Prognostification of ALL by Cytogenetics.
Srīnagar, India. In Indian J Hematol Blood Transfus, 30 Sep 2015
Some chromosomal abnormalities are associated with more favorable outcomes, such as high hyperdiploidy (51-65 chromosomes) and the ETV6-RUNX1 fusion.
Runx1 contributes to neurofibromatosis type 1 neurofibroma formation.
Cincinnati, United States. In Oncogene, 15 Jul 2015
By cross comparison of microarray gene lists on human neurofibroma-initiating cells and developed neurofibroma Schwann cells (SCs) we identified RUNX1 overexpression in human neurofibroma initiation cells, suggesting RUNX1 might relate to neurofibroma formation.
High MN1 expression increases the in vitro clonogenic activity of primary mouse B-cells.
Memphis, United States. In Leuk Res, 12 Jul 2015
Additional analysis of MN1 expression in sub-groups within our cohort carrying different chromosome translocations showed that carriers of the good prognostic marker t(12;21)(TEL-AML1) (n=27) expressed significantly more MN1 than both healthy controls (n=9) (P=0.02) and the group carrying the t(9;22)(BCR-ABL) (n=9) (P=0.001).
Epigenetic Aging Signatures Are Coherently Modified in Cancer.
Aachen, Germany. In Plos Genet, 30 Jun 2015
For example, in acute myeloid leukemia (AML) higher epigenetic age-predictions are associated with increased incidence of mutations in RUNX1, WT1, and IDH2, whereas mutations in TET2, TP53, and PML-PARA translocation are more frequent in younger age-predictions.
Harnessing the Therapeutic Potential of Th17 Cells.
Arbīl, Iraq. In Mediators Inflamm, Dec 2014
For development, Th17 cells require activation of the transcription factors STAT3 and RORγt while RUNX1, c-Maf, and Aiolos are involved in changes of phenotype/functions.
Targeting transcription regulation in cancer with a covalent CDK7 inhibitor.
Boston, United States. In Nature, Aug 2014
Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects transcription of RUNX1 and suggests that sensitivity to THZ1 may be due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core transcriptional regulatory circuitry of these tumour cells.
Reprogramming human endothelial cells to haematopoietic cells requires vascular induction.
New York City, United States. In Nature, Aug 2014
Highly purified non-haemogenic human umbilical vein endothelial cells or adult dermal microvascular endothelial cells were transduced with the transcription factors FOSB, GFI1, RUNX1 and SPI1 (hereafter referred to as FGRS), and then propagated on serum-free instructive vascular niche monolayers to induce outgrowth of haematopoietic colonies containing cells with functional and immunophenotypic features of multipotent progenitor cells (MPPs).