Oscar Ramirez
Address:
Yale University | YU
Yale Cancer Center-Section of Hematology
New Haven, CT.
Research Interests:
- PCR
 - Cell Culture
 - Gel Electrophoresis
 - Gene Expression
 - Western Blot Analysis
 - Cloning
 - Cancer Biology
 - Flow Cytometry
 - Immunohistochemistry
 - Cell Signaling
 - Molecular Cloning
 - Apoptosis.
 
Biography:
- 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..'
 
Research:
- 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.