UBC9 inhibits myeloid differentiation in collaboration with AML1-MTG8
Author:
Funder
Japan Society for the Promotion of Science
Children’s Cancer Association of Japan
Publisher
Springer Science and Business Media LLC
Subject
Hematology
Link
https://link.springer.com/content/pdf/10.1007/s12185-022-03303-1.pdf
Reference47 articles.
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2. Erickson P, Gao J, Chang KS, Look T, Whisenant E, Raimondi S, et al. Identification of breakpoints in t(8;21) acute myelogenous leukemia and isolation of a fusion transcript, AML1/ETO, with similarity to Drosophila segmentation gene, runt. Blood. 1992;80(7):1825–31.
3. Nisson PE, Watkins PC, Sacchi N. Transcriptionally active chimeric gene derived from the fusion of the AML1 gene and a novel gene on chromosome 8 in t(8;21) leukemic cells. Cancer Genet Cytogenet. 1992;63(2):81–8.
4. Miyoshi H, Kozu T, Shimizu K, Enomoto K, Maseki N, Kaneko Y, et al. The t(8;21) translocation in acute myeloid leukemia results in production of an AML1-MTG8 fusion transcript. Embo J. 1993;12(7):2715–21.
5. Kozu T, Miyoshi H, Shimizu K, Maseki N, Kaneko Y, Asou H, et al. Junctions of the AML1/MTG8(ETO) fusion are constant in t(8;21) acute myeloid leukemia detected by reverse transcription polymerase chain reaction. Blood. 1993;82(4):1270–6.
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