about
The Insulin/IGF System in Colorectal Cancer Development and Resistance to TherapyKnockout Serum Replacement Promotes Cell Survival by Preventing BIM from Inducing Mitochondrial Cytochrome C ReleaseMesenchymal Stem Cells (MSC) Regulate Activation of Granulocyte-Like Myeloid Derived Suppressor Cells (G-MDSC) in Chronic Myeloid Leukemia PatientsModelling of the ABL and ARG proteins predicts two functionally critical regions that are natively unfolded.Induction of apoptosis in chronic myelogenous leukemia cells through nuclear entrapment of BCR-ABL tyrosine kinase.Interplay between kinase domain autophosphorylation and F-actin binding domain in regulating imatinib sensitivity and nuclear import of BCR-ABL.Myeloid derived suppressor cells (MDSCs) are increased and exert immunosuppressive activity together with polymorphonuclear leukocytes (PMNs) in chronic myeloid leukemia patients.Charlson comorbidity index and adult comorbidity evaluation-27 scores might predict treatment compliance and development of pleural effusions in elderly patients with chronic myeloid leukemia treated with second-line dasatinib.Flow Cytometric Immunobead Assay for Detection of BCR-ABL1 Fusion Proteins in Chronic Myleoid Leukemia: Comparison with FISH and PCR TechniquesTargeting autophagy potentiates tyrosine kinase inhibitor-induced cell death in Philadelphia chromosome-positive cells, including primary CML stem cells.Frontline Dasatinib Treatment in a "Real-Life" Cohort of Patients Older than 65 Years with Chronic Myeloid Leukemia.Current management of CML patients: Summary of the Italian Consensus Meeting held in Rome, April 11-12, 2013.BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein.Biomarkers and prognostic factors for malignant pleural mesothelioma.Roles of Interferon Regulatory Factors in Chronic Myeloid Leukemia.Imatinib mesylate in chronic myeloid leukemia: frontline treatment and long-term outcomes.Biological effects of insulin and its analogs on cancer cells with different insulin family receptor expression.IRF5 is a target of BCR-ABL kinase activity and reduces CML cell proliferation.A population-based study of chronic myeloid leukemia patients treated with imatinib in first line.IRF5 promotes the proliferation of human thyroid cancer cells.New Insights in Thyroid Cancer and p53 Family Proteins.The BCR-ABL1 transcript type influences response and outcome in Philadelphia chromosome-positive chronic myeloid leukemia patients treated frontline with imatinib.Altered expression of c-IAP1, survivin, and Smac contributes to chemotherapy resistance in thyroid cancer cells.BCR-ABL nuclear entrapment kills human CML cells: ex vivo study on 35 patients with the combination of imatinib mesylate and leptomycin B.Discoidin domain receptor 1 modulates insulin receptor signaling and biological responses in breast cancer cells.Imatinib and polypharmacy in very old patients with chronic myeloid leukemia: effects on response rate, toxicity and outcome.Unsuccessful dasatinib therapy in a refractory patient with chronic lymphocytic leukemia.V gamma 9V delta 2 T lymphocytes efficiently recognize and kill zoledronate-sensitized, imatinib-sensitive, and imatinib-resistant chronic myelogenous leukemia cells.Infliximab therapy in hematologic malignancies: handle with care.Concomitant and feasible treatment with dasatinib and the anti-EGFR antibody cetuximab plus radiotherapy in a CML patient with multiple squamous neoplasias.Impact of BCR-ABL mutations on response to dasatinib after imatinib failure in elderly patients with chronic-phase chronic myeloid leukemia.Nuclear entrapment of BCR-ABL by combining imatinib mesylate with leptomycin B does not eliminate CD34+ chronic myeloid leukaemia cells.Targeting autophagy potentiates tyrosine kinaseinhibitor–induced cell death in Philadelphia chromosome–positivecells, including primary CML stem cells.High BCR-ABL/GUSIS Levels at Diagnosis of Chronic Phase CML Are Associated with Unfavorable Responses to Standard-Dose Imatinib.Non ABL-directed inhibitors as alternative treatment strategies for chronic myeloid leukemia.Predictive and Prognostic Value of Early Disease Progression by PET Evaluation in Advanced Non-Small Cell Lung Cancer.BRIT1/MCPH1 expression in chronic myeloid leukemia and its regulation of the G2/M checkpoint.Cancer stem cells and chemosensitivity.Personalized strategies for CML patients considering discontinuation of tyrosine kinase inhibitors treatment.Ground glass opacities management in the lung cancer screening era.
P50
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P50
description
researcher
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wetenschapper
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հետազոտող
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name
Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo VIGNERI
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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Paolo Vigneri
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P1053
K-8504-2016
P106
P1153
6602255102
P31
P496
0000-0002-5943-6066