A5034225897- RNA modifications and cancer
- RNA regulation and disease
- Histone Deacetylase Inhibitors Research
- PI3K/AKT/mTOR signaling in cancer
- Virus-based gene therapy research
- Pancreatic and Hepatic Oncology Research
- Cancer-related gene regulation
- Acute Lymphoblastic Leukemia research
- Renal and related cancers
- Acute Myeloid Leukemia Research
- Chronic Myeloid Leukemia Treatments
- RNA Interference and Gene Delivery
- Digestive system and related health
- Pancreatic function and diabetes
- T-cell and Retrovirus Studies
- Genomics and Chromatin Dynamics
- Gastrointestinal disorders and treatments
- Childhood Cancer Survivors' Quality of Life
- Folate and B Vitamins Research
- Biochemical and Molecular Research
- Genetic factors in colorectal cancer
- Ubiquitin and proteasome pathways
- Sirtuins and Resveratrol in Medicine
- Genetic Syndromes and Imprinting
- Pediatric Hepatobiliary Diseases and Treatments
Rutgers, The State University of New Jersey
2019-2022
Rutgers Cancer Institute of New Jersey
2020
Abstract The brush border is comprised of microvilli surface protrusions on the apical epithelia. This specialized structure greatly increases absorptive area and plays crucial roles in human health. However, transcriptional regulatory networks controlling genes are not fully understood. Here, we identify that hepatocyte nuclear factor 4 (HNF4) transcription a conserved important regulator gene program multiple organs, such as intestine, kidney yolk sac. Compromised signatures impaired...
As embryos mature, cells undergo remarkable transitions that are accompanied by shifts in transcription factor regulatory networks. Mechanisms driving developmental incompletely understood. The embryonic intestine from a rapidly proliferating tube with pseudostratified epithelium prior to murine day (E) 14.5 an exquisitely folded columnar fetal stages. We sought identify factors mouse intestinal maturation mining chromatin accessibility data for motifs. ATAC-seq accessible regions shift...
Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss expression PTEN associated with the pathogenesis various cancers, including T-cell leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts promoter multiple hematopoietic populations, T-cells, and acts as hub transcription factors T-ALL. Consistently, loss PE leads to reduced levels T-ALL cells....
Abstract T-cell acute lymphoblastic leukemia (T-ALL) is a NOTCH1-driven disease in need of novel therapies. Here, we identify NOTCH1–SIRT1–KAT7 link as therapeutic vulnerability T-ALL, which the histone deacetylase SIRT1 overexpressed downstream NOTCH1-bound enhancer. loss impaired generation, whereas overexpression accelerated and conferred resistance to NOTCH1 inhibition deacetylase-dependent manner. Moreover, pharmacologic or genetic resulted significant antileukemic effects. Global...
ABSTRACT As an embryo matures into a fetus, cells undergo remarkable transitions, accompanied by shifts in transcription factor regulatory networks and chromatin landscapes. The mechanisms of these developmental transitions are not completely understood. embryonic intestine from rapidly proliferating tube with pseudostratified epithelium prior to day (E) 14.5, exquisitely folded columnar the fetus. We sought define factors that drive fetal maturation intestine. ATAC-seq profiling revealed...
Intestinal stem cell (ISC) function is regulated by diet and cellular metabolism; however, regulatory mechanisms controlling ISC metabolism are not fully understood. HNF4 transcription factors important regulators of metabolism, but their functions in ISCs elucidated. Here, we demonstrate that fatty acid oxidation (FAO) supports renewal, bind to activate the FAO gene program. Loss paralogs reduces instead increases synthesis. Compound mutant mice reveal redundantly promote renewal. loss...
Abstract T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematologic malignancy. Despite recent advances in treatments with intensified chemotherapy regimens, relapse rates and associated morbidities remain high. In this context, metabolic dependencies have emerged as a druggable opportunity for the treatment of leukemia. Here, we tested antileukemic effects MB1-47, newly developed mitochondrial uncoupling compound. MB1-47 T-ALL cells robustly inhibited cell proliferation via...
<div>Abstract<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss expression PTEN associated with the pathogenesis various cancers, including T-cell acute lymphoblastic leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts <i>PTEN</i> promoter multiple hematopoietic populations, T cells, and acts as hub transcription factors...
<div>Abstract<p>Long-range oncogenic enhancers play an important role in cancer. Yet, whether similar regulation of tumor suppressor genes is relevant remains unclear. Loss expression PTEN associated with the pathogenesis various cancers, including T-cell acute lymphoblastic leukemia (T-ALL). Here, we identify a highly conserved distal enhancer (PE) that interacts <i>PTEN</i> promoter multiple hematopoietic populations, T cells, and acts as hub transcription factors...
<div>Abstract<p>T-cell acute lymphoblastic leukemia (T-ALL) is a NOTCH1-driven disease in need of novel therapies. Here, we identify NOTCH1–SIRT1–KAT7 link as therapeutic vulnerability T-ALL, which the histone deacetylase SIRT1 overexpressed downstream NOTCH1-bound enhancer. loss impaired generation, whereas overexpression accelerated and conferred resistance to NOTCH1 inhibition deacetylase-dependent manner. Moreover, pharmacologic or genetic resulted significant antileukemic...
<p>Supplementary Figures S1-S7 and Legends</p>
<div>Abstract<p>T-cell acute lymphoblastic leukemia (T-ALL) is a NOTCH1-driven disease in need of novel therapies. Here, we identify NOTCH1–SIRT1–KAT7 link as therapeutic vulnerability T-ALL, which the histone deacetylase SIRT1 overexpressed downstream NOTCH1-bound enhancer. loss impaired generation, whereas overexpression accelerated and conferred resistance to NOTCH1 inhibition deacetylase-dependent manner. Moreover, pharmacologic or genetic resulted significant antileukemic...
<p>Supplementary Figures S1-S7 and Legends</p>
<p>Supplementary Figures and Tables combined</p>