RUNX1/AML1 mutant collaborates with BMI1 overexpression in the development of human and murine myelodysplastic syndromes

Harada, Yuka; Inoue, Daichi; Ding, Ye; Imagawa, Jun; Doki, Noriko; Matsui, Hirotaka; Yahata, Takashi; Matsushita, Hiromichi; Ando, Kiyoshi; Sashida, Goro; Iwama, Atsushi; Kitamura, Toshio; Harada, Hironori

doi:10.1182/blood-2012-06-434423

Cited by 28 publications

(41 citation statements)

References 51 publications

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“…5 Gene expression levels were quantified with SYBR Select Master Mix and the following forward/reverse primer pairs: RUNX1a (59-GAACCACTCCACTGCCTTTAAC-39/59-ATTCTGAGGGCTGTCATCTTTC-39), RUNX1b Normal BM n=10…”

Section: Methods Patientsmentioning

confidence: 99%

“…Patients gave written informed consent, in accordance with the Declaration of Helsinki. Gene mutation analysis was performed by Sanger sequencing as described previously 5 using primer pairs listed in supplemental Table 1.…”

Section: Methods Patientsmentioning

confidence: 99%

“…Flow cytometry and immunoblot analysis were performed as reported previously. 5 Details are provided in supplemental Methods.…”

Section: Retrovirus Transductionmentioning

confidence: 99%

“…After GFP-based sorting, the cells were cultured on MS5 stromal cells as described previously. 5 The MDSderived cell line TF-1 was infected with retroviral SRSF2P95H vector, and transduced single cells were isolated using FACS Aria. Growing clones were then analyzed separately.…”

Section: Retrovirus Transductionmentioning

confidence: 99%

“…5 However, the relevance of the level of RUNX1 expression for the pathogenesis of hematological malignancies has not been explored.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of RUNX1 short isoform has an important role in the development of myelodysplastic/myeloproliferative neoplasms

et al. 2017

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Section: Methods Patientsmentioning

confidence: 99%

Section: Methods Patientsmentioning

confidence: 99%

“…Flow cytometry and immunoblot analysis were performed as reported previously. 5 Details are provided in supplemental Methods.…”

Section: Retrovirus Transductionmentioning

confidence: 99%

Section: Retrovirus Transductionmentioning

confidence: 99%

“…5 However, the relevance of the level of RUNX1 expression for the pathogenesis of hematological malignancies has not been explored.…”

Section: Introductionmentioning

confidence: 99%

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Overexpression of RUNX1 short isoform has an important role in the development of myelodysplastic/myeloproliferative neoplasms

et al. 2017

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RUNX1 and CBFβ Mutations and Activities of Their Wild-Type Alleles in AML

Hyde

Liu

Friedman

2017

Advances in Experimental Medicine and Biology

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Mutations in RUNX1 and CBFB have long been recognized as important in hematological malignancies. Point mutations and deletions of RUNX1 are frequently found in myelodysplastic syndrome, myeloproliferative disease, and acute myeloid leukemia. Germline mutations in RUNX1 are associated with familial platelet disorder with predisposition to AML. In addition, as will be discussed in other chapters, both RUNX1 and CBFB are involved in recurrent chromosomal rearrangements in leukemia. More recently, roles for the non-mutated RUNX1 and CBFB genes have been identified in multiple leukemia subtypes. This chapter will discuss the roles of RUNX1 and CBFB, both in diseases caused by their mutations or deletions, as well as in the context of chromosomal rearrangements.

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Lentiviral vector-mediate ATG3 overexpression inhibits growth and promotes apoptosis of human SKM-1 cells

et al. 2014

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Based on the nested case-control study cohort and gene expression profile, we have picked up a subset of six genes to distinguish the leukemia group and control group stably. ATG3 is the only down regulated gene. This research is to investigate the effect of ATG3 gene over expression by lentivirus on SKM-1 cell line and myelodysplastic syndrome to leukemic transformation. Human SKM-1 cells were transfected with ATG3-GFP recombinant lentiviral vectors and compared with cells transfected with GFP lentiviral vectors. Western blot was performed to detect the ATG3 protein. Cell proliferation was assessed by cell counting kit-8. Cell vitality was tested by Trypan Blue. Cell apoptosis was determined by Annexin V Apoptosis Detection Kit APC. Observe and compare the changes on growth curve, cell vitality and cell apoptosis. After 72 h of transfection, satisfactory transfection efficiency (> 90 %) was observed. SKM-1 cell line showed a statistically significant (P < 0.05) overexpression of ATG3, parallel to significantly (P < 0.05) inhibited cell proliferation. The cell vitality of ATG3 overexpression was significantly (P < 0.05) lower than negative control. Cell apoptosis analysis by flow cytometer demonstrated decreased proportion of early apoptosis and increased that of late apoptosis and death (P < 0.05). Over expressed ATG3 gene and protein, the SKM-1 cell line was inhibited in proliferation and cell vitality. It was promoted from early apoptosis to late apoptosis and death. The malignancy of SKM-1 cell line was decreased after transfection. ATG3 gene and its gene family may play an important role in transformation of myelodysplastic syndrome.

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RUNX1/AML1 mutant collaborates with BMI1 overexpression in the development of human and murine myelodysplastic syndromes

Cited by 28 publications

References 51 publications

Overexpression of RUNX1 short isoform has an important role in the development of myelodysplastic/myeloproliferative neoplasms

Overexpression of RUNX1 short isoform has an important role in the development of myelodysplastic/myeloproliferative neoplasms

RUNX1 and CBFβ Mutations and Activities of Their Wild-Type Alleles in AML

Lentiviral vector-mediate ATG3 overexpression inhibits growth and promotes apoptosis of human SKM-1 cells

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