Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) Proteins (RUNX1T1)

Human Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) interaction partners

1. 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.

2. 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.

3. 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.

4. 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.

5. 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.

6. 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.

7. RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells

8. Leukaemogenesis by AML1-ETO requires enhanced C/D box snoRNA/RNP formation.

9. 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

10. 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.

11. A feedback circuitry involving miR-9-1 and RUNX1-RUNX1T1.

12. The role of RUNX1T1 in t(8;21) acute myeloid leukemia and miRNA expression regulation

13. 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

14. Exon splicing patterns in the human RUNX1-RUNX1T1 fusion gene present in acute myeloid leukemia patients have been decoded.

15. 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).

16. AML1/ETO transactivates gene expression through recruiting AP-1 to the AML1/ETO-AML1 complex.

17. A substantial fraction of AML1-ETO/p300 co-localization occurs near TSSs in promoter regions associated with transcriptionally active loci.

18. 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

19. 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

20. RUNX1/ETO-induced DNA damage and apoptosis in human primary CD34+ hematopoietic progenitors are rescued by activating c-Kit mutations

Mouse (Murine) Runt-Related Transcription Factor 1, Translocated To, 1 (Cyclin D-Related) (RUNX1T1) interaction partners

1. Results suggest that AML1/ETO expression determines a more mobile and less adherent phenotype in preleukemic cells, therefore altering the interaction with the hematopoietic niche, potentially leading to the migration across the bone marrow barrier and to disease progression

2. 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.

3. RUNX1T1 serves as a common angiogenic driver for vaculogenesis and functionality of endothelial lineage cells

4. Leukaemogenesis by AML1-ETO requires enhanced C/D box snoRNA/RNP formation.

5. Data show that RUNX1-ETO;c-Kit(T417IDelta418-419) coexpression promoted exclusively acute myeloid leukemia (AML) in a fraction (51%) of reconstituted mice.

6. Self-renewal induced by AML1/ETO in primary murine progenitors was inhibited when Aes was decreased or absent.

7. AML1-ETO synergizes with an ICSBP deficiency to induce myeloblastic transformation in the bone marrow, reminiscent of acute myelogenous leukemia

8. molecular role for ETO in normal physiology as an inhibitor of C/EBPbeta and a novel regulator of early adipogenesis

9. the loss of the molecular events of AML1-ETO C-terminal NCoR/SMRT-interacting domain transforms AML1-ETO into a potent leukemogenic protein

10. p15(Ink4b) loss must be accompanied by additional oncogenic changes for RUNX1-ETO-associated AML to develop

11. AML1 DNA-binding domain and the ETO NHR2-dimerization domain, but not the ETO NHR1 domain, are critical for the induction of acute myeloid leukemia by AML1-ETO9a

12. the eTAFH-E protein interaction appears to contribute relatively little to the activity of AML1-ETO