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Chronic Myeloid Leukemia and Hepatoblastoma: Two Cancer Models to Link Metabolism to Stem CellsOne more stem cell niche: how the sensitivity of chronic myeloid leukemia cells to imatinib mesylate is modulated within a "hypoxic" environment.TNF-alpha-converting enzyme cleaves the macrophage colony-stimulating factor receptor in macrophages undergoing activation.Hypoxia selects bortezomib-resistant stem cells of chronic myeloid leukemia.Chromatin-associated CSF-1R binds to the promoter of proliferation-related genes in breast cancer cells.The colony-stimulating factor-1 (CSF-1) receptor sustains ERK1/2 activation and proliferation in breast cancer cell lines.The metabolically-modulated stem cell niche: a dynamic scenario regulating cancer cell phenotype and resistance to therapy.The Culture-Repopulating Ability assays and incubation in low oxygen: a simple way to test drugs on leukaemia stem or progenitor cells.Hypoxia-resistant profile implies vulnerability of cancer stem cells to physiological agents, which suggests new therapeutic targets.Different BCR/Abl protein suppression patterns as a converging trait of chronic myeloid leukemia cell adaptation to energy restriction.The complex metabolic network gearing the G1/S transition in leukemic stem cells: Hints to a rational use of antineoplastic agents.Lipid rafts: integrated platforms for vascular organization offering therapeutic opportunities.Mitogen-activated protein kinases and Hedgehog-GLI signaling in cancer: A crosstalk providing therapeutic opportunities?Low-dose methotrexate enhances cycling of highly anaplastic cancer cells.Salarin C inhibits the maintenance of chronic myeloid leukemia progenitor cells.Prostaglandin E2 transactivates the colony-stimulating factor-1 receptor and synergizes with colony-stimulating factor-1 in the induction of macrophage migration via the mitogen-activated protein kinase ERK1/2.Hypoxia up-regulates SERPINB3 through HIF-2α in human liver cancer cells.The involvement of a Nanog, Klf4 and c-Myc transcriptional circuitry in the intertwining between neoplastic progression and reprogramming.ERK5/BMK1 is indispensable for optimal colony-stimulating factor 1 (CSF-1)-induced proliferation in macrophages in a Src-dependent fashion.Selective anti-leukaemic activity of low-dose histone deacetylase inhibitor ITF2357 on AML1/ETO-positive cells.Severe hypoxia defines heterogeneity and selects highly immature progenitors within clonal erythroleukemia cells.Butyrates, as a single drug, induce histone acetylation and granulocytic maturation: possible selectivity on core binding factor-acute myeloid leukemia blasts.Tryptophan availability selectively limits NO-synthase induction in macrophages.Opposite effects of different doses of MCSF on ERK phosphorylation and cell proliferation in macrophages.Constitutive activation of the MAPK pathway mediates v-fes-induced mitogenesis in murine macrophages.The low-molecular-weight phosphotyrosine protein phosphatase, when overexpressed, reduces the mitogenic response to macrophage colony-stimulating factor and tyrosine phosphorylation of its receptor.Interleukin-4 rapidly down-modulates the macrophage colony-stimulating factor receptor in murine macrophages.Fibronectin induces macrophage migration through a SFK-FAK/CSF-1R pathway.Targeting chronic myeloid leukemia stem cells with the hypoxia-inducible factor inhibitor acriflavine.The Leukemic Stem Cell Niche: Adaptation to "Hypoxia" versus Oncogene Addiction.ERK5 is activated by oncogenic BRAF and promotes melanoma growth.The mitogen-activated protein kinase ERK5 regulates the development and growth of hepatocellular carcinoma.Possible mechanisms and function of nuclear trafficking of the colony-stimulating factor-1 receptor.Targeting the Extracellular Signal-Regulated Kinase 5 Pathway to Suppress Human Chronic Myeloid Leukemia Stem CellsINTERLEUKIN 2 DOWN-MODULATES THE MACROPHAGE COLONY-STIMULATING FACTOR RECEPTOR IN MURINE MACROPHAGESERK5 differentially regulates PDGF-induced proliferation and migration of hepatic stellate cellsImpact of ERK5 on the Hallmarks of CancerIncubation of murine bone marrow cells in hypoxia ensures the maintenance of marrow-repopulating ability together with the expansion of committed progenitorsThe expansion of murine bone marrow cells preincubated in hypoxia as an in vitro indicator of their marrow-repopulating abilityp38 and cancer: Yang gets Yin
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onderzoeker
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հետազոտող
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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Elisabetta Rovida
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7004469551
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0000-0002-5949-3239