A5036061134- CAR-T cell therapy research
- Multiple Myeloma Research and Treatments
- Immunotherapy and Immune Responses
- Prenatal Screening and Diagnostics
- Epigenetics and DNA Methylation
- Immune Cell Function and Interaction
- Synthesis and Biological Evaluation
- Genetic Syndromes and Imprinting
Kettering University
2019-2020
Memorial Sloan Kettering Cancer Center
2019
Génétique et biologie du développement
2010
The University of Texas Health Science Center at Houston
2010
Early clinical results of chimeric antigen receptor (CAR) T cell therapy targeting B maturation (BCMA) for multiple myeloma (MM) appear promising, but relapses associated with residual low-to-negative BCMA-expressing MM cells have been reported, necessitating identification additional targets. The orphan G protein-coupled receptor, class C group 5 member D (GPRC5D), normally expressed only in the hair follicle, was previously identified as by mRNA marrow aspirates from patients MM,...
Angelman syndrome (AS) and Prader–Willi (PWS) are neurodevelopmental disorders of genomic imprinting. AS results from loss function the ubiquitin protein ligase E3A ( UBE3A ) gene, whereas genetic defect in PWS is unknown. Although induced pluripotent stem cells (iPSCs) provide invaluable models human disease, nuclear reprogramming could limit usefulness iPSCs patients who have should imprint marks be disturbed by epigenetic process. Our derived with show no evidence DNA methylation erasure...
Abstract Chimeric antigen receptor (CAR) T-cell therapy for multiple myeloma targeting B-cell maturation (TNFRSF17; BCMA) induces high overall response rates; however, relapse occurs commonly. A reservoir of cells lacking sufficient BCMA surface expression (antigen escape) may be implicated in relapse. We demonstrate that simultaneous an additional antigen—here, G protein-coupled class-C group-5 member-D (GPRC5D)—can prevent escape–mediated a model myeloma. To identify optimal approach, we...