6 results on '"Conticello C"'
Search Results
2. High-density neutrophils in MGUS and multiple myeloma are dysfunctional and immune-suppressive due to increased STAT3 downstream signaling.
- Author
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Romano A, Parrinello NL, Simeon V, Puglisi F, La Cava P, Bellofiore C, Giallongo C, Camiolo G, D'Auria F, Grieco V, Larocca F, Barbato A, Cambria D, La Spina E, Tibullo D, Palumbo GA, Conticello C, Musto P, and Di Raimondo F
- Subjects
- Aged, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Case-Control Studies, Disease Progression, Female, Follow-Up Studies, Gene Expression Profiling, Gene Expression Regulation, Neoplastic immunology, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Monoclonal Gammopathy of Undetermined Significance drug therapy, Monoclonal Gammopathy of Undetermined Significance genetics, Monoclonal Gammopathy of Undetermined Significance mortality, Multiple Myeloma drug therapy, Multiple Myeloma genetics, Multiple Myeloma mortality, Neutrophils metabolism, Phagocytosis genetics, Phagocytosis immunology, Signal Transduction genetics, Tumor Escape genetics, Disease Susceptibility immunology, Monoclonal Gammopathy of Undetermined Significance immunology, Multiple Myeloma immunology, Neutrophils immunology, STAT3 Transcription Factor metabolism, Signal Transduction immunology
- Abstract
To understand neutrophil impairment in the progression from MGUS through active MM, we investigated the function of mature, high-density neutrophils (HDNs), isolated from peripheral blood. In 7 MM, 3 MGUS and 3 healthy subjects by gene expression profile, we identified a total of 551 upregulated and 343 downregulated genes in MM-HDN, involved in chemokine signaling pathway and FC-gamma receptor mediated phagocytosis conveying in the activation of STAT proteins. In a series of 60 newly diagnosed MM and 30 MGUS patients, by flow-cytometry we found that HDN from MM, and to a lesser extend MGUS, had an up-regulation of the inducible FcγRI (also known as CD64) and a down-regulation of the constitutive FcγRIIIa (also known as CD16) together with a reduced phagocytic activity and oxidative burst, associated to increased immune-suppression that could be reverted by arginase inhibitors in co-culture with lymphocytes. In 43 consecutive newly-diagnosed MM patients, who received first-line treatment based on bortezomib, thalidomide and dexamethasone, high CD64 could identify at diagnosis patients with inferior median overall survival (39.5 versus 86.7 months, p = 0.04). Thus, HDNs are significantly different among healthy, MGUS and MM subjects. In both MGUS and MM neutrophils may play a role in supporting both the increased susceptibility to infection and the immunological dysfunction that leads to tumor progression.
- Published
- 2020
- Full Text
- View/download PDF
3. The Notch2-Jagged1 interaction mediates stem cell factor signaling in erythropoiesis.
- Author
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Zeuner A, Francescangeli F, Signore M, Venneri MA, Pedini F, Felli N, Pagliuca A, Conticello C, and De Maria R
- Subjects
- Antigens, CD34 metabolism, Basic Helix-Loop-Helix Transcription Factors metabolism, Cell Differentiation, Cell Proliferation, Cells, Cultured, Erythroblasts cytology, Erythroblasts metabolism, GATA2 Transcription Factor metabolism, Homeodomain Proteins metabolism, Humans, Jagged-1 Protein, Receptor, Notch2 genetics, Serrate-Jagged Proteins, Signal Transduction, Transcription Factor HES-1, Calcium-Binding Proteins metabolism, Intercellular Signaling Peptides and Proteins metabolism, Membrane Proteins metabolism, Receptor, Notch2 metabolism, Stem Cell Factor metabolism
- Abstract
Stem cell factor (SCF), the ligand for the c-kit receptor, is essential for the production of red blood cells during development and stress erythropoiesis. SCF promotes erythroblast proliferation and survival, while delaying erythroid differentiation through mechanisms that are largely unknown. In cultures of primary human differentiating erythroblasts, we found that SCF induces an increase in the expression of Notch2, a member of the Notch family implicated in the control of cell growth and differentiation. Functional inhibition of either Notch or its ligand Jagged1 inhibited the effects of SCF on erythroid cell expansion. SCF also induced the expression of Hes-1 and GATA-2, which may contribute to transduce Notch2 signals in response to SCF. Transduction of primary erythroid precursors with a dominant-negative Notch2 mutant inhibited both basal and SCF-mediated erythroblast expansion, and counteracted the effects of SCF on erythroblast differentiation. These findings provide a clue to understand the effects of increased proliferation and delayed differentiation elicited by SCF on the erythroid compartment and indicate Notch2 as a new player in the regulation of red cell differentiation.
- Published
- 2011
- Full Text
- View/download PDF
4. Identification and expansion of the tumorigenic lung cancer stem cell population.
- Author
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Eramo A, Lotti F, Sette G, Pilozzi E, Biffoni M, Di Virgilio A, Conticello C, Ruco L, Peschle C, and De Maria R
- Subjects
- AC133 Antigen, Animals, Antigens, CD metabolism, Carcinoma, Non-Small-Cell Lung metabolism, Carcinoma, Small Cell metabolism, Cell Differentiation, Drug Resistance, Neoplasm, Female, Glycoproteins metabolism, Humans, Lung Neoplasms drug therapy, Lung Neoplasms metabolism, Mice, Mice, SCID, Neoplastic Stem Cells metabolism, Peptides metabolism, Phenotype, Tumor Cells, Cultured, Xenograft Model Antitumor Assays, Carcinoma, Non-Small-Cell Lung pathology, Carcinoma, Small Cell pathology, Lung Neoplasms pathology, Neoplastic Stem Cells pathology
- Abstract
Lung carcinoma is often incurable and remains the leading cancer killer in both men and women. Recent evidence indicates that tumors contain a small population of cancer stem cells that are responsible for tumor maintenance and spreading. The identification of the tumorigenic population that sustains lung cancer may contribute significantly to the development of effective therapies. Here, we found that the tumorigenic cells in small cell and non-small cell lung cancer are a rare population of undifferentiated cells expressing CD133, an antigen present in the cell membrane of normal and cancer-primitive cells of the hematopoietic, neural, endothelial and epithelial lineages. Lung cancer CD133(+) cells were able to grow indefinitely as tumor spheres in serum-free medium containing epidermal growth factor and basic fibroblast growth factor. The injection of 10(4) lung cancer CD133(+) cells in immunocompromised mice readily generated tumor xenografts phenotypically identical to the original tumor. Upon differentiation, lung cancer CD133(+) cells acquired the specific lineage markers, while loosing the tumorigenic potential together with CD133 expression. Thus, lung cancer contains a rare population of CD133(+) cancer stem-like cells able to self-renew and generates an unlimited progeny of non-tumorigenic cells. Molecular and functional characterization of such a tumorigenic population may provide valuable information to be exploited in the clinical setting.
- Published
- 2008
- Full Text
- View/download PDF
5. Involvement of interferon regulatory factor-1 in monocyte CD95 expression and CD95-mediated apoptosis.
- Author
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Conte E, Manzella L, Zeuner A, Cocchiaro G, Conticello C, Zammataro L, Messina CG, De Maria R, and Messina A
- Subjects
- Apoptosis drug effects, DNA-Binding Proteins genetics, Gene Expression, Humans, Interferon Regulatory Factor-1, Interferon-gamma pharmacology, Monocytes cytology, Monocytes drug effects, Oligonucleotides, Antisense pharmacology, Phosphoproteins genetics, Time Factors, U937 Cells, fas Receptor metabolism, Apoptosis genetics, DNA-Binding Proteins metabolism, Monocytes metabolism, Phosphoproteins metabolism, fas Receptor genetics
- Published
- 2003
- Full Text
- View/download PDF
6. Death in 2000 ways.
- Author
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Zeuner A, Ricci-Vitiani L, Conticello C, and De Maria R
- Subjects
- Animals, Apoptosis Regulatory Proteins, Humans, Models, Biological, Signal Transduction physiology, TNF-Related Apoptosis-Inducing Ligand, Apoptosis physiology, Caspases metabolism, Membrane Glycoproteins metabolism, Mitochondria physiology, Tumor Necrosis Factor-alpha metabolism
- Published
- 2000
- Full Text
- View/download PDF
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