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A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia
From the Bone Marrow Transplant Unit, University Hospital of Hamburg-Eppendorf, Hamburg, Germany (UB); MLL, Munich Leukemia Laboratory, Munich, Germany (TH, WK, CH, SS) Correspondence: Susanne Schnittger, MLL, Munich Leukemia Laboratory, Max-Lebsche-Platz 31 81377 Munich, Germany. E-mail: susanne.sc...
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| Published in: | Haematologica (Roma) 2007-06, Vol.92 (6), p.744-752 |
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| creator | Bacher, Ulrike Haferlach, Torsten Kern, Wolfgang Haferlach, Claudia Schnittger, Susanne |
| description | From the Bone Marrow Transplant Unit, University Hospital of Hamburg-Eppendorf, Hamburg, Germany (UB); MLL, Munich Leukemia Laboratory, Munich, Germany (TH, WK, CH, SS)
Correspondence: Susanne Schnittger, MLL, Munich Leukemia Laboratory, Max-Lebsche-Platz 31 81377 Munich, Germany. E-mail: susanne.schnittger{at}mll-online.com
Background and Objectives: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial. The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
Design and Methods: We compared the frequency of FLT3 -length mutations ( FLT3 -LM), FLT3 -TKD, MLL -partial tandem duplications ( MLL -PTD), NRAS , and KIT D816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML ( de novo : n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
Results: All mutations were more frequent in s-AML than in MDS and all but the FLT3 -TKD were more frequent in RAEB than in RA/RARS. The higher incidences in s-AML were significant for FLT3 -TKD ( p =0.032), MLL -PTD ( p =0.034), and FLT3 -LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p |
| doi_str_mv | 10.3324/haematol.10869 |
| format | article |
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Correspondence: Susanne Schnittger, MLL, Munich Leukemia Laboratory, Max-Lebsche-Platz 31 81377 Munich, Germany. E-mail: susanne.schnittger{at}mll-online.com
Background and Objectives: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial. The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
Design and Methods: We compared the frequency of FLT3 -length mutations ( FLT3 -LM), FLT3 -TKD, MLL -partial tandem duplications ( MLL -PTD), NRAS , and KIT D816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML ( de novo : n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
Results: All mutations were more frequent in s-AML than in MDS and all but the FLT3 -TKD were more frequent in RAEB than in RA/RARS. The higher incidences in s-AML were significant for FLT3 -TKD ( p =0.032), MLL -PTD ( p =0.034), and FLT3 -LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p <0.0001). The incidence of NRAS-mutations increased from 17/272 (6.3%) in MDS to 41/343 in s-AML (12.0%) and that of KIT D816-mutations from 2/290 (0.7%) to 5/341 (1.5%) ( p =n.s.). FLT3 -LM-acquisition occurred in 3/22 cases (13.6%) during MDS transformation; NRAS -acquisition occurred in 1/24 (4.2%). FLT3 -LM and MLL -PTD were more frequent in AML relapse than in de novo AML or s-AML ( p <0.0001).
Interpretation and Conclusions: The increase of molecular mutations from low- to high-risk MDS, to s-AML, and to relapsed AML emphasizes the value of these mutations as markers of progressing disease. Finally, we found a low rate of 5q- in the molecularly mutated cases in MDS which might explain the stability of this subtype.
Key words: myelodysplastic syndromes (MDS), acute myeloid leukemias (AML), molecular mutations, progression, leukemogenesis.
Related Article
The spectrum of molecular aberrations in myelodysplastic syndromes: in the shadow of acute myeloid leukemia
David P. Steensma
Haematologica 2007 92: 723-727.
[Full Text]
[PDF]</description><identifier>ISSN: 0390-6078</identifier><identifier>EISSN: 1592-8721</identifier><identifier>DOI: 10.3324/haematol.10869</identifier><identifier>PMID: 17550846</identifier><language>eng</language><publisher>Pavia: Haematologica</publisher><subject>Acute Disease ; Biological and medical sciences ; Disease Progression ; fms-Like Tyrosine Kinase 3 - genetics ; Gene Frequency ; Hematologic and hematopoietic diseases ; Histone-Lysine N-Methyltransferase ; Humans ; Leukemia, Myeloid - diagnosis ; Leukemia, Myeloid - genetics ; Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis ; Medical sciences ; Molecular Epidemiology ; Mutation ; Myelodysplastic Syndromes - diagnosis ; Myelodysplastic Syndromes - genetics ; Myeloid-Lymphoid Leukemia Protein - genetics ; Proto-Oncogene Proteins c-kit - genetics ; ras Proteins - genetics</subject><ispartof>Haematologica (Roma), 2007-06, Vol.92 (6), p.744-752</ispartof><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c459t-4df8cdb8b045031a7df67cca0f16be5a4e2e6e8a20ad502cc5577846eb10c2483</citedby></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=18853059$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17550846$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bacher, Ulrike</creatorcontrib><creatorcontrib>Haferlach, Torsten</creatorcontrib><creatorcontrib>Kern, Wolfgang</creatorcontrib><creatorcontrib>Haferlach, Claudia</creatorcontrib><creatorcontrib>Schnittger, Susanne</creatorcontrib><title>A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia</title><title>Haematologica (Roma)</title><addtitle>Haematologica</addtitle><description>From the Bone Marrow Transplant Unit, University Hospital of Hamburg-Eppendorf, Hamburg, Germany (UB); MLL, Munich Leukemia Laboratory, Munich, Germany (TH, WK, CH, SS)
Correspondence: Susanne Schnittger, MLL, Munich Leukemia Laboratory, Max-Lebsche-Platz 31 81377 Munich, Germany. E-mail: susanne.schnittger{at}mll-online.com
Background and Objectives: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial. The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
Design and Methods: We compared the frequency of FLT3 -length mutations ( FLT3 -LM), FLT3 -TKD, MLL -partial tandem duplications ( MLL -PTD), NRAS , and KIT D816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML ( de novo : n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
Results: All mutations were more frequent in s-AML than in MDS and all but the FLT3 -TKD were more frequent in RAEB than in RA/RARS. The higher incidences in s-AML were significant for FLT3 -TKD ( p =0.032), MLL -PTD ( p =0.034), and FLT3 -LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p <0.0001). The incidence of NRAS-mutations increased from 17/272 (6.3%) in MDS to 41/343 in s-AML (12.0%) and that of KIT D816-mutations from 2/290 (0.7%) to 5/341 (1.5%) ( p =n.s.). FLT3 -LM-acquisition occurred in 3/22 cases (13.6%) during MDS transformation; NRAS -acquisition occurred in 1/24 (4.2%). FLT3 -LM and MLL -PTD were more frequent in AML relapse than in de novo AML or s-AML ( p <0.0001).
Interpretation and Conclusions: The increase of molecular mutations from low- to high-risk MDS, to s-AML, and to relapsed AML emphasizes the value of these mutations as markers of progressing disease. Finally, we found a low rate of 5q- in the molecularly mutated cases in MDS which might explain the stability of this subtype.
Key words: myelodysplastic syndromes (MDS), acute myeloid leukemias (AML), molecular mutations, progression, leukemogenesis.
Related Article
The spectrum of molecular aberrations in myelodysplastic syndromes: in the shadow of acute myeloid leukemia
David P. Steensma
Haematologica 2007 92: 723-727.
[Full Text]
[PDF]</description><subject>Acute Disease</subject><subject>Biological and medical sciences</subject><subject>Disease Progression</subject><subject>fms-Like Tyrosine Kinase 3 - genetics</subject><subject>Gene Frequency</subject><subject>Hematologic and hematopoietic diseases</subject><subject>Histone-Lysine N-Methyltransferase</subject><subject>Humans</subject><subject>Leukemia, Myeloid - diagnosis</subject><subject>Leukemia, Myeloid - genetics</subject><subject>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</subject><subject>Medical sciences</subject><subject>Molecular Epidemiology</subject><subject>Mutation</subject><subject>Myelodysplastic Syndromes - diagnosis</subject><subject>Myelodysplastic Syndromes - genetics</subject><subject>Myeloid-Lymphoid Leukemia Protein - genetics</subject><subject>Proto-Oncogene Proteins c-kit - genetics</subject><subject>ras Proteins - genetics</subject><issn>0390-6078</issn><issn>1592-8721</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>DOA</sourceid><recordid>eNpdkUFvFCEYhidGY2v16tFw0duuwAADx6ap2qSJFz2Tb-CjS2WGFWbc7E_wXzvbXd3EEwGe9_ny5W2at4yu25aLjxvAAaac1oxqZZ41l0wavtIdZ8-bS9oaulK00xfNq1ofKeXUmO5lc8E6KakW6rL5fU1cHrZQYIq_kNRp9nuSAxlyQjcnKGSYp-Uvj5XEkbSake1yxXGqZBenDRn2mLLf122COkVH6n70JQ9IYPSHhGAt_S8Cbp7wGIyeJJx_4BDhdfMiQKr45nReNd8_3X67-bK6__r57ub6fuWENNNK-KCd73VPhaQtg84H1TkHNDDVowSBHBVq4BS8pNw5KbtuWRV7Rh0Xur1q7o5en-HRbkscoOxthmifHnJ5sFCWTRJax5ShQnEwXRCOhR6DCV72AltJUfHF9eHo2pb8c8Y62SFWhynBiHmutqNSGSUP4PoIupJrLRj-DWbUHoq0f4u0T0UugXcn89wP6M_4qbkFeH8CoDpIocDoYj1zWsuWSnPmNvFhs4sFbR0gpUXL7W63M9wq2wnR_gH9nrdy</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Bacher, Ulrike</creator><creator>Haferlach, Torsten</creator><creator>Kern, Wolfgang</creator><creator>Haferlach, Claudia</creator><creator>Schnittger, Susanne</creator><general>Haematologica</general><general>Ferrata Storti Foundation</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>7X8</scope><scope>DOA</scope></search><sort><creationdate>20070601</creationdate><title>A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia</title><author>Bacher, Ulrike ; Haferlach, Torsten ; Kern, Wolfgang ; Haferlach, Claudia ; Schnittger, Susanne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c459t-4df8cdb8b045031a7df67cca0f16be5a4e2e6e8a20ad502cc5577846eb10c2483</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Acute Disease</topic><topic>Biological and medical sciences</topic><topic>Disease Progression</topic><topic>fms-Like Tyrosine Kinase 3 - genetics</topic><topic>Gene Frequency</topic><topic>Hematologic and hematopoietic diseases</topic><topic>Histone-Lysine N-Methyltransferase</topic><topic>Humans</topic><topic>Leukemia, Myeloid - diagnosis</topic><topic>Leukemia, Myeloid - genetics</topic><topic>Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis</topic><topic>Medical sciences</topic><topic>Molecular Epidemiology</topic><topic>Mutation</topic><topic>Myelodysplastic Syndromes - diagnosis</topic><topic>Myelodysplastic Syndromes - genetics</topic><topic>Myeloid-Lymphoid Leukemia Protein - genetics</topic><topic>Proto-Oncogene Proteins c-kit - genetics</topic><topic>ras Proteins - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bacher, Ulrike</creatorcontrib><creatorcontrib>Haferlach, Torsten</creatorcontrib><creatorcontrib>Kern, Wolfgang</creatorcontrib><creatorcontrib>Haferlach, Claudia</creatorcontrib><creatorcontrib>Schnittger, Susanne</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>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Haematologica (Roma)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bacher, Ulrike</au><au>Haferlach, Torsten</au><au>Kern, Wolfgang</au><au>Haferlach, Claudia</au><au>Schnittger, Susanne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia</atitle><jtitle>Haematologica (Roma)</jtitle><addtitle>Haematologica</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>92</volume><issue>6</issue><spage>744</spage><epage>752</epage><pages>744-752</pages><issn>0390-6078</issn><eissn>1592-8721</eissn><abstract>From the Bone Marrow Transplant Unit, University Hospital of Hamburg-Eppendorf, Hamburg, Germany (UB); MLL, Munich Leukemia Laboratory, Munich, Germany (TH, WK, CH, SS)
Correspondence: Susanne Schnittger, MLL, Munich Leukemia Laboratory, Max-Lebsche-Platz 31 81377 Munich, Germany. E-mail: susanne.schnittger{at}mll-online.com
Background and Objectives: The precise relationship between myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML) is unclear and the role of molecular mutations in leukemic transformation in MDS is controversial. The aim of this study was to clarify the relationship between AML and MDS by comparing the frequency of molecular mutations in the two conditions.
Design and Methods: We compared the frequency of FLT3 -length mutations ( FLT3 -LM), FLT3 -TKD, MLL -partial tandem duplications ( MLL -PTD), NRAS , and KIT D816 in 381 patients with MDS refractory anemia with excess blasts [RAEB] n=49; with ringed sideroblasts [RARS] n=310; chronic monomyelocytic leukemia [CMML] n=22) and in 4130 patients with AML ( de novo : n=3139; secondary AML [s-AML] following MDS: n=397; therapy-related [t-AML]: n=233; relapsed: n=361).
Results: All mutations were more frequent in s-AML than in MDS and all but the FLT3 -TKD were more frequent in RAEB than in RA/RARS. The higher incidences in s-AML were significant for FLT3 -TKD ( p =0.032), MLL -PTD ( p =0.034), and FLT3 -LM (RA/RARS: 0/45; RAEB: 8/293; 2.7%; s-AML: 45/389; 11.6%; p <0.0001). The incidence of NRAS-mutations increased from 17/272 (6.3%) in MDS to 41/343 in s-AML (12.0%) and that of KIT D816-mutations from 2/290 (0.7%) to 5/341 (1.5%) ( p =n.s.). FLT3 -LM-acquisition occurred in 3/22 cases (13.6%) during MDS transformation; NRAS -acquisition occurred in 1/24 (4.2%). FLT3 -LM and MLL -PTD were more frequent in AML relapse than in de novo AML or s-AML ( p <0.0001).
Interpretation and Conclusions: The increase of molecular mutations from low- to high-risk MDS, to s-AML, and to relapsed AML emphasizes the value of these mutations as markers of progressing disease. Finally, we found a low rate of 5q- in the molecularly mutated cases in MDS which might explain the stability of this subtype.
Key words: myelodysplastic syndromes (MDS), acute myeloid leukemias (AML), molecular mutations, progression, leukemogenesis.
Related Article
The spectrum of molecular aberrations in myelodysplastic syndromes: in the shadow of acute myeloid leukemia
David P. Steensma
Haematologica 2007 92: 723-727.
[Full Text]
[PDF]</abstract><cop>Pavia</cop><pub>Haematologica</pub><pmid>17550846</pmid><doi>10.3324/haematol.10869</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Acute Disease Biological and medical sciences Disease Progression fms-Like Tyrosine Kinase 3 - genetics Gene Frequency Hematologic and hematopoietic diseases Histone-Lysine N-Methyltransferase Humans Leukemia, Myeloid - diagnosis Leukemia, Myeloid - genetics Leukemias. Malignant lymphomas. Malignant reticulosis. Myelofibrosis Medical sciences Molecular Epidemiology Mutation Myelodysplastic Syndromes - diagnosis Myelodysplastic Syndromes - genetics Myeloid-Lymphoid Leukemia Protein - genetics Proto-Oncogene Proteins c-kit - genetics ras Proteins - genetics |
| title | A comparative study of molecular mutations in 381 patients with myelodysplastic syndrome and in 4130 patients with acute myeloid leukemia |
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