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

Author

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, and Inghirami, G

Published
2015
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4. EFL students’ anxiety in remote learning during COVID-19 pandemic

Author

Landra, I Komang Gunawan, Dantes, I Nyoman, Suarni, Ni Ketut, Budiawan, Made, Permana, I Gede Yoga, Landra, I Komang Gunawan, Dantes, I Nyoman, Suarni, Ni Ketut, Budiawan, Made, and Permana, I Gede Yoga

Abstract

Since the outbreak of the Covid-19, the education system has undergone major changes. Learning that is carried out face-to-face is replaced with online-based learning. Students who have been through the online learning process for more than one year begin to show boredom. This directly impacts their psychological condition during learning. This study is aimed at investigating students’ anxiety during remote learning in covid-19 pandemic. There were 100 EFL students were invited to get involved in this study. The instrument to collect the data was Hamilton’s Anxiety Rating Scale (HAM-A). The result showed that there were fourteen symptoms during remote learning. Students were experiencing a moderate anxiety. This study also highlighted female students showed had higher anxiety compared to male students.

Published
2022

5. EFL students’ anxiety in remote learning during COVID-19 pandemic

Author

Gunawan Landra, I Komang, Dantes, Nyoman, Suarni, Ni Ketut, Budiawan, Made, and Yoga Permana, I Gede

Subjects
COVID-19, Anxiety, HAM-A, Remote Learning
Abstract

Since the outbreak of the Covid-19, the education system has undergone major changes. Learning that is carried out face-to-face is replaced with online-based learning. Students who have been through the online learning process for more than one year begin to show boredom. This directly impacts their psychological condition during learning. This study is aimed at investigating students’ anxiety during remote learning in covid-19 pandemic. In this study, there were 100 EFL students were involved. The instrument to collect the data was Hamilton’s Anxiety Rating Scale (HAM-A). The collected data were analyzed using descriptive statistics. The result showed that there were fourteen symptoms during remote learning. The highest mean score of anxiety was indicated in fears (M=2.96) meanwhile the lowest mean score was mood (M=1.52). Students were identified to have experienced a moderate anxiety. This study also highlighted female students showed higher anxiety compared to male students.

Published
2022
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8. PDGFR blockade is a rational and effective therapy for NPM-ALK\u2013driven lymphomas

Author

Laimer D, Dolznig H, Kollmann K, Vesely PW, Schlederer M, Merkel O, Schiefer AI, Hassler MR, Heider S, Amenitsch L, Thallinger C, Staber PB, Simonitsch-Klupp I, Artaker M, Lagger S, Turner SD, Pileri S, Piccaluga PP, Valent P, Messana K, Landra I, Weichhart T, Knapp S, Shehata M, Todaro M, Sexl V, Hxf6fler G, Piva R, Medico E, Ruggeri BA, Cheng M, Eferl R, Egger G, Penninger JM, Jaeger U, Moriggl R, Inghirami G, and Kenner L

Published
2012

9. 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

10. PDGFR blockade is a rational and effective therapy for NPM-ALK-driven lymphomas

Author

Giorgio Inghirami, Philipp B. Staber, Karoline Kollmann, Medhat Shehata, Olaf Merkel, Veronika Sexl, Katia Messana, Pier Paolo Piccaluga, Robert Eferl, Maria Todaro, Susi Heider, Peter Valent, Sylvia Knapp, Bruce Ruggeri, Enzo Medico, Christiane Thallinger, Thomas Weichhart, Ingrid Simonitsch-Klupp, Helmut Dolznig, Ulrich Jaeger, Sabine Lagger, Indira Landra, Mangeng Cheng, Lena Amenitsch, Melanie R. Hassler, Paul Vesely, Richard Moriggl, Josef M. Penninger, Suzanne D. Turner, Matthias Artaker, Roberto Piva, Daniela Laimer, Stefano Pileri, Michaela Schlederer, Gerda Egger, Ana Iris Schiefer, Lukas Kenner, Gerald Höfler, Laimer D, Dolznig H, Kollmann K, Vesely PW, Schlederer M, Merkel O, Schiefer AI, Hassler MR, Heider S, Amenitsch L, Thallinger C, Staber PB, Simonitsch-Klupp I, Artaker M, Lagger S, Turner SD, Pileri S, Piccaluga PP, Valent P, Messana K, Landra I, Weichhart T, Knapp S, Shehata M, Todaro M, Sexl V, Höfler G, Piva R, Medico E, Ruggeri BA, Cheng M, Eferl R, Egger G, Penninger JM, Jaeger U, Moriggl R, Inghirami G, and Kenner L

Subjects
Receptor, Platelet-Derived Growth Factor alpha, Oncogene Protein p65(gag-jun), lymphomas, Piperazines, Translocation, Genetic, Mice, 0302 clinical medicine, hemic and lymphatic diseases, Anaplastic Lymphoma Kinase, Molecular Targeted Therapy, Anaplastic large-cell lymphoma, 0303 health sciences, integumentary system, Remission Induction, Nuclear Proteins, General Medicine, Protein-Tyrosine Kinases, 3. Good health, Gene Expression Regulation, Neoplastic, 030220 oncology & carcinogenesis, Benzamides, Imatinib Mesylate, Lymphoma, Large-Cell, Anaplastic, Nucleophosmin, Platelet-derived growth factor receptor, Adult, JUNB, Mice, Transgenic, PDGFRB, PDGFRA, Biology, General Biochemistry, Genetics and Molecular Biology, Receptor, Platelet-Derived Growth Factor beta, 03 medical and health sciences, Growth factor receptor, Cell Line, Tumor, medicine, Animals, Humans, Neoplasm Staging, 030304 developmental biology, Receptor Protein-Tyrosine Kinases, medicine.disease, Lymphoma, Transcription Factor AP-1, Pyrimidines, Imatinib mesylate, Cancer research, biology.protein, Stem Cell Transplantation
Abstract

Anaplastic large cell lymphoma (ALCL) is an aggressive non-Hodgkin's lymphoma found in children and young adults. ALCLs frequently carry a chromosomal translocation that results in expression of the oncoprotein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). The key molecular downstream events required for NPM-ALK-triggered lymphoma growth have been only partly unveiled. Here we show that the activator protein 1 family members JUN and JUNB promote lymphoma development and tumor dissemination through transcriptional regulation of platelet-derived growth factor receptor-β (PDGFRB) in a mouse model of NPM-ALK-triggered lymphomagenesis. Therapeutic inhibition of PDGFRB markedly prolonged survival of NPM-ALK transgenic mice and increased the efficacy of an ALK-specific inhibitor in transplanted NPM-ALK tumors. Notably, inhibition of PDGFRA and PDGFRB in a patient with refractory late-stage NPM-ALK(+) ALCL resulted in rapid, complete and sustained remission. Together, our data identify PDGFRB as a previously unknown JUN and JUNB target that could be a highly effective therapy for ALCL.

Published
2012

11. Tailoring CD19xCD3-DART exposure enhances T-cells to eradication of B-cell neoplasms.

Author

Circosta P, Elia AR, Landra I, Machiorlatti R, Todaro M, Aliberti S, Brusa D, Deaglio S, Chiaretti S, Bruna R, Gottardi D, Massaia M, Giacomo FD, Guarini AR, Foà R, Kyriakides PW, Bareja R, Elemento O, Chichili GR, Monteleone E, Moore PA, Johnson S, Bonvini E, Cignetti A, and Inghirami G

Abstract

Many patients with B-cell malignancies can be successfully treated, although tumor eradication is rarely achieved. T-cell-directed killing of tumor cells using engineered T-cells or bispecific antibodies is a promising approach for the treatment of hematologic malignancies. We investigated the efficacy of CD19xCD3 DART bispecific antibody in a broad panel of human primary B-cell malignancies. The CD19xCD3 DART identified 2 distinct subsets of patients, in which the neoplastic lymphocytes were eliminated with rapid or slow kinetics. Delayed responses were always overcome by a prolonged or repeated DART exposure. Both CD4 and CD8 effector cytotoxic cells were generated, and DART-mediated killing of CD4 + cells into cytotoxic effectors required the presence of CD8 + cells. Serial exposures to DART led to the exponential expansion of CD4 + and CD8 + cells and to the sequential ablation of neoplastic cells in absence of a PD-L1-mediated exhaustion. Lastly, patient-derived neoplastic B-cells (B-Acute Lymphoblast Leukemia and Diffuse Large B Cell Lymphoma) could be proficiently eradicated in a xenograft mouse model by DART-armed cytokine induced killer (CIK) cells. Collectively, patient tailored DART exposures can result in the effective elimination of CD19 positive leukemia and B-cell lymphoma and the association of bispecific antibodies with unmatched CIK cells represents an effective modality for the treatment of CD19 positive leukemia/lymphoma.

Published
2018
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12. PDGFR blockade is a rational and effective therapy for NPM-ALK-driven lymphomas.

Author

Laimer D, Dolznig H, Kollmann K, Vesely PW, Schlederer M, Merkel O, Schiefer AI, Hassler MR, Heider S, Amenitsch L, Thallinger C, Staber PB, Simonitsch-Klupp I, Artaker M, Lagger S, Turner SD, Pileri S, Piccaluga PP, Valent P, Messana K, Landra I, Weichhart T, Knapp S, Shehata M, Todaro M, Sexl V, Höfler G, Piva R, Medico E, Ruggeri BA, Cheng M, Eferl R, Egger G, Penninger JM, Jaeger U, Moriggl R, Inghirami G, and Kenner L

Subjects
Adult, Anaplastic Lymphoma Kinase, Animals, Benzamides, Cell Line, Tumor, Gene Expression Regulation, Neoplastic drug effects, Humans, Imatinib Mesylate, Mice, Mice, Transgenic, Molecular Targeted Therapy, Neoplasm Staging, Nucleophosmin, Oncogene Protein p65(gag-jun) genetics, Oncogene Protein p65(gag-jun) metabolism, Piperazines administration & dosage, Pyrimidines administration & dosage, Remission Induction, Stem Cell Transplantation, Transcription Factor AP-1 genetics, Transcription Factor AP-1 metabolism, Translocation, Genetic, Lymphoma, Large-Cell, Anaplastic drug therapy, Lymphoma, Large-Cell, Anaplastic metabolism, Lymphoma, Large-Cell, Anaplastic pathology, Nuclear Proteins genetics, Nuclear Proteins metabolism, Protein-Tyrosine Kinases genetics, Protein-Tyrosine Kinases metabolism, Receptor Protein-Tyrosine Kinases antagonists & inhibitors, Receptor Protein-Tyrosine Kinases genetics, Receptor Protein-Tyrosine Kinases metabolism, Receptor, Platelet-Derived Growth Factor alpha antagonists & inhibitors, Receptor, Platelet-Derived Growth Factor alpha genetics, Receptor, Platelet-Derived Growth Factor alpha metabolism, Receptor, Platelet-Derived Growth Factor beta antagonists & inhibitors, Receptor, Platelet-Derived Growth Factor beta genetics, Receptor, Platelet-Derived Growth Factor beta metabolism
Abstract

Anaplastic large cell lymphoma (ALCL) is an aggressive non-Hodgkin's lymphoma found in children and young adults. ALCLs frequently carry a chromosomal translocation that results in expression of the oncoprotein nucleophosmin-anaplastic lymphoma kinase (NPM-ALK). The key molecular downstream events required for NPM-ALK-triggered lymphoma growth have been only partly unveiled. Here we show that the activator protein 1 family members JUN and JUNB promote lymphoma development and tumor dissemination through transcriptional regulation of platelet-derived growth factor receptor-β (PDGFRB) in a mouse model of NPM-ALK-triggered lymphomagenesis. Therapeutic inhibition of PDGFRB markedly prolonged survival of NPM-ALK transgenic mice and increased the efficacy of an ALK-specific inhibitor in transplanted NPM-ALK tumors. Notably, inhibition of PDGFRA and PDGFRB in a patient with refractory late-stage NPM-ALK(+) ALCL resulted in rapid, complete and sustained remission. Together, our data identify PDGFRB as a previously unknown JUN and JUNB target that could be a highly effective therapy for ALCL.

Published
2012
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