ; Female ; FLT3 ; Hematologic and hematopoietic diseases ; Hematology ; Humans ; inv ; Leukemia, Myeloid - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Membrane Proteins - genetics ; Middle Aged ; Mutation - genetics ; Prognosis ; Proto-Oncogene Proteins c-kit - genetics ; Recurrence ; Survival Analysis</subject><ispartof>British journal of haematology, 2003-06, Vol.121 (5), p.775-777</ispartof><rights>2003 INIST-CNRS</rights><rights>Copyright Blackwell Scientific Publications Ltd. Jun 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4882-ebdf22fee2b2bbc62e06bbb1db26b49bef8541f9851111a3b678b77d3f7c24993</citedby><cites>FETCH-LOGICAL-c4882-ebdf22fee2b2bbc62e06bbb1db26b49bef8541f9851111a3b678b77d3f7c24993</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14820283$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12780793$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Care, Rory S.</creatorcontrib><creatorcontrib>Valk, Peter J. M.</creatorcontrib><creatorcontrib>Goodeve, Anne C.</creatorcontrib><creatorcontrib>Abu‐Duhier, Faisel M.</creatorcontrib><creatorcontrib>Geertsma‐Kleinekoort, Wendy M. C.</creatorcontrib><creatorcontrib>Wilson, Giu A.</creatorcontrib><creatorcontrib>Gari, Mamdooh A.</creatorcontrib><creatorcontrib>Peake, Ian R.</creatorcontrib><creatorcontrib>Löwenberg, Bob</creatorcontrib><creatorcontrib>Reilly, John T.</creatorcontrib><title>Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias</title><title>British journal of haematology</title><addtitle>Br J Haematol</addtitle><description>DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) (n = 63) or t(8;21) (n = 47) was screened for mutations in the c‐KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(8;21) patients. c‐KIT Asp816 mutations were present in 5/63 (7·9%) inv(16) AML and 5/47 (10·6%) t(8;21) AML. FLT3 mutations were identified in five patients (7·9%) with inv(16) and three patients (5·6%) with t(8;21) AML. All mutations were mutually exclusive; 40% of inv(16) AML patients possessed either a c‐KIT or FLT3 mutation. c‐KIT exon 8 mutations were shown to be a significant factor adversely affecting relapse rate.</description><subject>Acute Disease</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>AML</subject><subject>Biological and medical sciences</subject><subject>CBF</subject><subject>c‐KIT</subject><subject>Female</subject><subject>FLT3</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Humans</subject><subject>inv</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins - genetics</subject><subject>Middle Aged</subject><subject>Mutation - genetics</subject><subject>Prognosis</subject><subject>Proto-Oncogene Proteins c-kit - genetics</subject><subject>Recurrence</subject><subject>Survival Analysis</subject><issn>0007-1048</issn><issn>1365-2141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><recordid>eNqNkc9u1DAQxi0EokvhFZCFBIJDgv9kHefQA12xdGElLsvZsp1x5W1iFzsR3RuPwDPyJCTdFZU4MRePNL9vNP4-hDAlJSWVeL8vKRfLgtGKlowQXpKKC1bePUKLv4PHaEEIqYtJIM_Qs5z3hFBOlvQpOqOslqRu-ALdbIL1LQQLWIcW36Z4HWL2GUeH7e-fv75sdveD9XbHcT8OevAxZOwDtjEBNj60Plxjp-0QE367uly_w9qOA-D-AF30Le5gvNHQe52foydOdxlenN5z9G39cbe6KrZfP21WH7aFraRkBZjWMeYAmGHGWMGACGMMbQ0TpmoMOLmsqGvkkk6luRG1NHXdcldbVjUNP0dvjnun33wfIQ-q99lC1-kAccyq5pwTWdUT-OofcB_HFKbbFG2koEJwOUHyCNkUc07g1G3yvU4HRYma01B7NZuuZtPVnIa6T0PdTdKXp_2j6aF9EJ7sn4DXJ0BnqzuX9JRGfuAqyQiTM3dx5H74Dg7_fYC6_Hw1d_wPkWmk8w</recordid><startdate>200306</startdate><enddate>200306</enddate><creator>Care, Rory S.</creator><creator>Valk, Peter J. M.</creator><creator>Goodeve, Anne C.</creator><creator>Abu‐Duhier, Faisel M.</creator><creator>Geertsma‐Kleinekoort, Wendy M. C.</creator><creator>Wilson, Giu A.</creator><creator>Gari, Mamdooh A.</creator><creator>Peake, Ian R.</creator><creator>Löwenberg, Bob</creator><creator>Reilly, John T.</creator><general>Blackwell Science Ltd</general><general>Blackwell</general><general>Blackwell Publishing Ltd</general><scope>IQODW</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200306</creationdate><title>Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias</title><author>Care, Rory S. ; Valk, Peter J. M. ; Goodeve, Anne C. ; Abu‐Duhier, Faisel M. ; Geertsma‐Kleinekoort, Wendy M. C. ; Wilson, Giu A. ; Gari, Mamdooh A. ; Peake, Ian R. ; Löwenberg, Bob ; Reilly, John T.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4882-ebdf22fee2b2bbc62e06bbb1db26b49bef8541f9851111a3b678b77d3f7c24993</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Acute Disease</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>AML</topic><topic>Biological and medical sciences</topic><topic>CBF</topic><topic>c‐KIT</topic><topic>Female</topic><topic>FLT3</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Humans</topic><topic>inv</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins - genetics</topic><topic>Middle Aged</topic><topic>Mutation - genetics</topic><topic>Prognosis</topic><topic>Proto-Oncogene Proteins c-kit - genetics</topic><topic>Recurrence</topic><topic>Survival Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Care, Rory S.</creatorcontrib><creatorcontrib>Valk, Peter J. M.</creatorcontrib><creatorcontrib>Goodeve, Anne C.</creatorcontrib><creatorcontrib>Abu‐Duhier, Faisel M.</creatorcontrib><creatorcontrib>Geertsma‐Kleinekoort, Wendy M. C.</creatorcontrib><creatorcontrib>Wilson, Giu A.</creatorcontrib><creatorcontrib>Gari, Mamdooh A.</creatorcontrib><creatorcontrib>Peake, Ian R.</creatorcontrib><creatorcontrib>Löwenberg, Bob</creatorcontrib><creatorcontrib>Reilly, John T.</creatorcontrib><collection>Pascal-Francis</collection><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>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>British journal of haematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Care, Rory S.</au><au>Valk, Peter J. M.</au><au>Goodeve, Anne C.</au><au>Abu‐Duhier, Faisel M.</au><au>Geertsma‐Kleinekoort, Wendy M. C.</au><au>Wilson, Giu A.</au><au>Gari, Mamdooh A.</au><au>Peake, Ian R.</au><au>Löwenberg, Bob</au><au>Reilly, John T.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias</atitle><jtitle>British journal of haematology</jtitle><addtitle>Br J Haematol</addtitle><date>2003-06</date><risdate>2003</risdate><volume>121</volume><issue>5</issue><spage>775</spage><epage>777</epage><pages>775-777</pages><issn>0007-1048</issn><eissn>1365-2141</eissn><coden>BJHEAL</coden><abstract>DNA from 110 adult de novo acute myeloid leukaemia (AML) patients exhibiting either inv(16) (n = 63) or t(8;21) (n = 47) was screened for mutations in the c‐KIT (exon 8 and Asp816) and FLT3 (ITD and Asp835) genes. c‐KIT exon 8 mutations were found in 15/63 (23·8%) inv(16) patients and 1/47 (2·1%) t(8;21) patients. c‐KIT Asp816 mutations were present in 5/63 (7·9%) inv(16) AML and 5/47 (10·6%) t(8;21) AML. FLT3 mutations were identified in five patients (7·9%) with inv(16) and three patients (5·6%) with t(8;21) AML. All mutations were mutually exclusive; 40% of inv(16) AML patients possessed either a c‐KIT or FLT3 mutation. c‐KIT exon 8 mutations were shown to be a significant factor adversely affecting relapse rate.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>12780793</pmid><doi>10.1046/j.1365-2141.2003.04362.x</doi><tpages>3</tpages></addata></record> |
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| ispartof | British journal of haematology, 2003-06, Vol.121 (5), p.775-777 |
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| subjects | Acute Disease Adolescent Adult Aged Aged, 80 and over AML Biological and medical sciences CBF c‐KIT Female FLT3 Hematologic and hematopoietic diseases Hematology Humans inv Leukemia, Myeloid - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Membrane Proteins - genetics Middle Aged Mutation - genetics Prognosis Proto-Oncogene Proteins c-kit - genetics Recurrence Survival Analysis |
| title | Incidence and prognosis of c‐KIT and FLT3 mutations in core binding factor (CBF) acute myeloid leukaemias |
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