AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: Implication in stepwise leukemogenesis and response to Gleevec
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AML1-ETO and C-KIT mutation/overexpression in t(8;21) leukemia: implication in stepwise leukemogenesis and response to Gleevec.
To explore the genetic abnormalities that cooperate with AML1-ETO (AE) fusion gene to cause acute myeloid leukemia (AML) with t(8;21), we screened a number of candidate genes and identified 11 types of mutations in C-KIT gene (mC-KIT), including 6 previously undescribed ones among 26 of 54 (48.1%) cases with t(8;21). To address a possible chronological order between AE and mC-KIT, we showed tha...
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The full-length AML1-ETO (AE) fusion gene resulting from t(8;21)(q22;q22) in human acute myeloid leukemia (AML) is not sufficient to induce leukemia in animals, suggesting that additional mutations are required for leukemogenesis. We and others have identified activating mutations of C-KIT in nearly half of patients with t(8;21) AML. To test the hypothesis that activating C-KIT mutations cooper...
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One of the most common genetic events in acute myeloid leukemia (AML) is the t(8;21) (q22;q22) translocation, which contributes to leukemic transformation. However, different lines of evidence suggest that the AML1-ETO rearrangement is not sufficient to cause the full leukemic phenotype. Secondary genetic alterations such as mutations in receptor tyrosine kinases are thus required to induce ove...
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170 words Text: 4977 words Blood First Edition Paper, prepublished online September 21, 2006; DOI 10.1182/blood-2006-02-003517 Copyright © 2006 American Society of Hematology only. For personal use at PENN STATE UNIVERSITY on February 23, 2013. bloodjournal.hematologylibrary.org From
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ژورنال
عنوان ژورنال: Proceedings of the National Academy of Sciences
سال: 2005
ISSN: 0027-8424,1091-6490
DOI: 10.1073/pnas.0408831102