A5040021547- MicroRNA in disease regulation
- Cancer-related molecular mechanisms research
- RNA Interference and Gene Delivery
- Cancer-related Molecular Pathways
- Circular RNAs in diseases
- Liver Disease Diagnosis and Treatment
- Virus-based gene therapy research
- RNA modifications and cancer
- Pregnancy and preeclampsia studies
- Peroxisome Proliferator-Activated Receptors
- Graphene and Nanomaterials Applications
- Cholangiocarcinoma and Gallbladder Cancer Studies
- Enzyme Catalysis and Immobilization
- Nanoparticle-Based Drug Delivery
- Genetics and Neurodevelopmental Disorders
- Cancer, Stress, Anesthesia, and Immune Response
- Liver physiology and pathology
- Microbial Metabolic Engineering and Bioproduction
- CRISPR and Genetic Engineering
- Biomedical Ethics and Regulation
- Cell death mechanisms and regulation
- Cancer Research and Treatments
- Macrophage Migration Inhibitory Factor
- Adenosine and Purinergic Signaling
- Epigenetics and DNA Methylation
Harvard University
2020-2024
Boston VA Research Institute
2024
Broad Institute
2024
Hadassah Medical Center
2016-2022
Hebrew University of Jerusalem
2010-2013
Pancreatic ductal adenocarcinoma (PDA) represents an unmet therapeutic challenge. PDA is addicted to the activity of mutated KRAS oncogene which considered so far undruggable target. We propose approach target effectively in patients using RNA interference. To meet this challenge, we have developed a local prolonged siRNA delivery system (Local Drug EluteR, LODER) shedding against (siG12D LODER). The siG12D LODER was assessed for its structural, release, and properties vitro vivo. effect on...
The H19-derived microRNA-675 (miR-675) has been implicated as both tumor promoter and suppressor also plays a role in liver inflammation. We found that miR-675 promotes cell death human hepatocellular carcinoma (HCC) lines. show Fas-associated protein with domain (FADD), mediator of apoptotic signaling, is downregulated by negative correlation exists between FADD expression mouse models HCC (p = 0.014) well samples 0.017). demonstrate model inflammation overexpression necroptosis, which can...
The tumor suppressor p53 is a central regulator of signaling pathways that controls the cell cycle and maintains integrity human genome. level regulated by mouse double minute 2 homolog (Mdm2), which marks for proteasomal degradation. p53‐Mdm2 circuitry subjected to complex regulation variety mechanisms, including microRNAs (miRNAs). We found novel effector this regulatory circuit, namely, miR‐122*, passenger strand abundantly expressed liver‐specific miR‐122. Here, we demonstrate miR‐122*...
Glycogen storage disease type Ia (GSD-Ia), also known as von Gierke disease, is caused by a deficiency of glucose-6-phosphatase-alpha (G6Pase), key enzyme in glucose homeostasis. From birth, affected individuals cannot maintain normal blood levels and suffer from variety metabolic disorders, leading to life-threatening complications. Gene therapy has been proposed possible option for treatment this illness. Vectors have constructed feline immunodeficiency virus (FIV), nonprimate lentivirus,...
Lentiviral vectors are widely used in basic research and clinical applications for gene transfer long-term expression; however, safety issues have not yet been completely resolved. In this study, we characterized hepatocarcinomas that developed mice 1 year after utero administration of a feline-derived lentiviral vector. Mapped viral integration sites differed among tumors did coincide with the regions chromosomal aberrations. Furthermore, expression profiling revealed no known...
Abstract The Cancer Dependency Map aims to accelerate precision cancer medicine by identifying the landscape of vulnerabilities across all tumors. To address underrepresented types, we have optimized a genome-wide CRISPR KO screening pipeline, utilizing condensed Cas12a library, for patient-derived 3D models. Here, present characterization cohort ovarian models which consist subtypes along with treatment-resistant cancers. In particular, our organoid dataset includes low-grade serous...
The master regulator of the DNA damage response, transcription factor p53, orchestrates multiple downstream responses and coordinates repair processes. In response to double-strand breaks, p53 exhibits pulses expression, but how it achieves temporal coordination remains unclear. Here, we show that p53's posttranslational modification state is altered between its first second expression. We acetylations at two sites, K373 K382, were reduced in pulse, these differentially affected target...