A5057167861- Glioma Diagnosis and Treatment
- Brain Metastases and Treatment
- RNA regulation and disease
- Tuberous Sclerosis Complex Research
- Intracerebral and Subarachnoid Hemorrhage Research
- Venous Thromboembolism Diagnosis and Management
- Cancer-related molecular mechanisms research
- Advanced MRI Techniques and Applications
- RNA Research and Splicing
- MicroRNA in disease regulation
- CRISPR and Genetic Engineering
- Neurofibromatosis and Schwannoma Cases
- Meningioma and schwannoma management
- Circular RNAs in diseases
- PI3K/AKT/mTOR signaling in cancer
- Medical Imaging Techniques and Applications
- Acute Ischemic Stroke Management
- Lung Cancer Research Studies
- Acute Myeloid Leukemia Research
- Cancer Treatment and Pharmacology
- Metabolomics and Mass Spectrometry Studies
- Renal and related cancers
- Lanthanide and Transition Metal Complexes
- Bone Tumor Diagnosis and Treatments
- RNA modifications and cancer
Harvard University
2016-2025
Beth Israel Deaconess Medical Center
2016-2025
Athinoula A. Martinos Center for Biomedical Imaging
2024
Brigham and Women's Hospital
2010-2024
Center for Neuro-Oncology
2012-2024
Dana-Farber Cancer Institute
2010-2024
Massachusetts General Hospital
2010-2024
Hadassah Medical Center
2023-2024
Beth Israel Deaconess Hospital
2020-2023
Washington University in St. Louis
2001-2023
Abstract Glioblastoma (GBM) is an incurable primary malignant brain cancer hallmarked with a substantial protumorigenic immune component. Knowledge of the GBM microenvironment during tumor evolution and standard care treatments limited. Using single-cell transcriptomics flow cytometry, we unveiled large-scale comprehensive longitudinal changes in cell composition throughout progression epidermal growth factor receptor-driven genetic mouse model. We identified subsets proinflammatory...
The adenovirus type 2/5 E1A proteins transform primary baby rat kidney (BRK) cells in cooperation with the activated Ras (T24 ras) oncoprotein. N-terminal half of (exon 1) is essential for this transformation activity. While C-terminal 2) dispensable, a region located between residues 225 and 238 243R protein negatively modulates vitro T24 ras cooperative as well tumorigenic potential E1A/T24 ras-transformed cells. same domain also required binding cellular 48-kDa phosphoprotein, (CtBP). We...
Abstract Persons affected with tuberous sclerosis complex (TSC) develop a wide range of neurological abnormalities including aberrant neuronal migration and seizures. In an effort to model TSC‐associated central nervous system in mice, we generated two independent lines astrocyte‐specific Tsc1 conditional knockout mice by using the Cre‐LoxP system. Astrocyte‐specific ‐null exhibit electroencephalographically proven seizures after first month age begin die at 3 4 months. show significant...
Abstract Somatic mutations of PTEN are found in many types cancers including glioblastoma, the most malignant astrocytic tumor. mutation occurs 25 to 40% glioblastomas but is rarely observed low-grade glial neoplasms. To determine role Pten astrocytes and tumor formation, we inactivated by a Cre-loxP approach with GFAP-cre transgenic mouse that induced Cre-mediated recombination astrocytes. conditional knockout mice showed striking progressive enlargement entire brain. Increased nuclear soma...
Abstract Excessive astrocytosis in cortical tubers tuberous sclerosis complex (TSC) suggests that astrocytes may be important for epileptogenesis TSC. We previously demonstrated astrocyte‐specific Tsc1 gene inactivation mice ( cKO mice) results progressive epilepsy. Here, we report glutamate transporter expression and function is impaired astrocytes. exhibit decreased GLT‐1 GLAST protein expression. Electrophysiological assays demonstrate a functional decrease transport currents of...
Research Article10 February 2016Open Access Source DataTransparent process Therapeutic potential of targeting microRNA-10b in established intracranial glioblastoma: first steps toward the clinic Nadiya M Teplyuk Department Neurology, Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Search more papers by this author Erik J Uhlmann Galina Gabriely Natalia Volfovsky Simons Foundation, New York, NY, Yang Wang Jian Teng Massachusetts...
Glioblastoma (GBM) brain tumor remains among the most lethal and incurable human diseases. Oncogenic microRNA-10b (miR-10b) is strongly universally upregulated in GBM, its inhibition by antisense oligonucleotides (ASOs) reduces growth of heterogeneous glioma cells; therefore, miR-10b represents a unique therapeutic target for GBM. Here we explored effects gene editing on Using clustered regularly interspaced short palindromic repeats (CRISPR)-Cas9 system, investigated cultured cells,...
Summary: Purpose: Individuals with tuberous sclerosis complex (TSC) frequently have intractable epilepsy. To gain insights into mechanisms of epileptogenesis in TSC, we previously developed a mouse model TSC conditional inactivation the Tsc1 gene glia ( GFAP CKO mice). These mice develop progressive seizures, suggesting that glial dysfunction may be involved TSC. Here, investigated hypothesis impairment potassium uptake through astrocyte inward rectifier (Kir) channels contribute to mice....
Using in silico analysis of The Cancer Genome Atlas (TCGA), we identified microRNAs associated with glioblastoma (GBM) survival, and predicted their functions glioma growth progression. Inhibition two "risky" miRNAs, miR-148a miR-31, orthotopic xenograft GBM mouse models suppressed tumor thereby prolonged animal survival. Intracranial tumors treated uncomplexed miR-31 antagomirs exhibited reduced proliferation, stem cell depletion, normalized vasculature. Growth-promoting these miRNAs were,...
Glioblastoma (GBM) may arise from astrocytes through a multistep process involving progressive accumulation of mutations. We explored whether GBM-derived extracellular vesicles (EVs) facilitate neoplastic transformation and malignant growth astrocytes. utilized conditioned media (CM) cultured glioma cells, its sequential filtration, diverse cell-based assays, RNA sequencing, metabolic assays to compare the effects EV-containing EV-depleted CM. GBM EVs facilitated pre-transformed but not...
Rheb GTPases represent a unique family of the Ras superfamily G-proteins. Studies on in Schizosaccharomyces pombe and Drosophila have shown that this small GTPase is essential involved cell growth cycle progression. The studies also raised possibility TOR/S6K signaling pathway. In paper, we first report identification dominant negative mutants S. (SpRheb). Screens randomly mutagenized SpRheb library yielded mutant, SpRhebD60V, whose expression results inhibition, G1 arrest, induction fnx1+,...
BACKGROUND: Febrile nonhemolytic transfusion reaction (FNHTR) has been identified as a pivotal reason for prestorage universal WBC reduction. A regional blood center implemented reduction RBCs on January 1, 2000. Whether of RBC units will affect FNHTR is not known. STUDY DESIGN AND METHODS: All reports reactions at Barnes‐Jewish Hospital submitted evaluation to the bank, before and after implementation RBCs, were retrospectively evaluated. RESULTS: For 36,303 allogeneic transfusions...
// Nadiya M. Teplyuk 1 , Erik J. Uhlmann Andus Hon-Kit Wong Priya Karmali 2 Meenakshi Basu Galina Gabriely Anant Jain Yang Wang E. Antonio Chiocca 3 Robert Stephens 4 Eric Marcusson Ming Yi Anna Krichevsky Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA Regulus Therapeutics, Inc., San Diego, CA, Neurosurgery, Cancer Research Technology Program, Frederick National Laboratory for Research, Leidos Biomedical Frederick, MD, Correspondence to:...
Abstract Individuals with tuberous sclerosis complex (TSC) develop central nervous system abnormalities that may reflect astrocyte dysfunction. In an effort to model dysfunction in TSC, we generated mice lacking Tsc1 (hamartin) expression astrocytes and demonstrated ‐null exhibit contact inhibition growth arrest. this study, demonstrate hamartin‐deficient are also defective cell size regulation. We show the increase is associated increased activation of S6‐kinase pathway. keeping recent...
Background Hyperhemolysis syndrome is a serious transfusion reaction mostly reported in association with sickle cell disease, characterized by destruction of both donor and host red blood cells ( RBCs ) an unknown mechanism. Case Report A 21‐year‐old man disease multiple prior transfusions received two phenotype‐matched, compatible RBC units during brief admission for pain crisis. He developed rapid‐onset progressive anemia hemoglobinuria. Methylprednisolone, erythropoietin, rituximab were...