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11 results on '"Martinoglio, B."'

2. Analysis of miRNAs and their correlation with early malignat melanoma (MM)

Author

Occelli, M., primary, Nigro, L.o., additional, Vivenza, D., additional, Cauchi, C., additional, Sciancalepore, G., additional, Rovera, M., additional, Silvia, V., additional, Varamo, C., additional, Martinoglio, B., additional, Seia, Z., additional, Bosio, P., additional, Errico, F., additional, Lavagna, F., additional, Forte, G., additional, Palazzini, S., additional, Quaranta, L., additional, Basso, D., additional, Gervasio, S., additional, and Merlano, M.C., additional

Published
2017
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3. Anaplastic lymphoma kinase in human cancer

Author

Barreca, A., Lasorsa, E., Riera, L., Machiorlatti, R., Piva, R., Ponzoni, M., Kwee, I., Bertoni, F., Piccaluga, P.P., Pileri, S.A., Inghirami, G.C.B.A., Chiarle, R., Cuccuru, G., Inghirami, G., Martinoglio, B., Medico, E., Pellegrino, E., Ruberto, M.L., Voena, C., Fornari, A., Novero, D., Chilosi, M., Zamó, A., Facchetti, F., Lonardi, S., De Chiara, A., Fulciniti, F., Doglioni, C., Agnelli, L., Neri, A., Todoerti, K., Pileri, S., Falini, B., Tiacci, E., Van Loo, P., Tousseyn, T., De Wolf-Peeters, C., Geissinger, E., Muller-Hermelink, H.K., Rosenwald, A., Piris, M.A., Maria, E.R., Barreca A, Lasorsa E, Riera L, Machiorlatti R, Piva R, Ponzoni M, Kwee I, Bertoni F, Piccaluga PP, Pileri SA, Inghirami G, and the European T-Cell Lymphoma Study Group, Barreca, A, Lasorsa, E, Riera, L, Machiorlatti, R, Piva, R, Ponzoni, Maurilio, Kwee, I, Bertoni, F, Piccaluga, Pp, Pileri, Sa, and Inghirami, G.

Subjects
Transcriptional Activation, Lymphoma, kinase, Settore MED/06 - Oncologia Medica, Pyridines, Receptor Protein-Tyrosine Kinases, Antineoplastic Agents, Receptor tyrosine kinase, Translocation, Genetic, CSK Tyrosine-Protein Kinase, Proto-Oncogene Proteins p21(ras), Phosphatidylinositol 3-Kinases, Endocrinology, Crizotinib, Piperidines, Neoplasms, Proto-Oncogene Proteins, hemic and lymphatic diseases, medicine, cancer, Anaplastic lymphoma kinase, Humans, Anaplastic Lymphoma Kinase, anaplastic lymphoma, Molecular Biology, Anaplastic large-cell lymphoma, Nucleophosmin, biology, Phospholipase C gamma, ALK, Intracellular Signaling Peptides and Proteins, Protein-Tyrosine Kinases, medicine.disease, BCL10, Up-Regulation, src-Family Kinases, Mutation, Cancer research, biology.protein, Pyrazoles, Signal transduction, medicine.drug, Signal Transduction
Abstract

The receptor tyrosine kinases (RTKs) play a critical role, controlling cell proliferation, survival, and differentiation of normal cells. Their pivotal function has been firmly established in the pathogenesis of many cancers as well. The anaplastic lymphoma kinase (ALK), a transmembrane RTK, originally identified in the nucleophosmin (NPM)–ALK chimera of anaplastic large cell lymphoma, has emerged as a novel tumorigenic player in several human cancers. In this review, we describe the expression of the ALK–RTK, its related fusion proteins, and their molecular mechanisms of activation. Novel tailored strategies are briefly illustrated for the treatment of ALK-positive neoplasms.

Published
2011

4. Molecular anatomy of peripheral T cell lymphomas

Author

Pellegrino, Elisa, Agnelli, L, Todoerti, K, Fornari, A, Novero, D, Cuccuru, G, Ferreri, C, Martinoglio, B, Medico, Enzo, Zamò, A, Facchetti, F, De Chiara, A, Ponzoni, M, Rosenwald, A, Müller Hermelink HK, De Wolf Peeters, C, Piccaluga, Pp, Pileri, S, Neri, A, Inghirami, Giorgio, and Piva, Roberto

Published
2009

7. Gene expression profiling uncovers molecular classifiers for therecognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms

Author

Katia Todoerti, Elisa Pellegrino, Alessandro Fornari, Fabio Facchetti, Roberto Piva, Maurilio Ponzoni, Valentina Grosso, Luca Agnelli, Christiane De Wolf-Peeters, Hans Konrad Müller-Hermelink, Alberto Zamò, Ilaria Tamagno, Barbara Martinoglio, Andreas Rosenwald, Stefano Pileri, Pier Paolo Piccaluga, Antonino Neri, Eva Geissinger, Enzo Medico, Giorgio Inghirami, Piva R, Agnelli L, Pellegrino E, Todoerti K, Grosso V, Tamagno I, Fornari A, Martinoglio B, Medico E, Zamò A, Facchetti F, Ponzoni M, Geissinger E, Rosenwald A, Müller-Hermelink HK, De Wolf-Peeters C, Piccaluga PP, Pileri S, Neri A, Inghirami G., Piva, R, Agnelli, L, Pellegrino, E, Todoerti, K, Grosso, V, Tamagno, I, Fornari, A, Martinoglio, B, Medico, E, Zamo, A, Facchetti, F, Ponzoni, Maurilio, Geissinger, E, Rosenwald, A, Muller Hermelink, Hk, De Wolf Peeters, C, Piccaluga, Pp, Pileri, S, Neri, A, and Inghirami, G.

Subjects
Cancer Research, Pathology, medicine.medical_specialty, Lymphoma, Peripheral T-Cell Neoplasms, Biology, Transcriptome, Cell Line, Tumor, hemic and lymphatic diseases, Biomarkers, Tumor, medicine, Humans, Anaplastic lymphoma kinase, Anaplastic, Anaplastic Lymphoma Kinase, Anaplastic large-cell lymphoma, gene expression, Anaplastic Large-Cell Lymphoma, Gene Expression Profiling, Large cell, Uncovers Molecular Classifiers, Large-cell lymphoma, Lymphoma, T-Cell, Peripheral, Nuclear Proteins, Receptor Protein-Tyrosine Kinases, Protein-Tyrosine Kinases, medicine.disease, Peripheral T-cell lymphoma, Gene expression profiling, Cell Transformation, Neoplastic, Oncology, Cancer research, Lymphoma, Large-Cell, Anaplastic, Nucleophosmin, Signal Transduction
Abstract

Purpose To unravel the regulatory network underlying nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) –mediated lymphomagenesis of anaplastic large-cell lymphoma (ALCL) and to discover diagnostic genomic classifiers for the recognition of patients with ALK-positive and ALK-negative ALCL among T-cell non-Hodgkin's lymphoma (T-NHL). Patients and Methods The transcriptome of NPM-ALK–positive ALCL cell lines was characterized by silencing the expression of ALK or STAT3, a major effector of ALK oncogenic activity. Gene expression profiling (GEP) was performed in a series of systemic primary T-NHL (n = 70), including a set of ALK-positive and ALK-negative ALCL (n = 36). Genomic classifiers for ALK-positive and ALK-negative ALCL were generated by prediction analyses and validated by quantitative reverse-transcriptase polymerase chain reaction and/or immunohistochemistry. Results In ALCL cell lines, two thirds of ALK-regulated genes were concordantly dependent on STAT3 expression. GEP of systemic primary T-NHL significantly clustered ALK-positive ALCL samples in a separate subgroup, underscoring the relevance of in vitro ALK/STAT3 signatures. A set of genomic classifiers for ALK-positive ALCL and for ALCL were identified by prediction analyses. These gene clusters were instrumental for the distinction of ALK-negative ALCL from peripheral T-cell lymphomas not otherwise specified (PTCLs-NOS) and angioimmunoblastic lymphomas. Conclusion We proved that experimentally controlled GEP in ALCL cell lines represents a powerful tool to identify meaningful signaling networks for the recognition of systemic primary T-NHL. The identification of a molecular signature specific for ALCL suggests that these T-NHLs may represent a unique entity discernible from other PTCLs, and that a restricted number of genes can be instrumental for clinical stratification and, possibly, therapy of T-NHL.

Published
2010

8. A novel patient-derived tumorgraft model with TRAF1-ALK anaplastic large-cell lymphoma translocation

Author

Thomas Tousseyn, Elena Lasorsa, M. Ponzoni, Cristina Abele, Andrea Acquaviva, S. A. Pileri, Pier Paolo Piccaluga, Domenico Novero, Maria Todaro, Antonella Barreca, Francesco Abate, Ivo Kwee, Giorgio Inghirami, F Di Giacomo, Javeed Iqbal, Indira Landra, Raul Rabadan, Silvio Aime, Wing C. Chan, Rodolfo Machiorlatti, Mangeng Cheng, Michela Boi, Enrico Tiacci, B Pera-Gresely, Francesco Bertoni, Leonard D. Shultz, J-A van der Krogt, Katia Messana, Bruce Ruggeri, Brunangelo Falini, Sabrina Aliberti, Fabrizio Tabbò, Marcello Gaudiano, Luca Bessone, Roberto Piva, R Crescenzo, Andrea Rinaldi, Iwona Wlodarska, Dario Livio Longo, Elisa Ficarra, Leandro Cerchietti, Abate, F., Todaro, M., Van Der Krogt, J.-A., Boi, M., Landra, I., Machiorlatti, R., Tabbò, F., Messana, K., Abele, C., Barreca, A., Novero, D., Gaudiano, M., Aliberti, S., Di Giacomo, F., Tousseyn, T., Lasorsa, E., Crescenzo, R., Bessone, L., Ficarra, E., Acquaviva, A., Rinaldi, A., Ponzoni, M., Longo, D.L., Aime, S., Cheng, M., Ruggeri, B., Piccaluga, P.P., Pileri, S., Tiacci, E., Falini, B., Pera-Gresely, B., Cerchietti, L., Iqbal, J., Chan, W.C., Shultz, L.D., Kwee, I., Piva, R., Wlodarska, I., Rabadan, R., Bertoni, F., Inghirami, G., The European T-cell Lymphoma Study Group [.., Agostinelli, C., ], European T-cell Lymphoma Study Group, Cavallo, F., Chiesa, N., Fienga, A., di Giacomo, F., Marchiorlatti, R., Martinoglio, B., Medico, E., Ferrero, GB., Mereu, E., Pellegrino, E., Scafò, I., Spaccarotella, E., Ubezzi, I., Urigu, S., Chiapella, A., Vitolo, U., Agnelli, L., Neri, A., Chilosi£££Anna Caliò Marco£££ AC., Zamó, A., Facchetti, F., Lonardi, S., De Chiara, A., Fulciniti, F., Ferreri, A., Piccaluga, PP., Van Loo, P., De Wolf-Peeters, C., Geissinger, E., Muller-Hermelink, HK., Rosenwald, A., Piris, MA., Rodriguez, ME., Chiattone, C., Paes, RA., Abate, F, Todaro, M, van der Krogt, Ja, Boi, M, Landra, I, Machiorlatti, R, Tabbò, F, Messana, K, Abele, C, Barreca, A, Novero, D, Gaudiano, M, Aliberti, S, Di Giacomo, F, Tousseyn, T, Lasorsa, E, Crescenzo, R, Bessone, L, Ficarra, E, Acquaviva, A, Rinaldi, A, Ponzoni, M, Longo, Dl, Aime, S, Cheng, M, Ruggeri, B, Piccaluga, Pp, Pileri, S, Tiacci, E, Falini, B, Pera-Gresely, B, Cerchietti, L, Iqbal, J, Chan, Wc, Shultz, Ld, Kwee, I, Piva, R, Wlodarska, I, Rabadan, R, Bertoni, F, Inghirami, G, and andThe European T-cell Lymphoma Study, Group

Subjects
Pathology, Cancer Research, Lymphoma, TRAF1, Messenger, Drug Resistance, Translocation, Genetic, Fusion gene, Mice, Mice, Inbred NOD, hemic and lymphatic diseases, Tumor Cells, Cultured, Anaplastic lymphoma kinase, Anaplastic, Anaplastic Lymphoma Kinase, Anaplastic large-cell lymphoma, Animals, Blotting, Western, Flow Cytometry, Gene Expression Profiling, High-Throughput Nucleotide Sequencing, Humans, Immunoprecipitation, In Situ Hybridization, Fluorescence, Lymphoma, Large-Cell, Anaplastic, NF-kappa B, Proteasome Inhibitors, Proto-Oncogene Proteins c-myc, RNA, Messenger, Real-Time Polymerase Chain Reaction, Receptor Protein-Tyrosine Kinases, Repressor Proteins, Reverse Transcriptase Polymerase Chain Reaction, Signal Transduction, TNF Receptor-Associated Factor 1, Tumor Suppressor Protein p53, Xenograft Model Antitumor Assays, Drug Resistance, Neoplasm, In Situ Hybridization, Hematology, Cultured, Blotting, Medicine (all), Large-Cell, Tumor Cells, Proteasome Inhibitor, Receptor Protein-Tyrosine Kinase, Oncology, Western, Human, medicine.medical_specialty, fusion detection tool, Xenograft Model Antitumor Assay, medicine.drug_class, Translocation, Anesthesiology and Pain Medicine, Biology, anaplastic large-cell lymphomas (ALCL), RNA-Seq data, Fluorescence, Article, Genetic, Internal medicine, PRDM1, medicine, traslocation, Animal, Repressor Protein, medicine.disease, ALK inhibitor, anaplastic lymphoma kinase (ALK), Cancer research, Inbred NOD, RNA, Neoplasm, Positive Regulatory Domain I-Binding Factor 1, Lymphoma, Large-Cell, Anaplastic/drug therapy, Lymphoma, Large-Cell, Anaplastic/genetics, NF-kappa B/genetics, NF-kappa B/metabolism, Proteasome Inhibitors/pharmacology, Proto-Oncogene Proteins c-myc/genetics, Proto-Oncogene Proteins c-myc/metabolism, RNA, Messenger/genetics, Receptor Protein-Tyrosine Kinases/genetics, Receptor Protein-Tyrosine Kinases/metabolism, Repressor Proteins/genetics, Repressor Proteins/metabolism, TNF Receptor-Associated Factor 1/genetics, TNF Receptor-Associated Factor 1/metabolism, Translocation, Genetic/genetics, Tumor Suppressor Protein p53/genetics, Tumor Suppressor Protein p53/metabolism
Abstract

Although anaplastic large-cell lymphomas (ALCL) carrying anaplastic lymphoma kinase (ALK) have a relatively good prognosis, aggressive forms exist. We have identified a novel translocation, causing the fusion of the TRAF1 and ALK genes, in one patient who presented with a leukemic ALK+ ALCL (ALCL-11). To uncover the mechanisms leading to high-grade ALCL, we developed a human patient-derived tumorgraft (hPDT) line. Molecular characterization of primary and PDT cells demonstrated the activation of ALK and nuclear factor kappa B (NF kappa B) pathways. Genomic studies of ALCL-11 showed the TP53 loss and the in vivo subclonal expansion of lymphoma cells, lacking PRDM1/Blimp1 and carrying c-MYC gene amplification. The treatment with proteasome inhibitors of TRAF1-ALK cells led to the downregulation of p50/p52 and lymphoma growth inhibition. Moreover, a NF kappa B gene set classifier stratified ALCL in distinct subsets with different clinical outcome. Although a selective ALK inhibitor (CEP28122) resulted in a significant clinical response of hPDT mice, nevertheless the disease could not be eradicated. These data indicate that the activation of NF kappa B signaling contributes to the neoplastic phenotype of TRAF1-ALK ALCL. ALCL hPDTs are invaluable tools to validate the role of druggable molecules, predict therapeutic responses and implement patient specific therapies.

Published
2015

9. The molecular landscape of colorectal cancer cell lines unveils clinically actionable kinase targets.

Author

Medico E, Russo M, Picco G, Cancelliere C, Valtorta E, Corti G, Buscarino M, Isella C, Lamba S, Martinoglio B, Veronese S, Siena S, Sartore-Bianchi A, Beccuti M, Mottolese M, Linnebacher M, Cordero F, Di Nicolantonio F, and Bardelli A

Subjects
Anaplastic Lymphoma Kinase, Cell Line, Tumor, Cetuximab, Colorectal Neoplasms genetics, Genes, erbB-1, Genetic Heterogeneity, Humans, Molecular Targeted Therapy, Proto-Oncogene Proteins c-ret metabolism, Receptor Protein-Tyrosine Kinases genetics, Receptor, Fibroblast Growth Factor, Type 2 metabolism, Colorectal Neoplasms enzymology, ErbB Receptors antagonists & inhibitors, Receptor Protein-Tyrosine Kinases metabolism
Abstract

The development of molecularly targeted anticancer agents relies on large panels of tumour-specific preclinical models closely recapitulating the molecular heterogeneity observed in patients. Here we describe the mutational and gene expression analyses of 151 colorectal cancer (CRC) cell lines. We find that the whole spectrum of CRC molecular and transcriptional subtypes, previously defined in patients, is represented in this cell line compendium. Transcriptional outlier analysis identifies RAS/BRAF wild-type cells, resistant to EGFR blockade, functionally and pharmacologically addicted to kinase genes including ALK, FGFR2, NTRK1/2 and RET. The same genes are present as expression outliers in CRC patient samples. Genomic rearrangements (translocations) involving the ALK and NTRK1 genes are associated with the overexpression of the corresponding proteins in CRC specimens. The approach described here can be used to pinpoint CRCs with exquisite dependencies to individual kinases for which clinically approved drugs are already available.

Published
2015
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10. Gene expression profiling uncovers molecular classifiers for the recognition of anaplastic large-cell lymphoma within peripheral T-cell neoplasms.

Author

Piva R, Agnelli L, Pellegrino E, Todoerti K, Grosso V, Tamagno I, Fornari A, Martinoglio B, Medico E, Zamò A, Facchetti F, Ponzoni M, Geissinger E, Rosenwald A, Müller-Hermelink HK, De Wolf-Peeters C, Piccaluga PP, Pileri S, Neri A, and Inghirami G

Subjects
Anaplastic Lymphoma Kinase, Cell Line, Tumor, Cell Transformation, Neoplastic genetics, Humans, Nuclear Proteins genetics, Nucleophosmin, Protein-Tyrosine Kinases genetics, Receptor Protein-Tyrosine Kinases, Signal Transduction, Biomarkers, Tumor genetics, Gene Expression Profiling, Lymphoma, Large-Cell, Anaplastic genetics, Lymphoma, T-Cell, Peripheral genetics
Abstract

Purpose: To unravel the regulatory network underlying nucleophosmin-anaplastic lymphoma kinase (NPM-ALK) -mediated lymphomagenesis of anaplastic large-cell lymphoma (ALCL) and to discover diagnostic genomic classifiers for the recognition of patients with ALK-positive and ALK-negative ALCL among T-cell non-Hodgkin's lymphoma (T-NHL)., Patients and Methods: The transcriptome of NPM-ALK-positive ALCL cell lines was characterized by silencing the expression of ALK or STAT3, a major effector of ALK oncogenic activity. Gene expression profiling (GEP) was performed in a series of systemic primary T-NHL (n = 70), including a set of ALK-positive and ALK-negative ALCL (n = 36). Genomic classifiers for ALK-positive and ALK-negative ALCL were generated by prediction analyses and validated by quantitative reverse-transcriptase polymerase chain reaction and/or immunohistochemistry., Results: In ALCL cell lines, two thirds of ALK-regulated genes were concordantly dependent on STAT3 expression. GEP of systemic primary T-NHL significantly clustered ALK-positive ALCL samples in a separate subgroup, underscoring the relevance of in vitro ALK/STAT3 signatures. A set of genomic classifiers for ALK-positive ALCL and for ALCL were identified by prediction analyses. These gene clusters were instrumental for the distinction of ALK-negative ALCL from peripheral T-cell lymphomas not otherwise specified (PTCLs-NOS) and angioimmunoblastic lymphomas., Conclusion: We proved that experimentally controlled GEP in ALCL cell lines represents a powerful tool to identify meaningful signaling networks for the recognition of systemic primary T-NHL. The identification of a molecular signature specific for ALCL suggests that these T-NHLs may represent a unique entity discernible from other PTCLs, and that a restricted number of genes can be instrumental for clinical stratification and, possibly, therapy of T-NHL.

Published
2010
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11. Multipotent mesenchymal stem cells from amniotic fluid originate neural precursors with functional voltage-gated sodium channels.

Author

Mareschi K, Rustichelli D, Comunanza V, De Fazio R, Cravero C, Morterra G, Martinoglio B, Medico E, Carbone E, Benedetto C, and Fagioli F

Subjects
Biomarkers metabolism, Cell Differentiation, Cell Separation, Cell Shape, Cells, Cultured, Culture Media, Female, Gene Expression Regulation, Developmental, Humans, Immunophenotyping, Ion Channel Gating, Mesenchymal Stem Cells metabolism, Multipotent Stem Cells metabolism, Pregnancy, Amniotic Fluid cytology, Mesenchymal Stem Cells cytology, Multipotent Stem Cells cytology, Neurons cytology, Neurons metabolism, Sodium Channels metabolism
Abstract

Background Aims: Amniotic fluid (AF) contains stem cells with high proliferative and differentiative potential that might be an attractive source of multipotent stem cells. We investigated whether human AF contains mesenchymal stem cells (MSC) and evaluated their phenotypic characteristics and differentiation potential in vitro., Methods: AF was harvested during routine pre-natal amniocentesis at 14-16 weeks of pregnancy. AF sample pellets were plated in alpha-minimum essential medium (MEM) with 10% fetal bovine serum (FBS). We evaluated cellular growth, immunophenotype, stemness markers and differentiative potential during in vitro expansion. Neural progenitor maintenance medium (NPMM), a medium normally used for the growth and maintenance of neural stem cells, containing hFGF, hEGF and NSF-1, was used for neural induction., Results: Twenty-seven AF samples were collected and primary cells, obtained from samples containing more than 6 mL AF, had MSC characteristics. AF MSC showed high proliferative potential, were positive for CD90, CD105, CD29, CD44, CD73 and CD166, showed Oct-4 and Nanog molecular and protein expression, and differentiated into osteoblasts, adypocytes and chondrocytes. The NPMM-cultured cells expressed neural markers and increased Na(+) channel density and channel inactivation rate, making the tetrodotoxin (TTX)-sensitive channels more kinetically similar to native neuronal voltage-gated Na(+) channels., Conclusions: These data suggest that AF is an important multipotent stem cell source with a high proliferative potential able to originate potential precursors of functional neurons.

Published
2009
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