Literature DB >> 21343549

TET2 mutations improve the new European LeukemiaNet risk classification of acute myeloid leukemia: a Cancer and Leukemia Group B study.

Klaus H Metzeler1, Kati Maharry, Michael D Radmacher, Krzysztof Mrózek, Dean Margeson, Heiko Becker, John Curfman, Kelsi B Holland, Sebastian Schwind, Susan P Whitman, Yue-Zhong Wu, William Blum, Bayard L Powell, Thomas H Carter, Meir Wetzler, Joseph O Moore, Jonathan E Kolitz, Maria R Baer, Andrew J Carroll, Richard A Larson, Michael A Caligiuri, Guido Marcucci, Clara D Bloomfield.   

Abstract

PURPOSE: To determine the frequency of TET2 mutations, their associations with clinical and molecular characteristics and outcome, and the associated gene- and microRNA-expression signatures in patients with primary cytogenetically normal acute myeloid leukemia (CN-AML). PATIENTS AND METHODS: Four-hundred twenty-seven patients with CN-AML were analyzed for TET2 mutations by polymerase chain reaction and direct sequencing and for established prognostic gene mutations. Gene- and microRNA-expression profiles were derived using microarrays.
RESULTS: TET2 mutations, found in 23% of patients, were associated with older age (P < .001) and higher pretreatment WBC (P = .04) compared with wild-type TET2 (TET2-wt). In the European LeukemiaNet (ELN) favorable-risk group (patients with CN-AML who have mutated CEBPA and/or mutated NPM1 without FLT3 internal tandem duplication [FLT3-ITD]), TET2-mutated patients had shorter event-free survival (EFS; P < .001) because of a lower complete remission (CR) rate (P = .007), and shorter disease-free survival (DFS; P = .003), and also had shorter overall survival (P = .001) compared with TET2-wt patients. TET2 mutations were not associated with outcomes in the ELN intermediate-I-risk group (CN-AML with wild-type CEBPA and wild-type NPM1 and/or FLT3-ITD). In multivariable models, TET2 mutations were associated with shorter EFS (P = .004), lower CR rate (P = .03), and shorter DFS (P = .05) only among favorable-risk CN-AML patients. We identified a TET2 mutation-associated gene-expression signature in favorable-risk but not in intermediate-I-risk patients and found distinct mutation-associated microRNA signatures in both ELN groups.
CONCLUSION: TET2 mutations improve the ELN molecular-risk classification in primary CN-AML because of their adverse prognostic impact in an otherwise favorable-risk patient subset. Our data suggest that these patients may be candidates for alternative therapies.

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Year:  2011        PMID: 21343549      PMCID: PMC3084003          DOI: 10.1200/JCO.2010.32.7742

Source DB:  PubMed          Journal:  J Clin Oncol        ISSN: 0732-183X            Impact factor:   44.544


  46 in total

1.  Favorable prognostic impact of NPM1 mutations in older patients with cytogenetically normal de novo acute myeloid leukemia and associated gene- and microRNA-expression signatures: a Cancer and Leukemia Group B study.

Authors:  Heiko Becker; Guido Marcucci; Kati Maharry; Michael D Radmacher; Krzysztof Mrózek; Dean Margeson; Susan P Whitman; Yue-Zhong Wu; Sebastian Schwind; Peter Paschka; Bayard L Powell; Thomas H Carter; Jonathan E Kolitz; Meir Wetzler; Andrew J Carroll; Maria R Baer; Michael A Caligiuri; Richard A Larson; Clara D Bloomfield
Journal:  J Clin Oncol       Date:  2009-12-21       Impact factor: 44.544

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7.  Genetic characterization of TET1, TET2, and TET3 alterations in myeloid malignancies.

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Journal:  Blood       Date:  2009-05-06       Impact factor: 22.113

8.  Loss of heterozygosity 4q24 and TET2 mutations associated with myelodysplastic/myeloproliferative neoplasms.

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9.  Genetic analysis of transforming events that convert chronic myeloproliferative neoplasms to leukemias.

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  133 in total

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5.  TET2 gene mutation is unfavorable prognostic factor in cytogenetically normal acute myeloid leukemia patients with NPM1+ and FLT3-ITD - mutations.

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7.  Identification of a 24-gene prognostic signature that improves the European LeukemiaNet risk classification of acute myeloid leukemia: an international collaborative study.

Authors:  Zejuan Li; Tobias Herold; Chunjiang He; Peter J M Valk; Ping Chen; Vindi Jurinovic; Ulrich Mansmann; Michael D Radmacher; Kati S Maharry; Miao Sun; Xinan Yang; Hao Huang; Xi Jiang; Maria-Cristina Sauerland; Thomas Büchner; Wolfgang Hiddemann; Abdel Elkahloun; Mary Beth Neilly; Yanming Zhang; Richard A Larson; Michelle M Le Beau; Michael A Caligiuri; Konstanze Döhner; Lars Bullinger; Paul P Liu; Ruud Delwel; Guido Marcucci; Bob Lowenberg; Clara D Bloomfield; Janet D Rowley; Stefan K Bohlander; Jianjun Chen
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