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4. Additional file 1 of High activity and low toxicity of a novel CD71-targeting nanotherapeutic named The-0504 on preclinical models of several human aggressive tumors

Author

Falvo, Elisabetta, Damiani, Verena, Giamaica Conti, Boschi, Federico, Messana, Katia, Giacomini, Patrizio, Milella, Michele, Laurenzi, Vincenzo De, Morea, Veronica, Sala, Gianluca, Fracasso, Giulio, and Ceci, Pierpaolo

Abstract

Additional file 1: Table S1. Free-drug content in lyophilized The-0504 after storage at 2–8 °C for eight months. Fig. S1. The-05 binding to pancreatic PaCa44 cells. Flow cytometric analysis of The-05. Mitoxantrone-containing The-05 (The-05-Mit) preparation was incubated for different times at 37 °C with human PaCa44 cells. Binding was revealed by direct fluorescence reading in a BD FACSCanto II flow cytometer. The-05-Mit provided at the predetermined optimal concentration of 0.5 μM (in Mitoxantrone). MFI refers to the median fluorescence intensity of the sample subtracted from the cell autofluorescence value. Fig. S2. MMP-9 and CD71 expression evaluation in cancer cells. Western blot using anti-MMP-9 antibody on SJSA-1 cells (A) or anti-CD71 antibody on SJSA-1, Panc-1 and MIA-PaCa-2 cells (B). GAPDH was used as a loading control. Fig. S3. Anti-tumor activity of The-0504 in mice bearing subcutaneous HepG2 liver tumors. Tumor-growth curves for each mouse groups are indicated. Animals were observed up to 60 days. At that time, 100% of The-0504-treated mice were still alive and with any residual sign of disease. Statistical significance according to the Student’s t-test: control vs The-0504 * p

Published
2021
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5. PDGFR blockade is a rational and effective therapy for NPM-ALK-driven lymphomas

Author

Laimer, Daniela, Dolznig, Helmut, Kollmann, Karoline, Vesely, Paul W., Schlederer, Michaela, Merkel, Olaf, Schiefer, Ana-Iris, Hassler, Melanie R., Heider, Susi, Amenitsch, Lena, Thallinger, Christiane, Staber, Philipp B., Simonitsch-Klupp, Ingrid, Artaker, Matthias, Lagger, Sabine, Turner, Suzanne D., Pileri, Stefano, Piccaluga, Pier Paolo, Valent, Peter, Messana, Katia, Landra, Indira, Weichhart, Thomas, Knapp, Sylvia, Shehata, Medhat, Todaro, Maria, Sexl, Veronika, Hofler, Gerald, Piva, Roberto, Medico, Enzo, Ruggeri, Bruce A., Cheng, Mangeng, Eferl, Robert, Egger, Gerda, Penninger, Josef M., Jaeger, Ulrich, Moriggl, Richard, Inghirami, Giorgio, and Kenner, Lukas

Subjects
Non-Hodgkin's lymphomas -- Genetic aspects -- Drug therapy -- Research, Protein kinases -- Physiological aspects -- Genetic aspects -- Research, Blood platelets -- Receptors, Biological sciences, Health
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.sup.+] 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., ALCLs are T cell lymphomas (1), (2) comprising 10-20% of all non-Hodgkin's lymphoma cases in children and 3% in adults (3). About half of ALCL cases are positive for the [...]

Published
2012
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6. Identification of a new subclass of ALK-negative ALCL expressing aberrant levels of ERBB4 transcripts

Author

Scarfò, Irene, Pellegrino, Elisa, Mereu, Elisabetta, Kwee, Ivo, Agnelli, Luca, Bergaggio, Elisa, Garaffo, Giulia, Vitale, Nicoletta, Caputo, Manuel, Machiorlatti, Rodolfo, Circosta, Paola, Abate, Francesco, Barreca, Antonella, Novero, Domenico, Mathew, Susan, Rinaldi, Andrea, Tiacci, Enrico, Serra, Sara, Deaglio, Silvia, Neri, Antonino, Falini, Brunangelo, Rabadan, Raul, Bertoni, Francesco, Inghirami, Giorgio, Piva, Roberto, Boi, Michela, Crescenzo, Ramona, Cuccuru, Giuditta, Gaudiano, Marcello, Lasorsa, Elena, Medico, Enzo, Messana, Katia, Spaccarotella, Elisa, Tabbò, Fabrizio, Todaro, Maria, Fornari, Alessandro, Chilosi, Marco, Zamò, Alberto, Facchetti, Fabio, Lonardi, Silvia, De Chiara, Anna, Fulciniti, Franco, Doglioni, Claudio, Ponzoni, Maurilio, Todoerti, Katia, De Wolf Peeters, Christiane, Tousseyn, Thomas, Van Loo, Peter, Geissinger, Eva, Muller Hermelink, Hans Konrad, Rosenwald, Andreas, Matolcsy, Andras, Piris, Miguel Angel, Rodriguez Pinilla, Maria E., AGOSTINELLI, CLAUDIO, PICCALUGA, PIER PAOLO, PILERI, STEFANO, Scarfò, Irene, Pellegrino, Elisa, Mereu, Elisabetta, Kwee, Ivo, Agnelli, Luca, Bergaggio, Elisa, Garaffo, Giulia, Vitale, Nicoletta, Caputo, Manuel, Machiorlatti, Rodolfo, Circosta, Paola, Abate, Francesco, Barreca, Antonella, Novero, Domenico, Mathew, Susan, Rinaldi, Andrea, Tiacci, Enrico, Serra, Sara, Deaglio, Silvia, Neri, Antonino, Falini, Brunangelo, Rabadan, Raul, Bertoni, Francesco, Inghirami, Giorgio, Piva, Roberto, Boi, Michela, Crescenzo, Ramona, Cuccuru, Giuditta, Gaudiano, Marcello, Lasorsa, Elena, Medico, Enzo, Messana, Katia, Spaccarotella, Elisa, Tabbò, Fabrizio, Todaro, Maria, Fornari, Alessandro, Chilosi, Marco, Zamò, Alberto, Facchetti, Fabio, Lonardi, Silvia, De Chiara, Anna, Fulciniti, Franco, Doglioni, Claudio, Ponzoni, Maurilio, Todoerti, Katia, Agostinelli, Claudio, Piccaluga, Pier Paolo, Pileri, Stefano, De Wolf-Peeters, Christiane, Tousseyn, Thoma, Van Loo, Peter, Geissinger, Eva, Muller-Hermelink, Hans Konrad, Rosenwald, Andrea, Matolcsy, Andra, Piris, Miguel Angel, Rodriguez-Pinilla, Maria E., Scarfò, I, Pellegrino, E, Mereu, E, Kwee, I, Agnelli, L, Bergaggio, E, Garaffo, G, Vitale, N, Caputo, M, Machiorlatti, R, Circosta, P, Abate, F, Barreca, A, Novero, D, Mathew, S, Rinaldi, A, Tiacci, E, Serra, S, Deaglio, S, Neri, A, Falini, B, Rabadan, R, Bertoni, F, Inghirami, G, Piva, R, the European T-Cell Lymphoma Study, Group, Doglioni, C, and Ponzoni, M

Subjects
0301 basic medicine, Untranslated region, Receptor, ErbB-4, Messenger, Mice, SCID, Biochemistry, Mice, 0302 clinical medicine, 5' Untranslated Region, HEK293 Cell, Mutant Protein, Mice, Inbred NOD, hemic and lymphatic diseases, 5' Untranslated RegionsAnimalsCodon, Anaplastic lymphoma kinase, Anaplastic Lymphoma Kinase, NIH 3T3 Cell, Regulation of gene expression, TransgenicMolecular Sequence DataMutant ProteinsNIH 3T3 CellsReceptor Protein-Tyrosine KinasesReceptor, Hematology, Long terminal repeat, Large-Cell, Gene Expression Regulation, Neoplastic, Receptor Protein-Tyrosine Kinase, Codon, Nonsense, 030220 oncology & carcinogenesis, Lymphoma, Large-Cell, Anaplastic, Human, Molecular Sequence Data, Immunology, ErbB-4RNA, Mice, Transgenic, Biology, 03 medical and health sciences, Complementary DNA, Animals, Humans, RNA, Messenger, Gene, NonsenseGene Expression Regulation, NeoplasticHEK293 CellsHumansLymphoma, Animal, Receptor Protein-Tyrosine Kinases, RNA, Cell Biology, Molecular biology, Gene expression profiling, HEK293 Cells, 030104 developmental biology, Inbred NODMice, NIH 3T3 Cells, Mutant Proteins, SCIDMice, AnaplasticMiceMice, 5' Untranslated Regions, 5' Untranslated RegionsAnimalsCodon, NonsenseGene Expression Regulation, NeoplasticHEK293 CellsHumansLymphoma, Large-Cell, AnaplasticMiceMice, Inbred NODMice, SCIDMice, TransgenicMolecular Sequence DataMutant ProteinsNIH 3T3 CellsReceptor Protein-Tyrosine KinasesReceptor, ErbB-4RNA, Messenger
Abstract

Anaplastic large-cell lymphoma (ALCL) is a clinical and biological heterogeneous disease that includes systemic anaplastic lymphoma kinase (ALK)-positive and ALK-negative entities. To discover biomarkers and/or genes involved in ALK-negative ALCL pathogenesis, we applied the cancer outlier profile analysis algorithm to a gene expression profiling data set including 249 cases of T-cell non-Hodgkin lymphoma and normal T cells. Ectopic coexpression of ERBB4 and COL29A1 genes was detected in 24% of ALK-negative ALCL patients. RNA sequencing and 5' RNA ligase-mediated rapid amplification of complementary DNA ends identified 2 novel ERBB4-truncated transcripts displaying intronic transcription start sites. By luciferase assays, we defined that the expression of ERBB4-aberrant transcripts is promoted by endogenous intronic long terminal repeats. ERBB4 expression was confirmed at the protein level by western blot analysis and immunohistochemistry. Lastly, we demonstrated that ERBB4-truncated forms show oncogenic potentials and that ERBB4 pharmacologic inhibition partially controls ALCL cell growth and disease progression in an ERBB4-positive patient-derived tumorgraft model. In conclusion, we identified a new subclass of ALK-negative ALCL characterized by aberrant expression of ERBB4-truncated transcripts carrying intronic 5' untranslated regions. © 2016 by The American Society of Hematology.

Published
2016

8. Beyond NPM-anaplastic lymphoma kinase driven lymphomagenesis

Author

Fabrizio Tabbò, Maurilio Ponzoni, Raul Rabadan, Francesco Bertoni, Giorgio Inghirami European T. cell Lymphoma Study Group, Aliberti Sabrina, Barreca Antonella, Besson Luca, Crescenzo Ramona, Di Giacomo Filomena, Gaudiano Marcello, Inghirami Giorgio, Landra Indira, Lasorsa Elena, Machiorlatti Rodolfo, Mereu Elisabetta, Messana Katia, Novero Domenico, Pellegrino Elisa, Pich Achille, Piva Roberto, Scarfo Irene, Spaccarotella Elisa, Tabbo Fabrizio, Todaro Maria, Ubezzi Ivana, Urigu Susanna, Vittone Francesco, Abage Francesco, Ficarra Elisa, Acquaviva Andrea, Ponzoni Maurilio, Stella Carmelo, AGOSTINELLI, CLAUDIO, PICCALUGA, PIER PAOLO, PILERI, STEFANO, Falini Brunangelo, Tiacci Enrico, Bertoni Francesco, Boi Michela, Kwee Ivo, Fabrizio Tabbò,Maurilio Ponzoni,Raul Rabadan,Francesco Bertoni,Giorgio Inghirami European T-cell Lymphoma Study Group, Aliberti Sabrina, Barreca Antonella, Besson Luca, Crescenzo Ramona, Di Giacomo Filomena, Gaudiano Marcello, Inghirami Giorgio, Landra Indira, Lasorsa Elena, Machiorlatti Rodolfo, Mereu Elisabetta, Messana Katia, Novero Domenico, Pellegrino Elisa, Pich Achille, Piva Roberto, Scarfo Irene, Spaccarotella Elisa, Tabbo Fabrizio, Todaro Maria, Ubezzi Ivana, Urigu Susanna, Vittone Francesco, Abage Francesco, Ficarra Elisa, Acquaviva Andrea, Ponzoni Maurilio, Stella Carmelo, Agostinelli Claudio, Piccaluga Pier Paolo, Pileri Stefano, Falini Brunangelo, Tiacci Enrico, Bertoni Francesco, Boi Michela, and Kwee Ivo

Subjects
Anaplastic lymphoma kinase, Kinase inhibitor, Signalling pathways, hemic and lymphatic diseases, Lymphoid differentiation, Mouse model
Abstract

PURPOSE OF REVIEW: Anaplastic large cell lymphomas (ALCLs) are rare entities whose somatic genetic lesions have been identified only in a subset of patients. Thus, an integrated and massive discovery programme is required to define their tumourigenic alterations and to design more successful tailored therapies. RECENT FINDINGS: The discovery of anaplastic lymphoma kinase (ALK) fusions has provided the basis for the characterization of distinct subsets among ALCL patients. Although the oncogenic addiction of ALK signalling is proven, the tumorigenic contribution of coactivating lesions is still missing. As ALK- and ALK+ share common signatures, it is plausible that analogous mechanisms of transformation may be operating in both subsets, as confirmed by the dysregulated activation of c-MYC, RAS and NFκB, and the loss of Blimp-1 and p53/p63 axis. Nonetheless, recurrent genetic alterations for ALK- ALCL or refractory leukaemic ALK+ ALCL are lacking. Moreover, although conventional chemotherapies (anthracycline-based) are most successful, that is in ALK+ ALCL patients, the implementation of ALK inhibitors or of anti-CD30 based treatments provides innovative solutions, particularly in paediatric ALK+ ALCL and in chemorefractory/relapsed patients. SUMMARY: The complete portrayal of the landscape of genetic alterations in ALCL will dictate the development of innovative chemotherapeutic and targeted therapies that will fit most with the molecular and clinical profiling of individual patients.

Published
2013

9. Identification of a New Subclass of ALK Negative Anaplastic Large Cell Lymphoma Expressing Aberrant Levels of ERBB4 Transcripts

Author

Scarfò, Irene, primary, Pellegrino, Elisa, additional, Kwee, Ivo, additional, Agnelli, Luca, additional, Mereu, Elisabetta, additional, Bergaggio, Elisa, additional, Abate, Francesco, additional, Machiorlatti, Rodolfo, additional, Messana, Katia, additional, Rinaldi, Andrea, additional, Tiacci, Enrico, additional, Serra, Sara, additional, Deaglio, Silvia, additional, Neri, Antonino, additional, Falini, Brunangelo, additional, Rabadan, Raul, additional, Bertoni, Francesco, additional, Inghirami, Giorgio, additional, and Piva, Roberto, additional

Published
2014
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10. Abstract 5531: OTX015, a novel BET inhibitor, is a promising anticancer agent for multiple myeloma

Author

Todaro, Maria, primary, Boi, Michela, additional, Vurchio, Valentina, additional, Ercole, Elisabetta, additional, Machiorlatti, Rodolfo, additional, Messana, Katia, additional, Landra, Indira, additional, Urigu, Susanna, additional, Aliberti, Sabrina, additional, Riveiro, Eugenia, additional, Bertoni, Francesco, additional, and Inghirami, Giorgio, additional

Published
2014
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11. Abstract 3853: Humanized NOD/Scid/IL2g-/- tumor grafts recapitulate primary anaplastic large cell lymphoma.

Author

Tabbo', Fabrizio, primary, Barreca, Antonella, additional, Machiorlatti, Rodolfo, additional, Messana, Katia, additional, Landra, Indira, additional, Abate, Francesco, additional, Boi, Michela, additional, Todaro, Maria, additional, Abele, Cristina, additional, Novero, Domenico, additional, Zamo', Alberto, additional, Chilosi, Marco, additional, Ponzoni, Maurilio, additional, Cheng, Mangeng, additional, Ruggeri, Bruce, additional, Piccaluga, Pierpaolo, additional, Pileri, Stefano, additional, Tiacci, Enrico, additional, Falini, Brunangelo, additional, Shultz, Lenny, additional, Piva, Roberto, additional, Medico, Enzo, additional, Bertoni, Francesco, additional, Rabadan, Raul, additional, and Inghirami, Giorgio, additional

Published
2013
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