X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

ShiPS-miFF3

RRID:CVCL_1E70

Organism

Homo sapiens

Comments

From: University of Sheffield; Sheffield; UK. DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Proper Citation

RRID:CVCL_1E70

Reference

PMID:26810087

Category

Induced pluripotent stem cell DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Sex

DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Synonyms

ShiPS-MIFF3, MIFF3, MIFF-3, mRNA Induced Foreskin Fibroblast-3, UOSi001-B DT Created: 08-07-15, Last updated: 05-07-19, Version: 6

Cross References

BioSamples; SAMEA5424900 hPSCreg; UOSi001-B SKIP; SKIP002499 Wikidata; Q54953347 DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Hierarchy

DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Originate from Same Individual

DT Created: 08-07-15; Last updated: 05-07-19; Version: 6

Publications that use this research resource

A Human IPS Model Implicates Embryonic B-Myeloid Fate Restriction as Developmental Susceptibility to B Acute Lymphoblastic Leukemia-Associated ETV6-RUNX1.

  • Böiers C
  • Dev. Cell
  • 2018 Feb 5

Literature context:


Abstract:

ETV6-RUNX1 is associated with childhood acute B-lymphoblastic leukemia (cALL) functioning as a first-hit mutation that initiates a clinically silent pre-leukemia in utero. Because lineage commitment hierarchies differ between embryo and adult, and the impact of oncogenes is cell-context dependent, we hypothesized that the childhood affiliation of ETV6-RUNX1 cALL reflects its origins in a progenitor unique to embryonic life. We characterize the first emerging B cells in first-trimester human embryos, identifying a developmentally restricted CD19-IL-7R+ progenitor compartment, which transitions from a myeloid to lymphoid program during ontogeny. This developmental series is recapitulated in differentiating human pluripotent stem cells (hPSCs), thereby providing a model for the initiation of cALL. Genome-engineered hPSCs expressing ETV6-RUNX1 from the endogenous ETV6 locus show expansion of the CD19-IL-7R+ compartment, show a partial block in B lineage commitment, and produce proB cells with aberrant myeloid gene expression signatures and potential: features (collectively) consistent with a pre-leukemic state.