Amplification or duplication of chromosome band 21q22 with multiple copies of the AML1 gene and mutation of the TP53 gene in therapy-related MDS and AML
Author:
Publisher
Springer Science and Business Media LLC
Subject
Oncology,Cancer Research,Hematology
Link
http://www.nature.com/articles/2403612.pdf
Reference26 articles.
1. Tanaka T, Tanaka K, Ogawa S, Kurokawa M, Mitani K, Nishida J et al. An acute myeloid leukaemia gene, AML1, regulates hemopoietic myeloid cell differentiation and transcriptional activation antagonistically by two alternative spliced forms. EMBO J 1995; 14: 341–350.
2. Okuda T, Cai Z, Yang S, Lenny N, Lyu CJ, van Deursen JM et al. Expression of a knocked-in AML1-ETO leukemia gene inhibits the establishment of normal definitive hematopoiesis and directly generates dysplastic hematopoietic progenitors. Blood 1998; 91: 3134–3143.
3. Rhoades KL, Hetherington CJ, Harakawa N, Yergeau DA, Zhou L, Liu LQ et al. Analysis of the role of AML1-ETO in leukemogenesis, using an inducible transgenic mouse model. Blood 2000; 96: 2108–2115.
4. Osato M, Asou N, Abdalla E, Hoshino K, Yamasaki H, Okubo T et al. Biallelic and heterozygous point mutations in the runt domain of the AML1/PEBP2alphaB gene associated with myeloblastic leukemias. Blood 1999; 93: 1817–1824.
5. Christiansen DH, Andersen MK, Pedersen-Bjergaard J . Mutations of AML1 are common in therapy-related myelodysplasia following therapy with alkylating agents and are significantly associated with deletion or loss of chromosome arm 7q and with subsequent leukemic transformation. Blood 2004; 104: 1474–1481.
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