A5068621499- T-cell and B-cell Immunology
- Immune Cell Function and Interaction
- DNA Repair Mechanisms
- CRISPR and Genetic Engineering
- Immunotherapy and Immune Responses
- Prostate Cancer Treatment and Research
- Epigenetics and DNA Methylation
- RNA and protein synthesis mechanisms
- RNA Research and Splicing
- Cytomegalovirus and herpesvirus research
- Genomics and Chromatin Dynamics
- interferon and immune responses
- RNA modifications and cancer
- Genetics and Neurodevelopmental Disorders
- Prostate Cancer Diagnosis and Treatment
- Ubiquitin and proteasome pathways
- Cancer, Lipids, and Metabolism
- MicroRNA in disease regulation
- Cytokine Signaling Pathways and Interactions
- Estrogen and related hormone effects
- Cancer-related Molecular Pathways
- Lymphoma Diagnosis and Treatment
- Polyamine Metabolism and Applications
- Immunodeficiency and Autoimmune Disorders
- CAR-T cell therapy research
Memorial Sloan Kettering Cancer Center
2016-2025
Cornell University
2016-2025
Kettering University
2009-2025
Albert Einstein College of Medicine
1993-2013
UNC Lineberger Comprehensive Cancer Center
2013
University of North Carolina at Chapel Hill
2013
Howard Hughes Medical Institute
1998-2007
Harvard University
2000-2007
Brigham and Women's Hospital
2002
Dana-Farber/Boston Children's Cancer and Blood Disorders Center
2000
Abstract We demonstrate that the androgen receptor (AR) regulates a transcriptional program of DNA repair genes promotes prostate cancer radioresistance, providing potential mechanism by which deprivation therapy synergizes with ionizing radiation. Using model castration-resistant cancer, we show second-generation antiandrogen results in downregulation genes. Next, primary cancers display significant spectrum AR output, correlates expression set RNA-seq and ChIP-seq, define these are both...
Changes in DNA methylation are required for the formation of germinal centers (GCs), but mechanisms such changes poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated demethylation through its activity coupled with repair. We investigated epigenetic function AID vivo center B cells (GCBs) isolated from wild-type (WT) and AID-deficient (Aicda−/−) mice. determined that transit GC is associated marked locus-specific loss increased diversity, both which lost...
Generation of cellular heterogeneity is an essential feature the adaptive immune system. This best exemplified during humoral response when expanding B cell clone assumes multiple fates, including class-switched cells, antibody-secreting plasma and memory cells. Although each type for immunity, their generation must be exquisitely controlled because a cannot revert back to parent isotype, terminally differentiated contribute pool. In this study, we show that environmental sensor, aryl...
The most aggressive B cell lymphomas frequently manifest extranodal distribution and carry somatic mutations in the poorly characterized gene TBL1XR1. Here, we show that TBL1XR1 skew humoral immune response toward generating abnormal immature memory cells (MB), while impairing plasma differentiation. At molecular level, mutants co-opt SMRT/HDAC3 repressor complexes binding MB transcription factor (TF) BACH2 at expense of germinal center (GC) TF BCL6, leading to pre-memory transcriptional...