257 results on '"Sashida, Goro"'
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2. TIF1β activates leukemic transcriptional program in HSCs and promotes BCR::ABL1-induced myeloid leukemia
3. Editorial: Recent Advance in MDS Research
4. Stem cell regulation and dynamics in myeloid malignancies
5. Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.
6. The acidic domain of Hmga2 and the domain’s linker region are critical for driving self-renewal of hematopoietic stem cell
7. Insufficiency of non-canonical PRC1 synergizes with JAK2V617F in the development of myelofibrosis
8. CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma
9. RUNX1-ETO (RUNX1-RUNX1T1) induces myeloid leukemia in mice in an age-dependent manner
10. Two faces of RUNX3 in myeloid transformation
11. PRC2 insufficiency causes p53-dependent dyserythropoiesis in myelodysplastic syndrome
12. Overexpression of Hmga2 activates Igf2bp2 and remodels transcriptional program of Tet2-deficient stem cells in myeloid transformation
13. Ascl1-induced Wnt11 regulates neuroendocrine differentiation, cell proliferation, and E-cadherin expression in small-cell lung cancer and Wnt11 regulates small-cell lung cancer biology
14. Low prevalence of the BCR–ABL1 fusion gene in a normal population in southern Sarawak
15. Ezh1 Targets Bivalent Genes to Maintain Self-Renewing Stem Cells in Ezh2-Insufficient Myelodysplastic Syndrome
16. Deregulated Polycomb functions in myeloproliferative neoplasms
17. Systematic review of pre-clinical chronic myeloid leukaemia
18. Multiple myeloma–associated DIS3 gene is essential for hematopoiesis, but loss of DIS3 is insufficient for myelomagenesis
19. Ezh2 loss propagates hypermethylation at T cell differentiation-regulating genes to promote leukemic transformation
20. Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs
21. Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
22. Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
23. Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
24. Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes
25. Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
26. Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
27. Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
28. Supplementary Figure 1-11 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
29. Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
30. Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
31. Supplementary Table 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
32. Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome
33. Data from The Mef/Elf4 Transcription Factor Fine Tunes the DNA Damage Response
34. Supplementary Figures 1-5 from The Mef/Elf4 Transcription Factor Fine Tunes the DNA Damage Response
35. A gain‐of‐function mutation in micro‐RNA ‐142 is sufficient to cause the development of T‐cell leukemia in mice
36. Antitumor immunity augments the therapeutic effects of p53 activation on acute myeloid leukemia
37. Author Correction: Lineage-specific RUNX2 super-enhancer activates MYC and promotes the development of blastic plasmacytoid dendritic cell neoplasm
38. Lineage-specific RUNX2 super-enhancer activates MYC and promotes the development of blastic plasmacytoid dendritic cell neoplasm
39. 3169 – PRIOR INFECTION STRESSES ACTIVATE ELF1 AND REMODEL HSCS TO PROMOTE DEVELOPMENT OF MYELODYSPLASTIC SYNDROME
40. Ezh2 loss in hematopoietic stem cells predisposes mice to develop heterogeneous malignancies in an Ezh1-dependent manner
41. Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator
42. TIF1β Enhances Self-Renewal Capacity of BCR-ABL Leukemic Stem Cells and Inhibits the Myeloid Differentiation
43. Multifaceted role of the polycomb-group gene EZH2 in hematological malignancies
44. A gain‐of‐function mutation in microRNA 142 is sufficient to cause the development of T‐cell leukemia in mice.
45. HMGN3 represses transcription of epithelial regulators to promote migration of cholangiocarcinoma in a SNAI2‐dependent manner
46. Correction to: Systematic review of pre-clinical chronic myeloid leukaemia
47. ATP citrate lyase controls hematopoietic stem cell fate and supports bone marrow regeneration
48. The effect of CARD11 mutation and HBZ expression accelerated lymphoproliferative diseases and formed the pathological basis for adult T-cell leukemia/lymphoma
49. 3179 – HMGA2 ACTIVATES IGF2BP2 BUT ALSO REPRESSES TRANSCRIPTION OF INFLAMMATORY RESPONSE GENES IN STRESS HEMATOPOIESIS
50. Overexpression of HMGN3 nucleosome binding protein is associated with tumor invasion and TGF-? expression in cholangiocarcinoma
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