Osteogenic potential of human adipose-tissue derived mesenchymal stromal cells cultured on 3D-printed porous structured titanium.
Rochester, United States. In Gene, Feb 2016
Compared to standard tissue culture plastic, AMSCs grown in the porous titanium microenvironment showed differences in temporal expression for genes involved in cell cycle progression (CCNB2, HIST2H4), extracellular matrix production (COL1A1, COL3A1), mesenchymal lineage identity (ACTA2, CD248, CD44), osteoblastic transcription factors (DLX3, DLX5, ID3) and epigenetic regulators (EZH1, EZH2).
Identification of gene expression signature for cigarette smoke exposure response-from man to mouse.
Neuchâtel, Switzerland. In Hum Exp Toxicol, Dec 2015
The signature consisted of LRRN3, SASH1, PALLD, RGL1, TNFRSF17, CDKN1C, IGJ, RRM2, ID3, SERPING1, and FUCA1.
Oncogenic mechanisms in Burkitt lymphoma.
Bethesda, United States. In Cold Spring Harb Perspect Med, 2014
TCF-3 is rendered constitutively active in Burkitt lymphoma by two related mechanisms: (1) somatic mutations that inactivate its negative regulator ID3, and (2) somatic mutations in TCF-3 that block the ability of ID3 to bind and interfere with its activity as a transcription factor.
Developments in Burkitt's lymphoma: novel cooperations in oncogenic MYC signaling.
Dundee, United Kingdom. In Cancer Manag Res, 2013
Recurrent mutations in ID3 or TCF3 (E2A) that promote signaling through PI3-kinase have recently been identified in human BL samples, and new therapeutic strategies based on coordinately targeting both the prosurvival factor, B-cell lymphoma-XL, and the PI3-kinase/AKT/mammalian target of rapamycin (mTOR) signaling pathway to synergistically induced BL apoptosis have been proposed.
New pathogenic mechanisms in Burkitt lymphoma.
Barcelona, Spain. In Nat Genet, 2012
Two studies in this issue identify the landscape of somatic mutations in Burkitt lymphoma and highlight the pathogenic and clinical relevance of inactivating mutations of ID3, an inhibitor of the TCF3 transcription factor.