A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia
Core binding factor (CBF) AML with the D816 C‐KIT gene mutation demonstrate inferior treatment outcomes. However, the remaining cases without the D816 C‐KIT mutation imply a requirement of more sophisticated dissection of the patients according to their prognosis. In this study, we analyzed the prog...
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creator | Huh, Jungwon Kim, Hee-Je Jung, Chul Won Kim, Hee-Jin Kim, Sun-Hee Kim, Yeo-Kyeoung Kim, Hyeoung-Joon Shin, Myung Geun Moon, Joon Ho Sohn, Sang Kyun Kim, Sung Hyun Lee, Won Sik Won, Jong Ho Mun, Yeung Chul Kim, Hawk Park, Jinny Min, Woo Sung Kim, Dong Hwan (Dennis) |
description | Core binding factor (CBF) AML with the D816 C‐KIT gene mutation demonstrate inferior treatment outcomes. However, the remaining cases without the D816 C‐KIT mutation imply a requirement of more sophisticated dissection of the patients according to their prognosis. In this study, we analyzed the prognostic value of a single nucleotide polymorphism array (SNP‐A) based karyotyping combined with metaphase cytogenetics (MC) to facilitate further stratification of CBF AML patients. A total of 98 CBF AML patients were included and genome‐wide Human SNP 6.0 Arrays (Affymetrix) were performed using marrow samples taken at diagnosis. Overall, 40 abnormal lesions were identified in 25 patients (26%). Survival of the patients with the abnormal lesion(s) detected by SNP‐A and/or MC was worse than those without lesions in terms of the 2‐year overall survival (OS; 57.5% vs. 76.4%, P = 0.028), event‐free (EFS; 45.7% vs. 66.2%, P = 0.072), and leukemia‐free survival (LFS; 49.0% vs. 77.4%, P = 0.015), specially in the subgroup with inv(16)/t(16;16) (40.9% vs. 80.2% OS, P = 0.040) and in the subgroup without the D816 C‐KIT mutation (61.6% vs. 82.7% OS, P = 0.038). Multivariate analysis confirmed the prognostic impact of the abnormal SNP‐A and/or MC lesion on EFS (HR 2.011, P = 0.047), and LFS (HR 3.231, P = 0.005) in the overall CBF AML. This study suggests that the combined use of SNP‐A with MC in the CBF AML can provide important prognostic value, especially in the inv(16)/t(16;16) subgroup or in the patients without the D816 C‐KIT mutation. Am. J. Hematol., 2012. © 2012 Wiley Periodicals, Inc. |
doi_str_mv | 10.1002/ajh.23281 |
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However, the remaining cases without the D816 C‐KIT mutation imply a requirement of more sophisticated dissection of the patients according to their prognosis. In this study, we analyzed the prognostic value of a single nucleotide polymorphism array (SNP‐A) based karyotyping combined with metaphase cytogenetics (MC) to facilitate further stratification of CBF AML patients. A total of 98 CBF AML patients were included and genome‐wide Human SNP 6.0 Arrays (Affymetrix) were performed using marrow samples taken at diagnosis. Overall, 40 abnormal lesions were identified in 25 patients (26%). Survival of the patients with the abnormal lesion(s) detected by SNP‐A and/or MC was worse than those without lesions in terms of the 2‐year overall survival (OS; 57.5% vs. 76.4%, P = 0.028), event‐free (EFS; 45.7% vs. 66.2%, P = 0.072), and leukemia‐free survival (LFS; 49.0% vs. 77.4%, P = 0.015), specially in the subgroup with inv(16)/t(16;16) (40.9% vs. 80.2% OS, P = 0.040) and in the subgroup without the D816 C‐KIT mutation (61.6% vs. 82.7% OS, P = 0.038). Multivariate analysis confirmed the prognostic impact of the abnormal SNP‐A and/or MC lesion on EFS (HR 2.011, P = 0.047), and LFS (HR 3.231, P = 0.005) in the overall CBF AML. This study suggests that the combined use of SNP‐A with MC in the CBF AML can provide important prognostic value, especially in the inv(16)/t(16;16) subgroup or in the patients without the D816 C‐KIT mutation. Am. J. Hematol., 2012. © 2012 Wiley Periodicals, Inc.</description><identifier>ISSN: 0361-8609</identifier><identifier>EISSN: 1096-8652</identifier><identifier>DOI: 10.1002/ajh.23281</identifier><identifier>PMID: 22886749</identifier><identifier>CODEN: AJHEDD</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Acute Disease ; Adolescent ; Adult ; Aged ; Antineoplastic Combined Chemotherapy Protocols - therapeutic use ; Biological and medical sciences ; Chromosome Inversion ; Core Binding Factors - genetics ; Cytarabine - administration & dosage ; Cytarabine - analogs & derivatives ; Disease-Free Survival ; Female ; Genome-Wide Association Study ; Hematologic and hematopoietic diseases ; Hematology ; Humans ; Idarubicin - administration & dosage ; Kaplan-Meier Estimate ; Karyotyping ; Leukemia, Myeloid - drug therapy ; Leukemia, Myeloid - genetics ; Leukemia, Myeloid - mortality ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Male ; Medical sciences ; Middle Aged ; Neoplasm Proteins - genetics ; Polymorphism, Single Nucleotide ; Prognosis ; Proportional Hazards Models ; Proto-Oncogene Proteins c-kit - genetics ; Remission Induction ; Translocation, Genetic ; Young Adult</subject><ispartof>American journal of hematology, 2012-10, Vol.87 (10), p.961-968</ispartof><rights>Copyright © 2012 Wiley Periodicals, Inc.</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4211-b0cf3c6f6ed969fcd1c0dc7ae248726a5e955e7ce495fae18d5bc387badaa9d83</citedby><cites>FETCH-LOGICAL-c4211-b0cf3c6f6ed969fcd1c0dc7ae248726a5e955e7ce495fae18d5bc387badaa9d83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fajh.23281$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fajh.23281$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,1427,27901,27902,45550,45551,46384,46808</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26395790$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22886749$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Huh, Jungwon</creatorcontrib><creatorcontrib>Kim, Hee-Je</creatorcontrib><creatorcontrib>Jung, Chul Won</creatorcontrib><creatorcontrib>Kim, Hee-Jin</creatorcontrib><creatorcontrib>Kim, Sun-Hee</creatorcontrib><creatorcontrib>Kim, Yeo-Kyeoung</creatorcontrib><creatorcontrib>Kim, Hyeoung-Joon</creatorcontrib><creatorcontrib>Shin, Myung Geun</creatorcontrib><creatorcontrib>Moon, Joon Ho</creatorcontrib><creatorcontrib>Sohn, Sang Kyun</creatorcontrib><creatorcontrib>Kim, Sung Hyun</creatorcontrib><creatorcontrib>Lee, Won Sik</creatorcontrib><creatorcontrib>Won, Jong Ho</creatorcontrib><creatorcontrib>Mun, Yeung Chul</creatorcontrib><creatorcontrib>Kim, Hawk</creatorcontrib><creatorcontrib>Park, Jinny</creatorcontrib><creatorcontrib>Min, Woo Sung</creatorcontrib><creatorcontrib>Kim, Dong Hwan (Dennis)</creatorcontrib><creatorcontrib>AML/MDS working party, Korean Society of Hematology</creatorcontrib><creatorcontrib>on behalf of AML/MDS working party, Korean Society of Hematology</creatorcontrib><title>A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia</title><title>American journal of hematology</title><addtitle>Am. J. Hematol</addtitle><description>Core binding factor (CBF) AML with the D816 C‐KIT gene mutation demonstrate inferior treatment outcomes. However, the remaining cases without the D816 C‐KIT mutation imply a requirement of more sophisticated dissection of the patients according to their prognosis. In this study, we analyzed the prognostic value of a single nucleotide polymorphism array (SNP‐A) based karyotyping combined with metaphase cytogenetics (MC) to facilitate further stratification of CBF AML patients. A total of 98 CBF AML patients were included and genome‐wide Human SNP 6.0 Arrays (Affymetrix) were performed using marrow samples taken at diagnosis. Overall, 40 abnormal lesions were identified in 25 patients (26%). Survival of the patients with the abnormal lesion(s) detected by SNP‐A and/or MC was worse than those without lesions in terms of the 2‐year overall survival (OS; 57.5% vs. 76.4%, P = 0.028), event‐free (EFS; 45.7% vs. 66.2%, P = 0.072), and leukemia‐free survival (LFS; 49.0% vs. 77.4%, P = 0.015), specially in the subgroup with inv(16)/t(16;16) (40.9% vs. 80.2% OS, P = 0.040) and in the subgroup without the D816 C‐KIT mutation (61.6% vs. 82.7% OS, P = 0.038). Multivariate analysis confirmed the prognostic impact of the abnormal SNP‐A and/or MC lesion on EFS (HR 2.011, P = 0.047), and LFS (HR 3.231, P = 0.005) in the overall CBF AML. This study suggests that the combined use of SNP‐A with MC in the CBF AML can provide important prognostic value, especially in the inv(16)/t(16;16) subgroup or in the patients without the D816 C‐KIT mutation. Am. J. Hematol., 2012. © 2012 Wiley Periodicals, Inc.</description><subject>Acute Disease</subject><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</subject><subject>Biological and medical sciences</subject><subject>Chromosome Inversion</subject><subject>Core Binding Factors - genetics</subject><subject>Cytarabine - administration & dosage</subject><subject>Cytarabine - analogs & derivatives</subject><subject>Disease-Free Survival</subject><subject>Female</subject><subject>Genome-Wide Association Study</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Hematology</subject><subject>Humans</subject><subject>Idarubicin - administration & dosage</subject><subject>Kaplan-Meier Estimate</subject><subject>Karyotyping</subject><subject>Leukemia, Myeloid - drug therapy</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemia, Myeloid - mortality</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neoplasm Proteins - genetics</subject><subject>Polymorphism, Single Nucleotide</subject><subject>Prognosis</subject><subject>Proportional Hazards Models</subject><subject>Proto-Oncogene Proteins c-kit - genetics</subject><subject>Remission Induction</subject><subject>Translocation, Genetic</subject><subject>Young Adult</subject><issn>0361-8609</issn><issn>1096-8652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp10d1qFDEUB_BBFLutXvgCEhChXkybzEc-LpdFW6VUBEXwJpxJzuxmOzPZJjPWfQmf2Wx3W0HwJgnhd_7nwMmyV4yeMUqLc1ivzoqykOxJNmNU8VzyuniazWjJWXpTdZQdx7imlLFK0ufZUVFIyUWlZtnvOVni4HvM75xFEt2w7DAfJtOhH3c_G99tex82Kxf7HEKALTEwENdvgv-JZFwlEvxy8HF0hsQxwOhaZ9LpB-Lbe2B8QNK4waZ00oIZfSBgphFJv8XOO0s6nG6wd_Aie9ZCF_Hl4T7Jvn14_3VxmV99vvi4mF_lpioYyxtq2tLwlqNVXLXGMkOtEYBFJUXBoUZV1ygMVqpuAZm0dWNKKRqwAMrK8iQ73eem2W8njKPuXTTYdTCgn6JmVFSC79ISffMPXfspDGk6zWrGq1oIUST1bq9M8DEGbPUmuB7CNkXp3ZJ0WpK-X1Kyrw-JU9OjfZQPW0ng7QFANNC1AQbj4l_HS1ULRZM737s71-H2_x31_NPlQ-t8X-HiiL8eKyDcaC5KUevv1xdaXS_KLwv6Q8vyD8OQuvI</recordid><startdate>201210</startdate><enddate>201210</enddate><creator>Huh, Jungwon</creator><creator>Kim, Hee-Je</creator><creator>Jung, Chul Won</creator><creator>Kim, Hee-Jin</creator><creator>Kim, Sun-Hee</creator><creator>Kim, Yeo-Kyeoung</creator><creator>Kim, Hyeoung-Joon</creator><creator>Shin, Myung Geun</creator><creator>Moon, Joon Ho</creator><creator>Sohn, Sang Kyun</creator><creator>Kim, Sung Hyun</creator><creator>Lee, Won Sik</creator><creator>Won, Jong Ho</creator><creator>Mun, Yeung Chul</creator><creator>Kim, Hawk</creator><creator>Park, Jinny</creator><creator>Min, Woo Sung</creator><creator>Kim, Dong Hwan (Dennis)</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley-Liss</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</scope><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>K9.</scope><scope>7X8</scope></search><sort><creationdate>201210</creationdate><title>A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia</title><author>Huh, Jungwon ; Kim, Hee-Je ; Jung, Chul Won ; Kim, Hee-Jin ; Kim, Sun-Hee ; Kim, Yeo-Kyeoung ; Kim, Hyeoung-Joon ; Shin, Myung Geun ; Moon, Joon Ho ; Sohn, Sang Kyun ; Kim, Sung Hyun ; Lee, Won Sik ; Won, Jong Ho ; Mun, Yeung Chul ; Kim, Hawk ; Park, Jinny ; Min, Woo Sung ; Kim, Dong Hwan (Dennis)</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4211-b0cf3c6f6ed969fcd1c0dc7ae248726a5e955e7ce495fae18d5bc387badaa9d83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acute Disease</topic><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Antineoplastic Combined Chemotherapy Protocols - therapeutic use</topic><topic>Biological and medical sciences</topic><topic>Chromosome Inversion</topic><topic>Core Binding Factors - genetics</topic><topic>Cytarabine - administration & dosage</topic><topic>Cytarabine - analogs & derivatives</topic><topic>Disease-Free Survival</topic><topic>Female</topic><topic>Genome-Wide Association Study</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Hematology</topic><topic>Humans</topic><topic>Idarubicin - administration & dosage</topic><topic>Kaplan-Meier Estimate</topic><topic>Karyotyping</topic><topic>Leukemia, Myeloid - drug therapy</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemia, Myeloid - mortality</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neoplasm Proteins - genetics</topic><topic>Polymorphism, Single Nucleotide</topic><topic>Prognosis</topic><topic>Proportional Hazards Models</topic><topic>Proto-Oncogene Proteins c-kit - genetics</topic><topic>Remission Induction</topic><topic>Translocation, Genetic</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Huh, Jungwon</creatorcontrib><creatorcontrib>Kim, Hee-Je</creatorcontrib><creatorcontrib>Jung, Chul Won</creatorcontrib><creatorcontrib>Kim, Hee-Jin</creatorcontrib><creatorcontrib>Kim, Sun-Hee</creatorcontrib><creatorcontrib>Kim, Yeo-Kyeoung</creatorcontrib><creatorcontrib>Kim, Hyeoung-Joon</creatorcontrib><creatorcontrib>Shin, Myung Geun</creatorcontrib><creatorcontrib>Moon, Joon Ho</creatorcontrib><creatorcontrib>Sohn, Sang Kyun</creatorcontrib><creatorcontrib>Kim, Sung Hyun</creatorcontrib><creatorcontrib>Lee, Won Sik</creatorcontrib><creatorcontrib>Won, Jong Ho</creatorcontrib><creatorcontrib>Mun, Yeung Chul</creatorcontrib><creatorcontrib>Kim, Hawk</creatorcontrib><creatorcontrib>Park, Jinny</creatorcontrib><creatorcontrib>Min, Woo Sung</creatorcontrib><creatorcontrib>Kim, Dong Hwan (Dennis)</creatorcontrib><creatorcontrib>AML/MDS working party, Korean Society of Hematology</creatorcontrib><creatorcontrib>on behalf of AML/MDS working party, Korean Society of Hematology</creatorcontrib><collection>Istex</collection><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>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>American journal of hematology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Huh, Jungwon</au><au>Kim, Hee-Je</au><au>Jung, Chul Won</au><au>Kim, Hee-Jin</au><au>Kim, Sun-Hee</au><au>Kim, Yeo-Kyeoung</au><au>Kim, Hyeoung-Joon</au><au>Shin, Myung Geun</au><au>Moon, Joon Ho</au><au>Sohn, Sang Kyun</au><au>Kim, Sung Hyun</au><au>Lee, Won Sik</au><au>Won, Jong Ho</au><au>Mun, Yeung Chul</au><au>Kim, Hawk</au><au>Park, Jinny</au><au>Min, Woo Sung</au><au>Kim, Dong Hwan (Dennis)</au><aucorp>AML/MDS working party, Korean Society of Hematology</aucorp><aucorp>on behalf of AML/MDS working party, Korean Society of Hematology</aucorp><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia</atitle><jtitle>American journal of hematology</jtitle><addtitle>Am. J. Hematol</addtitle><date>2012-10</date><risdate>2012</risdate><volume>87</volume><issue>10</issue><spage>961</spage><epage>968</epage><pages>961-968</pages><issn>0361-8609</issn><eissn>1096-8652</eissn><coden>AJHEDD</coden><abstract>Core binding factor (CBF) AML with the D816 C‐KIT gene mutation demonstrate inferior treatment outcomes. However, the remaining cases without the D816 C‐KIT mutation imply a requirement of more sophisticated dissection of the patients according to their prognosis. In this study, we analyzed the prognostic value of a single nucleotide polymorphism array (SNP‐A) based karyotyping combined with metaphase cytogenetics (MC) to facilitate further stratification of CBF AML patients. A total of 98 CBF AML patients were included and genome‐wide Human SNP 6.0 Arrays (Affymetrix) were performed using marrow samples taken at diagnosis. Overall, 40 abnormal lesions were identified in 25 patients (26%). Survival of the patients with the abnormal lesion(s) detected by SNP‐A and/or MC was worse than those without lesions in terms of the 2‐year overall survival (OS; 57.5% vs. 76.4%, P = 0.028), event‐free (EFS; 45.7% vs. 66.2%, P = 0.072), and leukemia‐free survival (LFS; 49.0% vs. 77.4%, P = 0.015), specially in the subgroup with inv(16)/t(16;16) (40.9% vs. 80.2% OS, P = 0.040) and in the subgroup without the D816 C‐KIT mutation (61.6% vs. 82.7% OS, P = 0.038). Multivariate analysis confirmed the prognostic impact of the abnormal SNP‐A and/or MC lesion on EFS (HR 2.011, P = 0.047), and LFS (HR 3.231, P = 0.005) in the overall CBF AML. This study suggests that the combined use of SNP‐A with MC in the CBF AML can provide important prognostic value, especially in the inv(16)/t(16;16) subgroup or in the patients without the D816 C‐KIT mutation. Am. J. Hematol., 2012. © 2012 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>22886749</pmid><doi>10.1002/ajh.23281</doi><tpages>8</tpages></addata></record> |
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subjects | Acute Disease Adolescent Adult Aged Antineoplastic Combined Chemotherapy Protocols - therapeutic use Biological and medical sciences Chromosome Inversion Core Binding Factors - genetics Cytarabine - administration & dosage Cytarabine - analogs & derivatives Disease-Free Survival Female Genome-Wide Association Study Hematologic and hematopoietic diseases Hematology Humans Idarubicin - administration & dosage Kaplan-Meier Estimate Karyotyping Leukemia, Myeloid - drug therapy Leukemia, Myeloid - genetics Leukemia, Myeloid - mortality Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Male Medical sciences Middle Aged Neoplasm Proteins - genetics Polymorphism, Single Nucleotide Prognosis Proportional Hazards Models Proto-Oncogene Proteins c-kit - genetics Remission Induction Translocation, Genetic Young Adult |
title | A genome-wide single-nucleotide polymorphism-array can improve the prognostic stratification of the core binding factor acute myeloid leukemia |
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