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33 results on '"Peola, Silvia"'

1. Targeting CCR7-PI3Kγ overcomes resistance to tyrosine kinase inhibitors in ALK-rearranged lymphoma

Author

Mastini, Cristina, primary, Campisi, Marco, additional, Patrucco, Enrico, additional, Mura, Giulia, additional, Ferreira, Antonio, additional, Costa, Carlotta, additional, Ambrogio, Chiara, additional, Germena, Giulia, additional, Martinengo, Cinzia, additional, Peola, Silvia, additional, Mota, Ines, additional, Vissio, Elena, additional, Molinaro, Luca, additional, Arigoni, Maddalena, additional, Olivero, Martina, additional, Calogero, Raffaele, additional, Prokoph, Nina, additional, Tabbò, Fabrizio, additional, Shoji, Brent, additional, Brugieres, Laurence, additional, Geoerger, Birgit, additional, Turner, Suzanne D., additional, Cuesta-Mateos, Carlos, additional, D’Aliberti, Deborah, additional, Mologni, Luca, additional, Piazza, Rocco, additional, Gambacorti-Passerini, Carlo, additional, Inghirami, Giorgio G., additional, Chiono, Valeria, additional, Kamm, Roger D., additional, Hirsch, Emilio, additional, Koch, Raphael, additional, Weinstock, David M., additional, Aster, Jon C., additional, Voena, Claudia, additional, and Chiarle, Roberto, additional

Published
2023
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2. Dysfunctional Vγ9Vδ2 T cells are negative prognosticators and markers of dysregulated mevalonate pathway activity in chronic lymphocytic leukemia cells

Author

Coscia, Marta, Vitale, Candida, Peola, Silvia, Foglietta, Myriam, Rigoni, Micol, Griggio, Valentina, Castella, Barbara, Angelini, Daniela, Chiaretti, Sabina, Riganti, Chiara, Guarini, Anna, Drandi, Daniela, Ladetto, Marco, Bosia, Amalia, Foà, Robin, Battistini, Luca, Boccadoro, Mario, Fournié, Jean-Jacques, and Massaia, Massimo

Published
2012
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3. CEP-18770: A novel, orally active proteasome inhibitor with a tumor-selective pharmacologic profile competitive with bortezomib

Author

Piva, Roberto, Ruggeri, Bruce, Williams, Michael, Costa, Giulia, Tamagno, Ilaria, Ferrero, Dario, Giai, Valentina, Coscia, Marta, Peola, Silvia, Massaia, Massimo, Pezzoni, Gabriella, Allievi, Cecilia, Pescalli, Nicoletta, Cassin, Mara, di Giovine, Stefano, Nicoli, Paola, de Feudis, Paola, Strepponi, Ivan, Roato, Ilaria, Ferracini, Riccardo, Bussolati, Benedetta, Camussi, Giovanni, Jones-Bolin, Susan, Hunter, Kathryn, Zhao, Hugh, Neri, Antonino, Palumbo, Antonio, Berkers, Celia, Ovaa, Huib, Bernareggi, Alberto, and Inghirami, Giorgio

Published
2008
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4. Abstract LT018: The perivascular niche protects ALK+ lymphoma cells from ALK inhibition through the CCL19/21-CCR7 axis

Author

Mastini, Cristina, primary, Campisi, Marco, additional, Costa, Carlotta, additional, Ambrogio, Chiara, additional, Germena, Giulia, additional, Peola, Silvia, additional, Martinengo, Cinzia, additional, Patrucco, Enrico, additional, Mota, Ines, additional, Arrigoni, Maddalena, additional, Olivero, Martina, additional, Calogero, Raffaele, additional, Chiono, Valeria, additional, Kamm, Roger D., additional, Hirsch, Emilio, additional, Aster, Jon C., additional, Voena, Claudia, additional, and Chiarle, Roberto, additional

Published
2021
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10. Soluble CD157 in pleural effusions: a complementary tool for the diagnosis of malignant mesothelioma

Author

Augeri, Stefania, primary, Capano, Stefania, additional, Morone, Simona, additional, Fissolo, Giulia, additional, Giacomino, Alice, additional, Peola, Silvia, additional, Drace, Zahida, additional, Rapa, Ida, additional, Novello, Silvia, additional, Volante, Marco, additional, Righi, Luisella, additional, Ferrero, Enza, additional, Ortolan, Erika, additional, and Funaro, Ada, additional

Published
2018
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12. Humoral immune responses toward tumor-derived antigens in previously untreated patients with chronic lymphocytic leukemia

Author

Griggio, Valentina, primary, Mandili, Giorgia, additional, Vitale, Candida, additional, Capello, Michela, additional, Macor, Paolo, additional, Serra, Sara, additional, Castella, Barbara, additional, Peola, Silvia, additional, Foglietta, Myriam, additional, Drandi, Daniela, additional, Omedé, Paola, additional, Sblattero, Daniele, additional, Cappello, Paola, additional, Chiarle, Roberto, additional, Deaglio, Silvia, additional, Boccadoro, Mario, additional, Novelli, Francesco, additional, Massaia, Massimo, additional, and Coscia, Marta, additional

Published
2016
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14. The Mevalonate Pathway As a Metabolic Target to Circumvent Multidrug-Resistance in Chronic Lymphocytic Leukemia Cells

Author

Coscia, Marta, primary, Rigoni, Micol, additional, Riganti, Chiara, additional, Campia, Ivana, additional, Vitale, Candida, additional, Griggio, Valentina, additional, Peola, Silvia, additional, Castella, Barbara, additional, Sciancalepore, Patrizia, additional, Drandi, Daniela, additional, Ladetto, Marco, additional, Bosia, Amalia, additional, Boccadoro, Mario, additional, and Massaia, Massimo, additional

Published
2011
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15. Immune Modulation by Zoledronic Acid in Human Myeloma: An Advantageous Cross-Talk between Vγ9Vδ2 T Cells, αβ CD8+ T Cells, Regulatory T Cells, and Dendritic Cells

Author

Castella, Barbara, primary, Riganti, Chiara, additional, Fiore, Francesca, additional, Pantaleoni, Francesca, additional, Canepari, Maria Elisa, additional, Peola, Silvia, additional, Foglietta, Myriam, additional, Palumbo, Antonio, additional, Bosia, Amalia, additional, Coscia, Marta, additional, Boccadoro, Mario, additional, and Massaia, Massimo, additional

Published
2011
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16. The Defective Proliferation of Vgamma9Vdelta2 T Cells to Zoledronic Acid In Chronic Lymphocytic Leukemia (CLL) Is a Powerful Time to First Treatment (TFT) Predictor Associated with the IGHV Mutational Status

Author

Coscia, Marta, primary, Vitale, Candida, additional, Peola, Silvia, additional, Riganti, Chiara, additional, Angelini, Daniela, additional, Foglietta, Myriam, additional, Pantaleoni, Francesca, additional, Matta, Giorgia, additional, Chiaretti, Sabina, additional, Guarini, Anna, additional, Drandi, Daniela, additional, Ladetto, Marco, additional, Bosia, Amalia, additional, Battistini, Luca, additional, Foà, Robin, additional, Boccadoro, Mario, additional, Fournié, Jean-Jacques, additional, and Massaia, Massimo, additional

Published
2010
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17. Identification by Serological Proteome Analysis (SERPA) of Tumor-Associated Antigens Eliciting Antibody Responses In Chronic Lymphocytic Leukemia (CLL)

Author

Coscia, Marta, primary, Capello, Michela, additional, Griggio, Valentina, additional, Linty, Federica, additional, Vitale, Candida, additional, Peola, Silvia, additional, Castella, Barbara, additional, Rigoni, Micol, additional, Drandi, Daniela, additional, Ruggeri, Marina, additional, Omedè, Paola, additional, Ladetto, Marco, additional, Novelli, Franco, additional, Boccadoro, Mario, additional, and Massaia, Massimo, additional

Published
2010
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18. IGHV Unmutated Chronic Lymphocytic Leukemia (CLL) B Cells Are More Susceptible to Spontaneous Apoptosis Than Mutated CLL B Cells and Are Subject to the Anti-Apoptotic Effect of Environmental Signals

Author

Coscia, Marta, primary, Pantaleoni, Francesca, additional, Riganti, Chiara, additional, Vitale, Candida, additional, Rigoni, Micol, additional, Peola, Silvia, additional, Drandi, Daniela, additional, Castella, Barbara, additional, Ruggeri, Marina, additional, Omedè, Paola, additional, Ladetto, Marco, additional, Bosia, Amalia, additional, Boccadoro, Mario, additional, and Massaia, Massimo, additional

Published
2010
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19. Differential Effects of Microenvironmental Elements On Tumor Cells Survival in Chronic Lymphocytic Leukemia Patient Subsets with Good or Poor Prognosis.

Author

Coscia, Marta, primary, Pantaleoni, Francesca, additional, Riganti, Chiara, additional, Rigoni, Micol, additional, Vitale, Candida, additional, Peola, Silvia, additional, Drandi, Daniela, additional, Ladetto, Marco, additional, Bosia, Amalia, additional, Boccadoro, Mario, additional, and Massaia, Massimo, additional

Published
2009
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21. Phenotypic and Functional Features of Vγ9/Vδ2 T Cells in Chronic Lymphocytic Leukemia Are Strongly Correlated with the Mutational Status of the Immunoglobulin Heavy Chain Variable Region (IgVH) and Metabolic Activity of the Mevalonate Pathway in Tumor Cells.

Author

Coscia, Marta, primary, Peola, Silvia, additional, Matta, Giorgia, additional, Pantaleoni, Francesca, additional, Foglietta, Myriam, additional, Angelini, Daniela, additional, Chiaretti, Sabina, additional, Riganti, Chiara, additional, Guarini, Anna, additional, Drandi, Daniela, additional, Ladetto, Marco, additional, Bosia, Amalia, additional, Foà, Robin, additional, Battistini, Luca, additional, Boccadoro, Mario, additional, Fournie, Jean Jacques, additional, and Massaia, Massimo, additional

Published
2007
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25. Generation of anti-tumour activity by OKT3-stimulation in multiple myeloma: in vitro inhibition of autologous haemopoiesis

Author

Attisano, Carmela, primary, Bianchi, Alberto, additional, Montacchini, Laura, additional, Carlesso, Nadia, additional, Peola, Silvia, additional, Bruno, Benedetto, additional, Roux, Viviana, additional, Ferrero, Dario, additional, Gallo, Eugenio, additional, Boccadoro, Mario, additional, Pileri, Alessandro, additional, and Massaia, Massimo, additional

Published
1994
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26. Increased expression of non-functional killer inhibitory receptor CD94 in CD8+ cells of myeloma patients.

Author

Besostri, Barbara, Beggiato, Eloise, Bianchi, Alberto, Mariani, Sara, Coscia, Marta, Peola, Silvia, Foglietta, Myriam, Boccadoro, Mario, Pileri, Alessandro, Moretta, Lorenzo, and Massaia, Massimo

Subjects
MULTIPLE myeloma, GLYCOPROTEINS, T cells, CYTOLOGY, PATIENTS
Abstract

Different MHC class I-specific killer inhibitory receptors (KIRs) are expressed in vivo by a minor fraction of activated memory CD8+ cells. It has been postulated that KIRs may ‘fine-tune’ specific responses by altering their threshold of activation by the TCR–CD3 complex. We have previously shown that, in multiple myeloma (MM) patients, a large fraction of peripheral blood CD8+ cells display the phenotype of chronically activated memory T cells (CD38+, HLA-DR+, CD25-, CD45R0+, CD28-). We investigated the expression of KIRs on MM T cells and determined their possible influence on cytolytic responses elicited via the CD3–TCR complex. The expression of CD94, a molecule that is part of a heterodimeric KIR recognizing the non-classical MHC surface HLA-E molecule, was almost threefold higher in MM T cells than in age-matched normal control subjects (P < 0·0001). CD94 expression was preferentially confined to CD8+ cells but not restricted to activated (HLA-DR+) and/or memory (CD45R0+) T cells. Unlike normal T cells, in which CD94 is assembled with glycoproteins of the NKG2 family to form functional receptors with activating or inhibitory properties, most CD94+ MM T cells were devoid of both the NKG2-A and NKG2-C glycoproteins detected in the inhibitory or activating form respectively. CD94 blockade did not significantly affect either T-cell proliferation or cytotoxic T-lymphocyte generation induced by the myeloma-derived cell lines NCI and RPMI 8226. Similarly, the cytolytic activity induced by direct anti-CD3-mediated targeting of MM T cells to FCR+ P815 target cells was unaffected by the addition of anti-CD94 and/or anti-NKG2-A/C monoclonal antibodies (mAbs). These data indicate that the large majority of MM CD8+ cells do not express a functional CD94 receptor. Thus, their ability to ‘fine-tune’ an appropriate immune response against tumour cells can be impaired. [ABSTRACT FROM AUTHOR]

Published
2000
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27. Detection of Hyperreactive T Cells in Multiple Myeloma by Multivalent Cross-Linking of the CD3/TCR Complex

Author

Massaia, Massimo, Bianchi, Alberto, Attisano, Carmela, Peola, Silvia, Redoglia, Valter, Dianzani, Umberto, and Pileri, Alessandro

Abstract

Cellular immunity was investigated in 43 patients with multiple myeloma (MM) by assessing 3HTdR uptake induced by monocyte-dependent [CD3 monoclonal antibodies (MoAbs), phytohemagglutinin (PHA)] and monocyte-indepen-dent (CD2 MoAbs, ionomycin + phorbolester) stimulations. The former were evaluated in peripheral blood mononuclear cells (PBMNC) and purified T cells; the latter were evaluated in purified T-cell preparations only. MM showed significantly lower PBMNC responses to PHA (P< .001), soluble OKT3 (CD3) (P= .01), and immobilized OKT3 MoAbs (P= .01). On purification of T cells, MM responses were still defective to soluble T112+ T113(CD2) MoAbs (P= .004), phorbol myristate acetate (PMA) plus ionomycin (P <.001), but significantly higher to plastic-immobilized OKT3 (P= .004). In some MM, 3HTdR uptake, interleukin-2 (IL-2) receptor (CD25) expression, and IL-2 production were as high on stimulation with plastic-immobilized OKT3 as that observed in normal subjects under optimal conditions (ie, plastic-immobilized OKT3 plus accessory signals). CD3 hyperreactivity correlated with the number of CD8+HLA-DR+ cells in MM T-cell preparations. MM patients with more than 10% CD8+HLA-DR+cells had significantly higher responses to immobilized OKT3 (P <.001), but lower responses to T112plus T113(P= .01), and PMA plus ionomycin (P =.03) than patients with less than 10% CD8+HLA-DR+cells. Phenotyping of CD45RA (naive) and CD45R0 (memory) expressions in resting MM T cells showed a lower ratio of CD45RA to CD45R0 in both CD4 (P <.05) and CD8 (P< .001) subpopulations. These data indicate that (a) some MM T cells require significantly fewer accessory signals (if any) to express the IL-2 receptor fully, secrete IL-2, and proliferate on multivalent cross-linking of the CD3/TCR complex; and (b) this peculiar state of activation is associated with high HLA-DR expression in CD8+lymphocytes.

Published
1991
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30. Immune Modulation by Zoledronic Acid in Human Myeloma: An Advantageous Cross-Talk between Vγ9Vδ2 T Cells, αβ CD8+ T Cells, Regulatory T Cells, and Dendritic Cells.

Author

Castella, Barbara, Riganti, Chiara, Fiore, Francesca, Pantaleoni, Francesca, Canepari, Maria Elisa, Peola, Silvia, Foglietta, Myriam, Palumbo, Antonio, Bosia, Amalia, Coscia, Marta, Boccadoro, Mario, and Massaia, Massimo

Subjects
*T cells, *IMMUNE response, *BACTERIA, *DENDRITIC cells, *ANTIGEN presenting cells
Abstract

Vγ9Vδ2 T cells play a major role as effector cells of innate immune responses against microbes, stressed cells, and tumor cells. They constitute <5% of PBLs but can be expanded by zoledronic acid (ZA)-treated monocytes or dendritic cells (DC). Much legs is known about their ability to act as cellular adjuvants bridging innate and adaptive immunity, especially in patients with cancer. We have addressed this issue in multiple myeloma (MM), a prototypic disease with several immune dysfunctions that also affect γδ T cells and DC. ZA-treated MM DC were highly effective in activating autologous γδ T cells, even in patients refractory to stimulation with ZA-treated monocytes. ZA inhibited the mevalonate pathway of MM DC and induced the intracellular accumulation and release into the supernatant of isopentenyl pyrophosphate, a selective γδ T cell activator, in sufficient amounts to induce the proliferation of γδ T cells. Immune responses against the tumor-associated Ag survivin (SRV) by MHC-restricted, SRV-specific CD8+ αβ T cells were amplified by the concurrent activation of αβ T cells driven by autologous DC copulsed with ZA and SRV-derived peptides. Ancillary to the isopentenyl pyrophosphate-induced γδ T cell proliferation was the mevalonate-independent ZA ability to directly antagonize regulatory T cells and downregulate PD-L2 expression on the DC cell surface. In conclusion, ZA has multiple immune modulatory activities that allow MM DC to effectively handle the concurrent activation of γδ T cells and MHC-restricted CD8+ αβ antitumor effector T cells. [ABSTRACT FROM AUTHOR]

Published
2011
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31. Humoral immune responses toward tumor-derived antigens in previously untreated patients with chronic lymphocytic leukemia

Author

Silvia Deaglio, Myriam Foglietta, Paola Cappello, Paolo Macor, Daniela Drandi, Candida Vitale, Valentina Griggio, Daniele Sblattero, Giorgia Mandili, Barbara Castella, Mario Boccadoro, Sara Serra, Michela Capello, Massimo Massaia, Roberto Chiarle, Silvia Peola, Paola Omedè, Marta Coscia, Francesco Novelli, Griggio, Valentina, Mandili, Giorgia, Vitale, Candida, Capello, Michela, Macor, Paolo, Serra, Sara, Castella, Barbara, Peola, Silvia, Foglietta, Myriam, Drandi, Daniela, Omedé, Paola, Sblattero, Daniele, Cappello, Paola, Chiarle, Roberto, Deaglio, Silvia, Boccadoro, Mario, Novelli, Francesco, Massaia, Massimo, and Coscia, Marta

Subjects
0301 basic medicine, Proteomics, Humoral responses, Chronic lymphocytic leukemia, Serological proteomics, Apoptosis, Immunogenetics, Lymphocyte Activation, Tumor antigens, Serology, hemic and lymphatic diseases, Humoral responses, chronic lymphocytic leukemia, Humoral response, Lymphocytes, Hematology, biology, DNA-Binding Proteins, Oncology, Disease Progression, Antibody, Research Paper, Alpha-enolase, medicine.medical_specialty, Serological proteomic, 03 medical and health sciences, Antigen, Antigens, Neoplasm, Internal medicine, medicine, Biomarkers, Tumor, Humans, Neoplasm Staging, business.industry, Tumor Suppressor Proteins, Antibody-Dependent Cell Cytotoxicity, Complement System Proteins, medicine.disease, Leukemia, Lymphocytic, Chronic, B-Cell, Immunity, Humoral, Transplantation, 030104 developmental biology, Phosphopyruvate Hydratase, Immunology, Antibody Formation, biology.protein, chronic lymphocytic leukemia, Lymph Nodes, business, Tumor antigen, Progressive disease, Biomarkers
Abstract

// Valentina Griggio 1, 2 , Giorgia Mandili 2, 3 , Candida Vitale 1, 2 , Michela Capello 2, 3 , Paolo Macor 4 , Sara Serra 5 , Barbara Castella 1, 2, 3 , Silvia Peola 2, 3 , Myriam Foglietta 1, 2, 3 , Daniela Drandi 1, 2 , Paola Omede 1 , Daniele Sblattero 4 , Paola Cappello 2, 3, 6 , Roberto Chiarle 2, 3, 7 , Silvia Deaglio 5 , Mario Boccadoro 1, 2 , Francesco Novelli 2, 3, 6, 8 , Massimo Massaia 1, 2, 3 , Marta Coscia 1, 2 1 Division of Hematology, University of Torino, AOU Citta della Salute e della Scienza di Torino, Torino, Italy 2 Department of Molecular Biotechnology and Health Sciences, University of Torino, Torino, Italy 3 Center for Experimental Research and Medical Studies (CeRMS), AOU Citta della Salute e della Scienza di Torino, Torino, Italy 4 Department of Life Sciences – University of Trieste, Trieste, Italy 5 Department of Medical Sciences, University of Torino and Immunogenetics Unit - Human Genetics Foundation (HuGeF), Torino, Italy 6 Molecular Biotechnology Center, Torino, Italy 7 Department of Pathology, Boston Children’s Hospital, Boston, Massachusetts, USA 8 Service of Immunogenetics and Transplantation, AOU Citta della Salute e della Scienza di Torino, Torino, Italy Correspondence to: Marta Coscia, email: marta.coscia@unito.it Keywords: chronic lymphocytic leukemia, humoral responses, tumor antigens, serological proteomics, alpha-enolase Received: July 13, 2016 Accepted: November 22, 2016 Published: November 30, 2016 ABSTRACT In chronic lymphocytic leukemia (CLL) the occurrence and the impact of antibody responses toward tumor-derived antigens are largely unexplored. Our serological proteomic data show that antibodies toward 47 identified antigens are detectable in 29 out of 35 patients (83%) with untreated CLL. The glycolytic enzyme alpha-enolase (ENO1) is the most frequently recognized antigen (i.e. 54% of CLL sera). We show that ENO1 is upregulated in the proliferating B-cell fraction of CLL lymph nodes. In CLL cells of the peripheral blood, ENO1 is exclusively expressed at the intracellular level, whereas it is exposed on the surface of apoptotic leukemic cells. From the clinical standpoint, patients with progressive CLL show a higher number of antigen recognitions compared to patients with stable disease. Consistently, the anti-ENO1 antibodies are prevalent in sera from patients with progressive disease and their presence is predictive of a shorter time to first treatment. This clinical inefficacy associates with the inability of patients’ sera to trigger complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity against leukemic cells. Together, these results indicate that antibody responses toward tumor-derived antigens are frequently detectable in sera from patients with CLL, but they are expression of a disrupted immune system and unable to hamper disease progression.

Published
2016

32. Humoral immune responses toward tumor-derived antigens in previously untreated patients with chronic lymphocytic leukemia.

Author

Griggio V, Mandili G, Vitale C, Capello M, Macor P, Serra S, Castella B, Peola S, Foglietta M, Drandi D, Omedé P, Sblattero D, Cappello P, Chiarle R, Deaglio S, Boccadoro M, Novelli F, Massaia M, and Coscia M

Subjects
Antibody Formation immunology, Antibody-Dependent Cell Cytotoxicity, Antigens, Neoplasm metabolism, Apoptosis genetics, Apoptosis immunology, Biomarkers, Biomarkers, Tumor immunology, Biomarkers, Tumor metabolism, Complement System Proteins immunology, Complement System Proteins metabolism, DNA-Binding Proteins immunology, DNA-Binding Proteins metabolism, Disease Progression, Humans, Leukemia, Lymphocytic, Chronic, B-Cell blood, Leukemia, Lymphocytic, Chronic, B-Cell diagnosis, Lymph Nodes immunology, Lymph Nodes metabolism, Lymphocyte Activation immunology, Lymphocytes immunology, Lymphocytes metabolism, Neoplasm Staging, Phosphopyruvate Hydratase immunology, Phosphopyruvate Hydratase metabolism, Proteomics methods, Tumor Suppressor Proteins immunology, Tumor Suppressor Proteins metabolism, Antigens, Neoplasm immunology, Immunity, Humoral, Leukemia, Lymphocytic, Chronic, B-Cell immunology
Abstract

In chronic lymphocytic leukemia (CLL) the occurrence and the impact of antibody responses toward tumor-derived antigens are largely unexplored. Our serological proteomic data show that antibodies toward 47 identified antigens are detectable in 29 out of 35 patients (83%) with untreated CLL. The glycolytic enzyme alpha-enolase (ENO1) is the most frequently recognized antigen (i.e. 54% of CLL sera). We show that ENO1 is upregulated in the proliferating B-cell fraction of CLL lymph nodes. In CLL cells of the peripheral blood, ENO1 is exclusively expressed at the intracellular level, whereas it is exposed on the surface of apoptotic leukemic cells.From the clinical standpoint, patients with progressive CLL show a higher number of antigen recognitions compared to patients with stable disease. Consistently, the anti-ENO1 antibodies are prevalent in sera from patients with progressive disease and their presence is predictive of a shorter time to first treatment. This clinical inefficacy associates with the inability of patients' sera to trigger complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity against leukemic cells.Together, these results indicate that antibody responses toward tumor-derived antigens are frequently detectable in sera from patients with CLL, but they are expression of a disrupted immune system and unable to hamper disease progression.

Published
2017
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33. The anaplastic lymphoma kinase as an oncogene in solid tumors.

Author

Voena C, Peola S, and Chiarle R

Subjects
Anaplastic Lymphoma Kinase, Animals, Antineoplastic Agents pharmacology, Humans, Neoplasms drug therapy, Protein Kinase Inhibitors pharmacology, Receptor Protein-Tyrosine Kinases antagonists & inhibitors, Neoplasms enzymology, Neoplasms genetics, Oncogenes, Receptor Protein-Tyrosine Kinases genetics
Abstract

Twenty years ago anaplastic lymphoma kinase (ALK) was discovered in anaplastic large cell lymphoma (ALCL), but the interest in ALK as an oncogene grew only in recent years when ALK rearrangements were reported as recurrent genetic lesions in lung carcinoma and activating single point mutations were described in neuroblastoma. In this review we will describe the main features of ALK-rearranged solid tumors, with particular emphasis to NSCLC and neuroblastoma. We will discuss the numerous in vitro and in vivo studies that confirmed ALK as the driver oncogene in these tumors and the achievements in clinical settings with ALK inhibitors that validated ALK as a therapeutic target. We will finally end with the description of putative innovative therapeutic approaches that are on going to overcome acquired resistance that invariably occurs in crizotinib treated NSCLC patients or intrinsic resistance to crizotinb therapy reported in neuroblastoma.

Published
2015
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