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1. 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

2. Anaplastic large cell lymphoma. Sem. Diagn. Pathol

Author

Inghirami G, European T. Cell Lymphoma Study Group: […, R. Chiarle, G. Cuccuru, B. Martinoglio, E. Medico, E. Pellegrino, R. Piva M.L. Ruberto, A. Fornari, D. Novero, M. Chilosi, A. Zamó, F. Facchetti, S. Lonardi, A. De Chiara, F. Fulciniti, C. Doglioni, M. Ponzoni, L. Agnelli, A. Neri, K. Todoerti, B. Falini, E. Tiacci, P. Van Loo, T. Tousseyn, C. De Wolf Peeters, E. Geissinger, H.K. Muller Hermelink, A. Rosenwald, M.A. Piris MA, M.E. Rodriguez, PILERI, STEFANO, AGOSTINELLI, CLAUDIO, PICCALUGA, PIER PAOLO, Inghirami G, Pileri S A, European T-Cell Lymphoma Study Group: […, R. Chiarle, G. Cuccuru, B. Martinoglio, E. Medico, E. Pellegrino, R. Piva ML. Ruberto, A. Fornari, D. Novero, M. Chilosi, A. Zamó, F. Facchetti, S. Lonardi, A. De Chiara, F. Fulciniti, C. Doglioni, M. Ponzoni, L. Agnelli, A. Neri, K. Todoerti, C. Agostinelli, PP. Piccaluga, B. Falini, E. Tiacci, P. Van Loo, T. Tousseyn, C. De Wolf-Peeter, E. Geissinger, HK. Muller-Hermelink, A. Rosenwald, MA. Piris MA, ME.Rodriguez, and …]

Subjects
Peripheral T-cell lymphoma (PTCL), Chimeric fusion protein, Phenotype, Signaling pathways, Molecular biology, hemic and lymphatic diseases, Anaplastic large-cell lymphoma (ALCL), Anaplastic lymphoma kinase (ALK), Immunohistochemistry
Abstract

The concept of anaplastic large-cell lymphoma (ALCL) has changed over the years because of a stream of new information and novel understanding regarding the cell of origin, biology, genetics, and clinical features of these neoplasms. This new information has led to the current classification proposed by the expert reviewers of the World Health Organization. The objective of this review is to present the most updated information on the cytologic and histologic features of these entities, with a special reference to diagnostic algorithms. A detailed description of the genetic aberrations and the pathogenetic mechanisms leading to transformation is presented. The clinical features of ALCL and novel tailored strategies are briefly illustrated

Published
2011

4. 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

5. 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

6. Identification of a 3-gene model as a powerful diagnostic tool for the recognition of ALK-negative anaplastic large-cell lymphoma

Author

Agnelli L., Mereu E., Pellegrino E., Limongi T., Kwee I., Bergaggio E., Ponzoni M., Zamò A., Iqbal J., Neri A., Chan W. C., Bertoni F., Inghirami G., Piva R., European T. Cell Lymphoma Study G.r.o.u.p. Barreca A., Cuccuru G., Medico E., Spaccarotella E., Scarfò I., Fornari A., Ferreri C., Novero D., Chilosi M., Facchetti F., Lonardi S., De Chiara A., Fulciniti F., Doglioni C., Todoerti K., Falini B., Tiacci E., Van Loo P., Tousseyn T., De Wolf Peeters C., Geissinger E., Muller Hermelink H. K., Rosenwald A., Piris M. A., Rodriguez M. E., Boi M., PICCALUGA, PIER PAOLO, PILERI, STEFANO, AGOSTINELLI, CLAUDIO, Agnelli L., Mereu E., Pellegrino E., Limongi T., Kwee I., Bergaggio E., Ponzoni M., Zamò A., Iqbal J., Piccaluga P.P., Neri A., Chan W.C., Pileri S., Bertoni F., Inghirami G., Piva R., European T-Cell Lymphoma Study Group. Barreca A., Cuccuru G., Medico E., Spaccarotella E., Scarfò I., Fornari A., Ferreri C., Novero D., Chilosi M., Facchetti F., Lonardi S., De Chiara A., Fulciniti F., Doglioni C., Todoerti K., Agostinelli C., Falini B., Tiacci E., Van Loo P., Tousseyn T., De Wolf-Peeters C., Geissinger E., Muller-Hermelink H.K., Rosenwald A., Piris M.A., Rodriguez M.E., Boi M., Agnelli, L, Mereu, E, Pellegrino, E, Limongi, T, Kwee, I, Bergaggio, E, Ponzoni, Maurilio, Zamo, A, Iqbal, J, Piccaluga, Pp, Neri, A, Chan, Wc, Pileri, S, Bertoni, F, Inghirami, G, Piva, R, European T., Cell Lymphoma Study Grp, and Doglioni, Claudio

Subjects
Lymphoma, Bioinformatics, Adult, Biomarkers, Tumor, Case-Control Studies, Diagnosis, Differential, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Humans, Lymphoma, Large-Cell, Anaplastic, Microarray Analysis, Models, Statistical, Molecular Diagnostic Techniques, Predictive Value of Tests, Prognosis, Receptor Protein-Tyrosine Kinases, Genes, Neoplasm, Immunology, Biochemistry, Hematology, Cell Biology, GENE-EXPRESSION ANALYSIS, Models, hemic and lymphatic diseases, PERIPHERAL T-CELL, Diagnosis, Anaplastic, Anaplastic lymphoma kinase, Anaplastic Lymphoma Kinase, Anaplastic large-cell lymphoma, Tumor, Not Otherwise Specified, Statistical, CANCER, Large-Cell, NEOPLASMS, Computational biology, ABERRATIONS, PROFILE, CLASSIFICATION, HODGKIN-LYMPHOMA, KINASE, medicine, TRANSLOCATIONS, Neoplastic, business.industry, Microarray analysis techniques, Large cell, medicine.disease, Gene expression profiling, Gene Expression Regulation, Genes, Differential, Neoplasm, Differential diagnosis, business, Biomarkers
Abstract

Anaplastic large-cell lymphomas (ALCLs) are a group of clinically and biologically heterogeneous diseases including the ALK(+) and ALK(-) systemic forms. Whereas ALK(+) ALCLs are molecularly characterized and can be readily diagnosed, specific immunophenotypic or genetic features to define ALK(-) ALCL are missing, and their distinction from other T-cell non-Hodgkin lymphomas (T-NHLs) remains controversial. In the present study, we undertook a transcriptional profiling meta-analysis of 309 cases, including ALCL and other primary T-NHL samples. Pathway discovery and prediction analyses defined a minimum set of genes capable of recognizing ALK(-) ALCL. Application of quantitative RT-PCR in independent datasets from cryopreserved and formalin-fixed paraffin-embedded samples validated a 3-gene model (TNFRSF8, BATF3, and TMOD1) able to successfully separate ALK(-) ALCL from peripheral T-cell lymphoma not otherwise specified, with overall accuracy near 97%. In conclusion, our data justify the possibility of translating quantitative RT-PCR protocols to routine clinical settings as a new approach to objectively dissect T-NHL and to select more appropriate therapeutic protocols. (Blood. 2012;120(6):1274-1281) Anaplastic large-cell lymphomas (ALCLs) are a group of clinically andbiologically heterogeneous diseases including the ALK(+) and ALK(-) systemicforms. Whereas ALK(+) ALCLs are molecularly characterized and can be readilydiagnosed, specific immunophenotypic or genetic features to define ALK(-) ALCLare missing, and their distinction from other T-cell non-Hodgkin lymphomas(T-NHLs) remains controversial. In the present study, we undertook atranscriptional profiling meta-analysis of 309 cases, including ALCL and otherprimary T-NHL samples. Pathway discovery and prediction analyses defined aminimum set of genes capable of recognizing ALK(-) ALCL. Application ofquantitative RT-PCR in independent datasets from cryopreserved and formalin-fixedparaffin-embedded samples validated a 3-gene model (TNFRSF8, BATF3, and TMOD1)able to successfully separate ALK(-) ALCL from peripheral T-cell lymphoma nototherwise specified, with overall accuracy near 97%. In conclusion, our datajustify the possibility of translating quantitative RT-PCR protocols to routineclinical settings as a new approach to objectively dissect T-NHL and to selectmore appropriate therapeutic protocols

Published
2012

7. 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

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