Yale University | YU Â· Yale Cancer Center-Section of Hematology.
Yale University | YU
Yale Cancer Center-Section of Hematology
New Haven, CT.
- Cell Culture
- Gel Electrophoresis
- Gene Expression
- Western Blot Analysis
- Cancer Biology
- Flow Cytometry
- Cell Signaling
- Molecular Cloning
- Oscar Ramirez currently works at the Yale Cancer Center-Section of Hematology, Yale University.
- Oscar does research in Immunology, Cell Biology and Molecular Biology.
- Their most recent publication is 'E2F-2 Promotes Nuclear Condensation and Enucleation of Terminally Differentiated Erythroblasts..'
- E2F-2 Promotes Nuclear Condensation and Enucleation of Terminally Differentiated Erythroblasts.
- Small interfering RNA targeting NF-κB attenuates lipopolysaccharide-induced acute lung injury in rats.
- Cancer-associated SF3B1 mutants recognize otherwise inaccessible cryptic 3' splice sites within RNA secondary structures.
- Time Series Analyses of Hand, Foot and Mouth Disease Integrating Weather Variables
- Correction: A Small Library of Synthetic Di-Substituted 1, 4-Naphthoquinones Induces ROS-Mediated Cell Death in Murine Fibroblasts
- Leptin deficiency in vivo enhances the ability of splenic dendritic cells to activate T cells
- Myeloid-derived suppressor cells are associated with disease progression and decreased overall survival in advanced-stage melanoma patients
- Abstract A98: Young women's breast cancer demonstrates increased immune suppression through ciculating regulatory T cells and myeloid-derived supressor cells independent of stage or subtype.
- Abstract P4-04-06: Young women's breast cancer is characterized by increased immune suppression through circulating myeloid derived supressor cells
- Influence of human immune cells on cancer: Studies at the University of Colorado
- Abstract 5405: Immuno-phenotyping reveals cell types present in circulation of breast cancer patients and elucidates their funstional potential
- Implication for the role of leptin-induced signaling as a negative regulator of dendritic cell function.