A5087995616- Chronic Myeloid Leukemia Treatments
- Chronic Lymphocytic Leukemia Research
- Acute Myeloid Leukemia Research
- Lymphoma Diagnosis and Treatment
- Acute Lymphoblastic Leukemia research
- Hemoglobinopathies and Related Disorders
- Eosinophilic Disorders and Syndromes
- Diabetes Treatment and Management
- Erythrocyte Function and Pathophysiology
- T-cell and Retrovirus Studies
- Myeloproliferative Neoplasms: Diagnosis and Treatment
- Cancer-related Molecular Pathways
- Pharmacology and Obesity Treatment
- Protein Degradation and Inhibitors
- NF-κB Signaling Pathways
- Viral-associated cancers and disorders
- Ubiquitin and proteasome pathways
- PI3K/AKT/mTOR signaling in cancer
- Multiple Myeloma Research and Treatments
- Antiplatelet Therapy and Cardiovascular Diseases
- DNA and Nucleic Acid Chemistry
- Cytokine Signaling Pathways and Interactions
- Iron Metabolism and Disorders
- Pancreatitis Pathology and Treatment
- Multiple Sclerosis Research Studies
University of Turin
2009-2021
Ospedale San Luigi Gonzaga
1994-2021
University of Foggia
2003
Sapienza University of Rome
1994
Columbia University
1992
University of Perugia
1992
Ospedale Sant'Anna
1992
Istituto di Ematologia di Bologna
1990
Kaplan (United States)
1987
New York University
1987
Glucagon-like peptide 1 (GLP-1) is object of intensive investigation for not only its metabolic effects but also the protective vascular actions. Since platelets exert a primary role in pathogenesis atherosclerosis, inflammation and complications, we investigated whether GLP-1 directly influences platelet reactivity. For this purpose, from 72 healthy volunteers evaluated receptor (GLP-1R) expression 15-minute incubation with native form GLP-1(7-36), N-terminally truncated GLP-1(9-36)...
Chronic Lymphocytic Leukemia (CLL) is a lymphoproliferative disorder with either indolent or aggressive clinical course. Current treatment regiments have significantly improved the overall outcomes even if higher risk subgroups - those harboring TP53 mutations deletions of short arm chromosome 17 (del17p) remain highly challenging. In present work, we identified USP7, known de-ubiquitinase multiple roles in cellular homeostasis, as potential therapeutic target CLL. We demonstrated that...
The authors investigated the efficacy and safety of histone deacetylase inhibitors valproic acid (VPA) all-trans retinoic (ATRA) as differentiation agents in a cohort older, poor-risk patients with acute myeloid leukemia (AML) or myelodysplastic syndrome (MDS).Twenty older recurrent refractory AML MDS were treated Phase II protocol sequential VPA ATRA therapy. was started at dose 10 mg/kg per day then escalated to achieve serum concentration 45-100 microg/mL. added 45 mg/square meters (sm)...
The tumor suppressive function of PTEN is exerted within 2 different cellular compartments. In the cytosol-membrane, it negatively regulates PI3K-AKT pathway through de-phosphorylation phosphatidylinositol (3,4,5)-triphosphate (PIP3), therefore blocking one major signaling transduction pathways in tumorigenesis. nucleus, controls genomic stability and proliferation phosphatase independent mechanisms. Importantly, impairments compartmentalization, changes protein levels post-transductional...
Nuclear factor κB (NF‑κB) is an essential component of tumorigenesis and resistance to cancer treatments. NFKB inhibitor α (IκB‑α) acts as a negative regulator the classical NF‑κB pathway through its ability maintain presence in cytoplasm. However, IκB‑α also able form complex with tumor protein p53, promoting inactivation. Recently, we demonstrated that mediate p53 nuclear exclusion inactivation chronic myeloid leukemia, indicating can modulate either oncogenic or tumor‑suppressive...
The identification of cystic lesions within the retroperitoneal space is a rare event that poses clinicians challenge difficult diagnosis and disease management. Retroperitoneal account for group range from common benign (e.g., lymphoceles developing as surgical complication) to aggressive malignant neoplasms. Currently, in majority cases, image‑guided procedures allow pathological be achieved these challenging lesions, thus offering chance an appropriate treatment; however, overall clinical...
Abstract BACKGROUND The objective of this study was to evaluate the ability clinically available histone deacetylase (HDAC) inhibitor valproate enhance cytotoxicity Bcr‐Abl imatinib in imatinib‐resistant cell lines. METHODS Interactions between imatinib, and have been examined imatinib‐sensitive ‐resistant chronic myeloid leukemia (CML)cell lines (K562, KCL‐22, CML‐T1) bone marrow mononuclear cells (MNCs) derived from CML patients. RESULTS In lines, cotreatment with 0.5 μM 5 for 48 hours...
Abstract We have analyzed the type of MYC/IG heavy‐chain locus ( IGH ) rearrangement present in 15 patients affected by t(8; 14)‐positive primary Burkitt's lymphoma or acute lymphoblastic leukemia L3 an attempt to map detail locations chromosome 8 and 14 breakpoints. The almost constant position breakpoint (within immediately 5′ MYC gene) together with two distinct clusters breakpoints on resulted main types MYC/IGH (present 12 cases). In first (six cases), gene at least its coding portion...
Chronic myeloid leukemia (CML) is a myeloproliferative disorder characterized by the t(9;22) translocation coding for chimeric protein p210 BCR-ABL. The tumor suppressor PTEN plays critical role in pathogenesis of CML chronic phase, through non genomic loss function mechanisms, such as down-regulation and impaired nuclear/cytoplasmic shuttling. Here we demonstrate that BCR-ABL promotes downregulation MEK dependent pathway. Furthermore, describe novel not recurrent N212D-PTEN point mutation...
// Sabrina Crivellaro 1 , Cristina Panuzzo Giovanna Carrà Alessandro Volpengo Francesca Crasto Enrico Gottardi Ubaldo Familiari 2 Mauro Papotti Davide Torti Rocco Piazza 3 Sara Redaelli Riccardo Taulli 4 Angelo Guerrasio Giuseppe Saglio Morotti Department of Clinical and Biological Sciences, University Turin, Orbassano, Italy Division Pathology, Oncology, Turin at St Luigi Hospital, Torino, Health Milano-Bicocca, Monza, Correspondence to: Morotti, e-mail: alessandro.morotti@unito.it...
Abstract The development of drugs able to target BTK, PI3k‐delta and BCL2 has dramatically improved chronic lymphocytic leukaemia (CLL) therapies. However, drug resistance these therapies already been reported due non‐recurrent changes in oncogenic pathways genes expression signatures. In this study, we investigated the cooperative role inhibitor venetoclax BRD4 JQ1. particular, found that JQ1 shows additional activity with venetoclax, CLL cell lines ex vivo isolated primary CD19 +...