A5031530382- Cytokine Signaling Pathways and Interactions
- Cancer Cells and Metastasis
- Angiogenesis and VEGF in Cancer
- interferon and immune responses
- Cellular Mechanics and Interactions
- Cancer, Hypoxia, and Metabolism
- Immune cells in cancer
- Neurogenesis and neuroplasticity mechanisms
- Telomeres, Telomerase, and Senescence
- Viral Infectious Diseases and Gene Expression in Insects
- Melanoma and MAPK Pathways
- Cancer Research and Treatments
- Cell death mechanisms and regulation
- Cancer Immunotherapy and Biomarkers
- Neuroinflammation and Neurodegeneration Mechanisms
- RNA regulation and disease
- Cancer Mechanisms and Therapy
- Metastasis and carcinoma case studies
- Lymphoma Diagnosis and Treatment
- Glioma Diagnosis and Treatment
- Chemokine receptors and signaling
- Phagocytosis and Immune Regulation
- Calpain Protease Function and Regulation
- Hedgehog Signaling Pathway Studies
- Mitochondrial Function and Pathology
Case Western Reserve University
2018-2024
Cleveland Clinic Lerner College of Medicine
2016-2024
University School
2019-2022
Cleveland Clinic
2014-2015
Italian Institute of Technology
2013
University of Verona
2010
University of Milan
2010
KU Leuven
2010
University of Würzburg
2010
Brescia University
2010
Glioblastoma is the most common and aggressive primary brain tumour. Standard of care consists surgical resection followed by radiotherapy concomitant maintenance temozolomide (temozolomide/radiotherapy→temozolomide). Corticosteroids are commonly used perioperatively to control cerebral oedema frequently continued throughout subsequent treatment, notably radiotherapy, for amelioration side effects. The effects corticosteroids such as dexamethasone on cell growth in glioma models patient...
// Xi Feng 1 , Frank Szulzewsky 2,* Alexan Yerevanian 1,3,* Zhihong Chen David Heinzmann 1,4 Rikke Darling Rasmussen Virginia Alvarez-Garcia Yeonghwan Kim 5 Bingcheng Wang 6 Ilaria Tamagno Hao Zhou 7 Xiaoxia Li Helmut Kettenmann 2 Richard M. Ransohoff 1,8 and Dolores Hambardzumyan Department of Neurosciences at Cleveland Clinic, Cleveland, Ohio, USA Cellular Neurosciences, Max Delbrück Center for Molecular Medicine, Berlin, Germany 3 Case Western Reserve University School 4 Cardiology...
To unravel the regulatory network underlying nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) -mediated lymphomagenesis of anaplastic large-cell (ALCL) and to discover diagnostic genomic classifiers for recognition patients with ALK-positive ALK-negative ALCL among T-cell non-Hodgkin's (T-NHL).The transcriptome NPM-ALK-positive cell lines was characterized by silencing expression ALK or STAT3, a major effector oncogenic activity. Gene profiling (GEP) performed in series systemic primary...
Highly aggressive, metastatic and therapeutically resistant triple-negative breast cancers (TNBCs) are often enriched for cancer stem cells (CSC). Cytokines within the tumor microenvironment (TME) influence CSC state by regulating cell differentiation programs. Two prevalent TME cytokines oncostatin-M (OSM) interferon-β (IFN-β). OSM is a member of IL-6 family can drive de-differentiation TNBC to highly aggressive state. Conversely, IFN-β induces TNBC, resulting in repression properties....
In response to neurodegeneration, the adult mammalian brain activates a cellular cascade that results in reactive astrogliosis and microgliosis. The mechanism through which astrocytes become physiological consequences of their activation neurodegeneration is complex. While proliferation has been shown occur during massive neuronal cell death, functional relationship between these two events not clearly elucidated. Here we show kainic acid‐ (KA) induced mitogen sonic hedgehog (SHH)...
Genomic instability is a hallmark of human cancer; yet the underlying mechanisms remain poorly understood. Here, we report that cytoplasmic unconventional Myosin X (MYO10) regulates genome stability, through which it mediates inflammation in cancer. MYO10 an unstable protein undergoes ubiquitin-conjugating enzyme H7 (UbcH7)/β-transducin repeat containing 1 (β-TrCP1)–dependent degradation. upregulated both and mouse tumors its expression level predisposes tumor progression response to immune...
The Journal of Cancer Metastasis and Treatment is an open access journal focused on cancer metastasis treatment, including the occurrence, development, progression, metastasis, treatment oncologic disease. It covers basic, translational clinical research related to cell biology, genomics, precision medicine, oncology internal radiotherapy radiology, obstetrics gynecology, pediatrics, surgery, hematology, neurooncology, etc.
Abstract Patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) frequently present advanced metastatic disease and exhibit a poor response to therapy, resulting in outcomes. The tumor microenvironment cytokine Oncostatin-M (OSM) initiates PDAC plasticity, inducing the reprogramming stem-like/mesenchymal state, which enhances metastasis therapy resistance. Using panel of cells driven through epithelial–mesenchymal transition (EMT) by OSM or transcription factors ZEB1 SNAI1, we find...
Glutamyl-prolyl-tRNA synthetase (EPRS1) is a bifunctional aminoacyl-tRNA-synthetase (aaRS) essential for decoding the genetic code. EPRS1 resides, with seven other aaRSs and three noncatalytic proteins, in cytoplasmic multi-tRNA complex (MSC). Multiple MSC-resident aaRSs, including EPRS1, exhibit stimulus-dependent release from MSC to perform noncanonical activities distinct their primary function protein synthesis. Here, we show present both cytoplasm nucleus of breast cancer cells...
Abstract Although frequently associated with tumor progression, inflammatory cytokines initially restrain transformation by inducing senescence, a key tumor-suppressive barrier. Here, we demonstrate that the cytokine, oncostatin M, activates mesenchymal/stem cell (SC) program engages cytokine-induced senescence (CIS) in normal human epithelial cells. CIS is driven Snail induction and requires cooperation between STAT3 TGFβ effector, SMAD3. Importantly, as cells escape CIS, they retain...
<p>Supplementary Figure Legends 1-6</p>
<p>S5. MEK inhibitors block OSM-driven conversion to a CD44HI/mesenchymal state.</p>
<p>S3. Generation of OSMR knock-out cells.</p>
<p>S1. OSM induces tumor initiation.</p>
<p>S2. Kaplan Meier comparison of IL-6 family member receptors.</p>