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  1. AU="Bergaggio, Elisa"
  2. AU="Yu, Haizong"
  3. AU="Corey M Peak"
  4. AU="Larsen, Mona L.V."
  5. AU=Yang Ying
  6. AU="Dekić Rozman, Svjetlana"
  7. AU="Rowe, Ashlee H"
  8. AU="Perrevoort, A"
  9. AU="Bhardwaj, Shashank"
  10. AU=Li Bo
  11. AU=Ramani Rama
  12. AU="Várnai-Händel, Alinda"
  13. AU="Kucher, Michael"
  14. AU="Blucher, E."
  15. AU="Muffels, Ruud"
  16. AU="Roufos, I"
  17. AU="Ammad Ahmad Farooqi"
  18. AU="Zawadka-Kunikowska, Monika"
  19. AU="Young, A P"
  20. AU="Danielle M. Matriano"
  21. AU="Ancona, Jennifer"
  22. AU="Abdallah G. Kfoury"
  23. AU="Zaeske, C"
  24. AU="Hammerich, Kristoff"
  25. AU="Paul J. Burgess"
  26. AU="Valek, Lucie"
  27. AU="Mandal, Surajit"
  28. AU="Krumm, Laura"
  29. AU="Shimura, Hidetoshi"
  30. AU="Munguia-Lopez, Jose Gil"
  31. AU="Eysert, Fanny"
  32. AU="Qazi Arisa, Fakhar Ali"
  33. AU="Guan, Yunshan"
  34. AU="Ayachi, Jihene"
  35. AU="Boulvard Chollet, Xavier L E"
  36. AU="Kwon, Sohee"
  37. AU=Fra-Bido Sigrid
  38. AU="Delgado, Teresa Cardoso"
  39. AU="Judy Ly"
  40. AU="E Richtig"
  41. AU="Jones, D. C."
  42. AU="Revillet, Hélène" AU="Revillet, Hélène"
  43. AU="Lee, Ji Ye"
  44. AU="Yoshinaga, Kazuaki"
  45. AU="Moturi, Krishna"
  46. AU="Loizeau, J"
  47. AU="Gentry, Matthew S"
  48. AU="Drury, Lucy S"
  49. AU="Caraman, Irina"

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  1. Artikel: Wild-Type IDH Enzymes as Actionable Targets for Cancer Therapy.

    Bergaggio, Elisa / Piva, Roberto

    Cancers

    2019  Band 11, Heft 4

    Abstract: Isocitrate dehydrogenases (IDHs) are enzymes that catalyze the oxidative decarboxylation of isocitrate, producing α-ketoglutarate (αKG) and ... ...

    Abstract Isocitrate dehydrogenases (IDHs) are enzymes that catalyze the oxidative decarboxylation of isocitrate, producing α-ketoglutarate (αKG) and CO
    Sprache Englisch
    Erscheinungsdatum 2019-04-19
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers11040563
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel: Directed evolution-based discovery of ligands for in vivo restimulation of CAR-T cells.

    Ma, Leyuan / Ramasubramanian, Ranjani / Mehta, Naveen / Cossette, Benjamin / Morgan, Duncan / Sukaj, Ina / Bergaggio, Elisa / Kadauke, Stephan / Myers, Regina / Paruzzo, Luca / Ghilardi, Guido / Grzywa, Tomasz / Cozzone, Austin / Schuster, Stephen / Frey, Noelle / Zhang, Libin / Yousefpour, Parisa / Abraham, Wuhbet / Suh, Heikyung /
    Ruella, Marco / Grupp, Stephan / Chiarle, Roberto / Wittrup, K Dane / Irvine, Darrell J

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Chimeric antigen receptor (CAR) T cell therapy targeting CD19 elicits remarkable clinical efficacy in B-cell malignancies, but many patients relapse due to failed expansion and/or progressive loss of CAR-T cells. We recently reported a strategy to ... ...

    Abstract Chimeric antigen receptor (CAR) T cell therapy targeting CD19 elicits remarkable clinical efficacy in B-cell malignancies, but many patients relapse due to failed expansion and/or progressive loss of CAR-T cells. We recently reported a strategy to potently restimulate CAR-T cells in vivo, enhancing their functionality by administration of a vaccine-like stimulus comprised of surrogate peptide ligands for a CAR linked to a lymph node-targeting amphiphilic PEG-lipid (termed CAR-T-vax). Here, we demonstrate a general strategy to generate and optimize peptide mimotopes enabling CAR-T-vax generation for any CAR. Using the clinical CD19 CAR FMC63 as a test case, we employed yeast surface display to identify peptide binders to soluble IgG versions of FMC63, which were subsequently affinity matured by directed evolution. CAR-T vaccines using these optimized mimotopes triggered marked expansion of both murine CD19 CAR-T cells in a syngeneic model and human CAR-T cells in a humanized mouse model of B cell acute lymphoblastic leukemia (B-ALL), and enhanced control of leukemia progression. This approach thus enables vaccine boosting to be applied to any clinically-relevant CAR-T cell product.
    Sprache Englisch
    Erscheinungsdatum 2024-04-30
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.04.16.589780
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: ALK inhibitors increase ALK expression and sensitize neuroblastoma cells to ALK.CAR-T cells.

    Bergaggio, Elisa / Tai, Wei-Tien / Aroldi, Andrea / Mecca, Carmen / Landoni, Elisa / Nüesch, Manuel / Mota, Ines / Metovic, Jasna / Molinaro, Luca / Ma, Leyuan / Alvarado, Diego / Ambrogio, Chiara / Voena, Claudia / Blasco, Rafael B / Li, Tongqing / Klein, Daryl / Irvine, Darrell J / Papotti, Mauro / Savoldo, Barbara /
    Dotti, Gianpietro / Chiarle, Roberto

    Cancer cell

    2023  Band 41, Heft 12, Seite(n) 2100–2116.e10

    Abstract: Selection of the best tumor antigen is critical for the therapeutic success of chimeric antigen receptor (CAR) T cells in hematologic malignancies and solid tumors. The anaplastic lymphoma kinase (ALK) receptor is expressed by most neuroblastomas while ... ...

    Abstract Selection of the best tumor antigen is critical for the therapeutic success of chimeric antigen receptor (CAR) T cells in hematologic malignancies and solid tumors. The anaplastic lymphoma kinase (ALK) receptor is expressed by most neuroblastomas while virtually absent in most normal tissues. ALK is an oncogenic driver in neuroblastoma and ALK inhibitors show promising clinical activity. Here, we describe the development of ALK.CAR-T cells that show potent efficacy in monotherapy against neuroblastoma with high ALK expression without toxicity. For neuroblastoma with low ALK expression, combination with ALK inhibitors specifically potentiates ALK.CAR-T cells but not GD2.CAR-T cells. Mechanistically, ALK inhibitors impair tumor growth and upregulate the expression of ALK, thereby facilitating the activity of ALK.CAR-T cells against neuroblastoma. Thus, while neither ALK inhibitors nor ALK.CAR-T cells will likely be sufficient as monotherapy in neuroblastoma with low ALK density, their combination specifically enhances therapeutic efficacy.
    Mesh-Begriff(e) Humans ; Anaplastic Lymphoma Kinase/genetics ; Anaplastic Lymphoma Kinase/metabolism ; Neuroblastoma/drug therapy ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Protein Kinase Inhibitors/pharmacology ; Protein Kinase Inhibitors/therapeutic use ; Antigens, Neoplasm ; T-Lymphocytes ; Cell Line, Tumor
    Chemische Substanzen Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Protein Kinase Inhibitors ; Antigens, Neoplasm
    Sprache Englisch
    Erscheinungsdatum 2023-11-30
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccell.2023.11.004
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: ALK peptide vaccination restores the immunogenicity of ALK-rearranged non-small cell lung cancer.

    Mota, Ines / Patrucco, Enrico / Mastini, Cristina / Mahadevan, Navin R / Thai, Tran C / Bergaggio, Elisa / Cheong, Taek-Chin / Leonardi, Giulia / Karaca-Atabay, Elif / Campisi, Marco / Poggio, Teresa / Menotti, Matteo / Ambrogio, Chiara / Longo, Dario L / Klaeger, Susan / Keshishian, Hasmik / Sztupinszki, Zsófia M / Szallasi, Zoltan / Keskin, Derin B /
    Duke-Cohan, Jonathan S / Reinhold, Bruce / Carr, Steven A / Wu, Catherine J / Moynihan, Kelly D / Irvine, Darrell J / Barbie, David A / Reinherz, Ellis L / Voena, Claudia / Awad, Mark M / Blasco, Rafael B / Chiarle, Roberto

    Nature cancer

    2023  Band 4, Heft 7, Seite(n) 1016–1035

    Abstract: Anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer (NSCLC) is treated with ALK tyrosine kinase inhibitors (TKIs), but the lack of activity of immune checkpoint inhibitors (ICIs) is poorly understood. Here, we identified immunogenic ... ...

    Abstract Anaplastic lymphoma kinase (ALK)-rearranged non-small cell lung cancer (NSCLC) is treated with ALK tyrosine kinase inhibitors (TKIs), but the lack of activity of immune checkpoint inhibitors (ICIs) is poorly understood. Here, we identified immunogenic ALK peptides to show that ICIs induced rejection of ALK
    Mesh-Begriff(e) Mice ; Animals ; Humans ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Anaplastic Lymphoma Kinase/genetics ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Cancer Vaccines/therapeutic use ; Receptor Protein-Tyrosine Kinases/therapeutic use ; CD8-Positive T-Lymphocytes/pathology ; Vaccines, Subunit/therapeutic use ; Protein Kinase Inhibitors/pharmacology ; Protein-Tyrosine Kinases/therapeutic use ; Mice, Transgenic ; Vaccination
    Chemische Substanzen Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Cancer Vaccines ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Vaccines, Subunit ; Protein Kinase Inhibitors ; Protein-Tyrosine Kinases (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2023-07-10
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-023-00591-2
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel: ALK expression favorably impacts the prognosis of

    Osella-Abate, Simona / Mereu, Elisabetta / Pellegrino, Elisa / Bergaggio, Elisa / Ribero, Simone / Bertero, Luca / Lisa, Francesco / Fierro, Maria Teresa / Giulio Papotti, Mauro / Piva, Roberto

    Oncology letters

    2018  Band 16, Heft 6, Seite(n) 7091–7096

    Abstract: Recent studies reported the expression of anaplastic lymphoma kinase (ALK) in malignant melanomas. The aim of this study was to investigate whether ALK expression is associated with specific clinical and molecular characteristics of melanoma metastases, ... ...

    Abstract Recent studies reported the expression of anaplastic lymphoma kinase (ALK) in malignant melanomas. The aim of this study was to investigate whether ALK expression is associated with specific clinical and molecular characteristics of melanoma metastases, and to evaluate its correlation with survival outcomes. Seventy-one patients with metastatic melanoma were investigated. Clinical features and survival outcomes were analyzed and correlated to ALK expression, as detected by immunohistochemistry and reverse transcription-quantitative polymerase chain reaction, and to the mutational status of
    Sprache Englisch
    Erscheinungsdatum 2018-10-09
    Erscheinungsland Greece
    Dokumenttyp Journal Article
    ZDB-ID 2573196-8
    ISSN 1792-1082 ; 1792-1074
    ISSN (online) 1792-1082
    ISSN 1792-1074
    DOI 10.3892/ol.2018.9560
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: IDH2 inhibition enhances proteasome inhibitor responsiveness in hematological malignancies.

    Bergaggio, Elisa / Riganti, Chiara / Garaffo, Giulia / Vitale, Nicoletta / Mereu, Elisabetta / Bandini, Cecilia / Pellegrino, Elisa / Pullano, Verdiana / Omedè, Paola / Todoerti, Katia / Cascione, Luciano / Audrito, Valentina / Riccio, Anna / Rossi, Antonio / Bertoni, Francesco / Deaglio, Silvia / Neri, Antonino / Palumbo, Antonio / Piva, Roberto

    Blood

    2018  Band 133, Heft 2, Seite(n) 156–167

    Abstract: Proteasome inhibitors (PI) are extensively used for the therapy of multiple myeloma (MM) and mantle cell lymphoma. However, patients continuously relapse or are intrinsically resistant to this class of drugs. Here, to identify targets that synergize with ...

    Abstract Proteasome inhibitors (PI) are extensively used for the therapy of multiple myeloma (MM) and mantle cell lymphoma. However, patients continuously relapse or are intrinsically resistant to this class of drugs. Here, to identify targets that synergize with PI, we carried out a functional screening in MM cell lines using a short hairpin RNA library against cancer driver genes. Isocitrate dehydrogenase 2 (
    Mesh-Begriff(e) Animals ; Apoptosis ; Cell Proliferation ; Cytokines/antagonists & inhibitors ; Cytokines/genetics ; Drug Resistance, Neoplasm ; Hematologic Neoplasms/drug therapy ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/pathology ; Humans ; Isocitrate Dehydrogenase/antagonists & inhibitors ; Isocitrate Dehydrogenase/genetics ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Nicotinamide Phosphoribosyltransferase/antagonists & inhibitors ; Nicotinamide Phosphoribosyltransferase/genetics ; Oligopeptides/pharmacology ; Proteasome Inhibitors/pharmacology ; RNA, Small Interfering/genetics ; Sirtuin 3/antagonists & inhibitors ; Sirtuin 3/genetics ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
    Chemische Substanzen Cytokines ; Oligopeptides ; Proteasome Inhibitors ; RNA, Small Interfering ; carfilzomib (72X6E3J5AR) ; IDH2 protein, human (EC 1.1.1.41) ; Isocitrate Dehydrogenase (EC 1.1.1.41) ; Nicotinamide Phosphoribosyltransferase (EC 2.4.2.12) ; nicotinamide phosphoribosyltransferase, human (EC 2.4.2.12) ; SIRT3 protein, human (EC 3.5.1.-) ; Sirtuin 3 (EC 3.5.1.-)
    Sprache Englisch
    Erscheinungsdatum 2018-11-19
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2018-05-850826
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Identification of a new subclass of ALK-negative ALCL expressing aberrant levels of ERBB4 transcripts.

    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

    Blood

    2015  Band 127, Heft 2, Seite(n) 221–232

    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 ... ...

    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.
    Mesh-Begriff(e) 5' Untranslated Regions ; Anaplastic Lymphoma Kinase ; Animals ; Codon, Nonsense ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Lymphoma, Large-Cell, Anaplastic/classification ; Lymphoma, Large-Cell, Anaplastic/genetics ; Lymphoma, Large-Cell, Anaplastic/pathology ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Mice, Transgenic ; Molecular Sequence Data ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; NIH 3T3 Cells ; RNA, Messenger/metabolism ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, ErbB-4/genetics ; Receptor, ErbB-4/metabolism
    Chemische Substanzen 5' Untranslated Regions ; Codon, Nonsense ; Mutant Proteins ; RNA, Messenger ; ALK protein, human (EC 2.7.10.1) ; Alk protein, mouse (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; ERBB4 protein, human (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; Receptor, ErbB-4 (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2015-10-13
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2014-12-614503
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: Identification of a 3-gene model as a powerful diagnostic tool for the recognition of ALK-negative anaplastic large-cell lymphoma.

    Agnelli, Luca / Mereu, Elisabetta / Pellegrino, Elisa / Limongi, Tania / Kwee, Ivo / Bergaggio, Elisa / Ponzoni, Maurilio / Zamò, Alberto / Iqbal, Javeed / Piccaluga, Pier Paolo / Neri, Antonino / Chan, Wing C / Pileri, Stefano / Bertoni, Francesco / Inghirami, Giorgio / Piva, Roberto

    Blood

    2012  Band 120, Heft 6, Seite(n) 1274–1281

    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 ... ...

    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.
    Mesh-Begriff(e) Adult ; Anaplastic Lymphoma Kinase ; Biomarkers, Tumor/genetics ; Biomarkers, Tumor/isolation & purification ; Biomarkers, Tumor/physiology ; Case-Control Studies ; Diagnosis, Differential ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Genes, Neoplasm/physiology ; Humans ; Lymphoma, Large-Cell, Anaplastic/diagnosis ; Lymphoma, Large-Cell, Anaplastic/genetics ; Microarray Analysis ; Models, Statistical ; Molecular Diagnostic Techniques/methods ; Predictive Value of Tests ; Prognosis ; Receptor Protein-Tyrosine Kinases/genetics ; Receptor Protein-Tyrosine Kinases/metabolism
    Chemische Substanzen Biomarkers, Tumor ; ALK protein, human (EC 2.7.10.1) ; Anaplastic Lymphoma Kinase (EC 2.7.10.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
    Sprache Englisch
    Erscheinungsdatum 2012-06-27
    Erscheinungsland United States
    Dokumenttyp Evaluation Study ; Journal Article ; Research Support, Non-U.S. Gov't ; Validation Study
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2012-01-405555
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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