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3. WT1 transcript amount discriminates secondary or reactive eosinophilia from idiopathic hypereosinophilic syndrome or chronic eosinophilic leukemia.

Author

Cilloni, D, Messa, F, Martinelli, G, Gottardi, E, Arruga, F, Defilippi, I, Carturan, S, Messa, E, Fava, M, Giugliano, E, Rosso, V, Catalano, R, Merante, S, Nicoli, P, Rondoni, M, Ottaviani, E, Soverini, S, Tiribelli, M, Pane, F, and Baccarani, M

Subjects
EOSINOPHILIA, EOSINOPHIL disorders, HEMATOPOIETIC stem cells, MYELOPROLIFERATIVE neoplasms, LEUKEMIA
Abstract

Idiopathic hypereosinophilic syndromes (HES) comprise a spectrum of indolent to aggressive diseases characterized by persistent hypereosinophilia. Hypereosinophilia can result from the presence of a defect in the hematopoietic stem cell giving rise to eosinophilia, it can be present in many myeloproliferative disorders or alternatively it may be a reactive form, secondary to many clinical conditions. The hybrid gene FIP1L1-PDGRFα was identified in a subset of patients presenting with HES or chronic eosinophilic leukemia (CEL). In spite of this, the majority of HES patients do not present detectable molecular lesions and for many of them the diagnosis is based on exclusion criteria and sometimes it remains doubt. In this study we explored the possibility to distinguish between HES/CEL and reactive hypereosinophilia based on WT1 transcript amount. For this purpose, 312 patients with hypereosinophilia were characterized at the molecular and cytogenetic level and analyzed for WT1 expression at diagnosis and during follow-up. This study clearly demonstrates that WT1 quantitative assessment allows to discriminate between HES/CEL and reactive eosinophilia and represents a useful tool for disease monitoring especially in the patients lacking a marker of clonality.Leukemia (2007) 21, 1442–1450; doi:10.1038/sj.leu.2404670; published online 17 May 2007 [ABSTRACT FROM AUTHOR]

Published
2007
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4. The NF-κB pathway blockade by the IKK inhibitor PS1145 can overcome Imatinib resistance.

Author

Cilloni, D., Messa, F., Arruga, F., Defilippi, I., Morotti, A., Messa, E., Carturan, S., Giugliano, E., Pautasso, M., Bracco, E., Rosso, V., Sen, A., Martinelli, G., Baccarani, M., and Saglio, G.

Subjects
IMATINIB, ANTINEOPLASTIC agents, LEUKEMIA, ANEMIA, CELL lines, CELL culture
Abstract

Imatinib represents at present the most attractive therapy for BCR-ABL positive leukemias, even though a percentage of CML patients develop resistance to this compound. For these resistant patients a therapeutic approach based on a combination of drugs is more likely to be effective. In the last years, constitutive NF-κB/Rel activity has been demonstrated in several hematological malignancies. As a result, NFkB/Rel-blocking approaches have been proposed as antineoplastic strategies. Furthermore, the identification of specific kinases within the NF-κB activation pathway offers a selective target to address tailored therapies. In the current study, we show that the IKK inhibitor PS1145 is able to inhibit the proliferation of CML cell lines and primary BM cells. Moreover, the addition of Imatinib increases the effects of PS1145 in resistant cell lines and BM cells from resistant patients, with a further increase of apoptosis and inhibition of proliferation and colony growth. Our data provide the rational for a new therapeutic approach, which combines Imatinib and the IKK inhibitor PS1145 in CML resistant patients.Leukemia (2006) 20, 61–67. doi:10.1038/sj.leu.2403998; published online 3 November 2005 [ABSTRACT FROM AUTHOR]

Published
2006
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5. Imatinib and pegylated human recombinant interferon-alpha2b in early chronic-phase chronic myeloid leukemia

Author

Baccarani, Michele, Martinelli, Giovanni, Rosti, Gianantonio, Trabacchi, Elena, Testoni, Nicoletta, Bassi, Simona, Amabile, Marilina, Soverini, Simona, Castagnetti, Fausto, Cilloni, Daniela, Izzo, Barbara, De Vivo, Antonio, Messa, Emanuela, Bonifazi, Francesca, Poerio, Angela, Luatti, Simona, Giugliano, Emilia, Alberti, Daniele, Fincato, Gianluca, Russo, Domenico, Pane, Fabrizio, Saglio, Giuseppe, GIMEMA CML Working Party, Bocchia, Monica, Baccarani, M, Martinelli, G, Rosti, G, Trabacchi, E, Testoni, N, Bassi, S, Amabile, M, Soverini, S, Castagnetti, F, Cilloni, D, Izzo, Barbara, DE VIVO, A, Messa, E, Bonifazi, F, Poerio, A, Luatti, S, Giugliano, E, Alberti, D, Fincato, G, Russo, D, Pane, Fabrizio, Saglio, G, GIMEMA WORKING PARTY ON CHRONIC MYELOID, L. E. U. K. E. M. I. A., BACCARANI M., MARTINELLI G., ROSTI G., TRABACCHI E., TESTONI N., BASSI S., AMABILE M., SOVERINI S., CASTAGNETTI F., CILLONI D., IZZO B., DE VIVO A., MESSA E., BONIFAZI F., POERIO A., LUATTI S., GIUGLIANO E., ALBERTI D., FINCATO G., RUSSO D., PANE F., SAGLIO G., and GIMEMA WORKING PARTY ON CHRONIC MYELOID LEUKEMIA

Subjects
Male, PHILADELPHIA-CHROMOSOME, Biochemistry, Gastroenterology, Piperazines, hemic and lymphatic diseases, Antineoplastic Combined Chemotherapy Protocols, Chronic, BCR-ABL, Leukemia, CLINICAL RESISTANCE, CHRONIC MYELOGENOUS LEUKEMIA, Myeloid leukemia, TYROSINE KINASE INHIBITOR, ABL-POSITIVE CELLS, SEQUENCE BINDING-PROTEIN, FUSION GENE TRANSCRIPTS, CYTOGENETIC RESPONSES, ANTILEUKEMIC AGENTS, Hematology, Middle Aged, Recombinant Proteins, Toxicity, Benzamides, Imatinib Mesylate, Female, Drug, medicine.drug, Adult, medicine.medical_specialty, Immunology, Alpha interferon, Interferon alpha-2, Dose-Response Relationship, chronic myeloid leukemia, Aged, Dose-Response Relationship, Drug, Humans, Interferon-alpha, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Pyrimidines, Internal medicine, medicine, Adverse effect, business.industry, Imatinib, Cell Biology, medicine.disease, Imatinib mesylate, imatinib, BCR-ABL Positive, recombinant alpha2b interferon, business, Chronic myelogenous leukemia, Myelogenous
Abstract

Since interferon-α and imatinib (IM; STI571, Glivec, Gleevec) are effective for the treatment of chronic myeloid leukemia (CML), and their mechanisms of action are different, we designed an exploratory study investigating the effects of a standard IM dose (400 mg/d) and a variable pegylated interferon-α (PegIFN) dose (50 μg/wk, 100 μg/wk, and 150 μg/wk). The criteria for dose adjustment were designed so as to ensure the delivery of the IM dose and to protect life quality. There were 76 patients with previously untreated Philadelphia (Ph)–positive CML enrolled in the study. There were 3 patients who discontinued IM and 45 patients who discontinued PegIFN. The severity of adverse events increased with increasing PegIFN dose. The IM dose could be administered to the patients who were assigned to receive 50 μg/wk or 100 μg/wk PegIFN but not to those who were assigned to receive 150 μg/wk. The median administered dose of PegIFN ranged between 32 μg/wk and 36 μg/wk. The cytogenetic response was 70% complete (Ph-neg 100%) and 83% major (Ph-neg > 65%). The BCR/ABL transcript was reduced by at least 3 logs in 68% of complete cytogenetic responders. These data of toxicity, compliance, and efficacy may assist in the design and preparation of prospective studies.

Published
2004

6. Increase sensitivity to chemotherapeutical agents and cytoplasmatic interaction between NPM leukemic mutant and NF-kappaB in AML carrying NPM1 mutations

Author

Ilaria Iacobucci, Ilaria Defilippi, Alessandro Morotti, Paolo Nicoli, Francesca Messa, Enrico Bracco, Francesca Arruga, Giuseppe Saglio, Sonia Carturan, Valentina Rosso, Daniela Cilloni, Renata Catalano, Cristina Panuzzo, Emanuela Messa, Marisa Pautasso, Giovanni Martinelli, Cilloni D, Messa F, Rosso V, Arruga F, Defilippi I, Carturan S, Catalano R, Pautasso M, Panuzzo C, Nicoli P, Messa E, Morotti A, Iacobucci I, Martinelli G, Bracco E, and Saglio G.

Subjects
Cancer Research, medicine.medical_specialty, NPM1, Antimetabolites, Antineoplastic, Cytoplasm, Myeloid, NPM, Blotting, Western, Fluorescent Antibody Technique, Apoptosis, Electrophoretic Mobility Shift Assay, medicine.disease_cause, Bone Marrow, Internal medicine, Tumor Cells, Cultured, Medicine, Humans, Immunoprecipitation, Etoposide, Cell Nucleus, Nucleophosmin, Acute leukemia, Mutation, Hematology, Antibiotics, Antineoplastic, business.industry, Gene Expression Regulation, Leukemic, Daunorubicin, Cytarabine, NF-kappa B, Myeloid leukemia, Nuclear Proteins, medicine.disease, Flow Cytometry, Antineoplastic Agents, Phytogenic, Leukemia, Leukemia, Myeloid, Acute, medicine.anatomical_structure, Oncology, Cancer research, ACUTE MYELOID LEUKEMIA, business
Abstract

Mutations in nucleophosmin (NPM) exon 12 and the resulting delocalization of NPM into the cytoplasm are the most specific and frequent cellular events in acute myeloid leukemia patients (AML) with normal karyotype. Cytoplasmatic NPM (NPMc+) is associated with responsiveness to chemotherapy and better prognosis. The activation of nuclear factor-kappaB (NF-kappaB) has been demonstrated to occur in a subset of AML patients and is thought to induce resistance to many chemotherapeutical agents. In this study, we demonstrate the increased in vitro sensitivity of NPMc+ cells to chemotherapeutical agents and their reduced NF-kappaB activity. Furthermore, we provide evidence of the interaction between NPMc+ and NF-kappaB in the cytoplasm, resulting in the sequestration and inactivation of NF-kappaB. The cytosolic localization and consequent inactivation of NF-kappaB justifies the reduced NF-kappaB DNA-binding activity observed in NPMc+ patients. These data, taken together, may provide a possible explanation for the increased rate of chemosensitivity observed among the NPMc+ patients.

Published
2008

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