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PKM2 as a novel target of RUNX1-ETO and is specifically downregulated in RUNX1-ETO positive AML patients, indicating that PKM2 level might have a diagnostic potential in RUNX1-ETO associated AML.
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The specific association of ZBTB7A mutations with t(8;21) rearranged acute myeloid leukaemia points towards leukemogenic cooperativity between mutant ZBTB7A and the RUNX1/RUNX1T1 fusion protein has been reported.
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Data indicate miR-29b-1 as a regulator of the AML1-ETO protein (RUNX1-RUNX1T1), and that miR-29b-1 expression in t(8;21)-carrying leukemic cell lines partially rescues the leukemic phenotype.
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Altogether, these results revealed an unexpected and important epigenetic mini-circuit of AML1-ETO/THAP10/miR-383 in t(8;21) acute myeloid leukaemia, in which epigenetic suppression of THAP10 predicts a poor clinical outcome and represents a novel therapeutic target.
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RUNX1-RUNX1T1 transcript levels were measured in bone marrow samples collected from 208 patients at scheduled time points after transplantation. Over 90% of the 175 patients who were in continuous complete remission had a >/=3-log reduction in RUNX1-RUNX1T1 transcript levels from the time of diagnosis at each time point after transplantation and a >/=4-log reduction at >/=12 months.
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The data suggest that the tumor suppressor activity of both RUNX1t1 and TFF1 are mechanistically connected to CEBPB and that cross-regulation between CEBPB-RUNX1t1-TFF1 plays an important role in gastric carcinogenesis.
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RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells
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Leukaemogenesis by AML1-ETO requires enhanced C/D box snoRNA/RNP formation.
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Study demonstrated that TRiC's contribution to the activity of the DNA-binding domain (AML1-175) of AML1-ETO is consistent with its contribution to the activity of full-length AML1-ETO and is mediated through its direct association with the DNA-binding domain
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the AML1-ETO fusion protein increases the expression of SIRT1, possibly by binding to the promoter region of SIRT1 to activate its transcription in t(8;21) AML.
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A feedback circuitry involving miR-9-1 and RUNX1-RUNX1T1.
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The role of RUNX1T1 in t(8;21) acute myeloid leukemia and miRNA expression regulation
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Our data revealed a novel role for RUNX1T1 as a tumor-suppressor gene in colorectal cancer through modulation of multiple cellular pathways affecting the cell cycle, DNA damage, DNA replication, estrogen signaling, and drug resistance
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Exon splicing patterns in the human RUNX1-RUNX1T1 fusion gene present in acute myeloid leukemia patients have been decoded.
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Data suggest that biosynthesis and folding of leukemogenic fusion oncoprotein AML1-ETO/RUNX1-RUNX1T1 is facilitated by interaction with the chaperonin TRiC/CCT1/TCP1 and HSP70 (heat shock protein 70).
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AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex.
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A substantial fraction of AML1-ETO/p300 co-localization occurs near TSSs in promoter regions associated with transcriptionally active loci.
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minimal residual disease determined by RUNX1/RUNX1T1 transcript levels could identify allogeneic hematopoietic stem cell transplantation t(8;21) (q22;q22) acute myeloid leukemia patients who are at high risk for relapse, together with c-KIT mutations
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identify a high-frequency mutation in t(8;21)/RUNX1-RUNX1T1 acute myekoid leukemia (AML) and identify the need for future studies to investigate the clinical and biological relevance of ASXL2 mutations in this unique subset of AML
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RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors are rescued by activating c-Kit mutations
