15 results on '"Agostinelli, Claudio"'
Search Results
2. A three-gene signature based on MYC, BCL-2 and NFKBIA improves risk stratification in diffuse large B-cell lymphoma
- Author
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Derenzini, Enrico, Mazzara, Saveria, Melle, Federica, Motta, Giovanna, Fabbri, Marco, Bruna, Riccardo, Agostinelli, Claudio, Cesano, Alessandra, Corsini, Chiara Antonia, Chen, Ning, Righi, Simona, Sabattini, Elena, Chiappella, Annalisa, Calleri, Angelica, Fiori, Stefano, Tabanelli, Valentina, Cabras, Antonello, Pruneri, Giancarlo, Vitolo, Umberto, Gianni, Alessandro Massimo, Rambaldi, Alessandro, Corradini, Paolo, Zinzani, Pier Luigi, Tarella, Corrado, and Pileri, Stefano
- Subjects
Proto-Oncogene Proteins c-myc ,NF-KappaB Inhibitor alpha ,Proto-Oncogene Proteins c-bcl-2 ,Gene Expression Profiling ,Antineoplastic Combined Chemotherapy Protocols ,Proto-Oncogene Proteins c-bcl-6 ,Humans ,Lymphoma, Large B-Cell, Diffuse ,Prognosis ,Risk Assessment ,Article - Abstract
Recent randomized trials focused on gene expression-based determination of the cell of origin in diffuse large B-cell lymphoma could not show significant improvements by adding novel agents to standard chemoimmunotherapy. The aim of this study was the identification of a gene signature able to refine current prognostication algorithms and applicable to clinical practice. Here we used a targeted gene expression profiling panel combining the Lymph2Cx signature for cell of origin classification with additional targets including MYC, BCL-2 and NFKBIA, in 186 patients from two randomized trials (discovery cohort) (clinicaltrials gov. Identifier: NCT00355199 and NCT00499018). Data were validated in three independent series (two large public datasets and a real-life cohort). By integrating the cell of origin, MYC/BCL-2 double expressor status and NFKBIA expression, we defined a three-gene signature combining MYC, BCL-2 and NFKBIA (MBN-signature), which outperformed the MYC/BCL-2 double expressor status in multivariate analysis, and allowed further risk stratification within the germinal center B-cell/unclassified subset. The high-risk (MBN Sig-high) subgroup identified the vast majority of double hit cases and a significant fraction of activated B-cell-derived diffuse large B-cell lymphomas. These results were validated in three independent series including a cohort from the REMoDL-B trial, where, in an exploratory ad hoc analysis, the addition of bortezomib in the MBN Sig-high subgroup provided a progression free survival advantage compared with standard chemoimmunotherapy. These data indicate that a simple three-gene signature based on MYC, BCL-2 and NFKBIA could refine the prognostic stratification in diffuse large B-cell lymphoma, and might be the basis for future precision-therapy approaches.
- Published
- 2020
3. Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target
- Author
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Sapienza, Maria Rosaria, primary, Abate, Francesco, additional, Melle, Federica, additional, Orecchioni, Stefania, additional, Fuligni, Fabio, additional, Etebari, Maryam, additional, Tabanelli, Valentina, additional, Laginestra, Maria Antonella, additional, Pileri, Alessandro, additional, Motta, Giovanna, additional, Rossi, Maura, additional, Agostinelli, Claudio, additional, Sabattini, Elena, additional, Pimpinelli, Nicola, additional, Truni, Mauro, additional, Falini, Brunangelo, additional, Cerroni, Lorenzo, additional, Talarico, Giovanna, additional, Piccioni, Rossana, additional, Amente, Stefano, additional, Indio, Valentina, additional, Tarantino, Giuseppe, additional, Brundu, Francesco, additional, Paulli, Marco, additional, Berti, Emilio, additional, Facchetti, Fabio, additional, Dellino, Gaetano Ivan, additional, Bertolini, Francesco, additional, Tripodo, Claudio, additional, Rabadan, Raul, additional, and Pileri, Stefano A., additional
- Published
- 2018
- Full Text
- View/download PDF
4. Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target
- Author
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Fabio Facchetti, Emilio Berti, Claudio Tripodo, Maryam Etebari, Giovanna Motta, Nicola Pimpinelli, Fabio Fuligni, Stefano Pileri, Gaetano Ivan Dellino, Alessandro Pileri, Claudio Agostinelli, Valentina Indio, Marco Paulli, Stefania Orecchioni, Stefano Amente, Federica Melle, Giovanna Talarico, Maria Antonella Laginestra, Giuseppe Tarantino, Francesco Bertolini, Maura Rossi, Elena Sabattini, Francesco Abate, Raul Rabadan, Valentina Tabanelli, Lorenzo Cerroni, Francesco Gavino Brundu, Mauro Truni, Rossana Piccioni, Maria Rosaria Sapienza, Brunangelo Falini, Sapienza M.R., Abate F., Melle F., Orecchioni S., Fuligni F., Etebari M., Tabanelli V., Laginestra M.A., Pileri A., Motta G., Rossi M., Agostinelli C., Sabattini E., Pimpinelli N., Truni M., Falini B., Cerroni L., Talarico G., Piccioni R., Amente S., Indio V., Tarantino G., Brundu F., Paulli M., Berti E., Facchetti F., Dellino G.I., Bertolini F., Tripodo C., Rabadan R., Pileri S.A., Sapienza, M. R., Abate, F., Melle, F., Orecchioni, S., Fuligni, F., Etebari, M., Tabanelli, V., Laginestra, M. A., Pileri, A., Motta, G., Rossi, M., Agostinelli, C., Sabattini, E., Pimpinelli, N., Truni, M., Falini, B., Cerroni, L., Talarico, G., Piccioni, R., Amente, S., Indio, V., Tarantino, G., Brundu, F., Paulli, M., Berti, E., Facchetti, F., Dellino, G. I., Bertolini, F., Tripodo, C., Rabadan, R., Pileri, S. A., Sapienza, Maria Rosaria, Abate, Francesco, Melle, Federica, Orecchioni, Stefania, Fuligni, Fabio, Etebari, Maryam, Tabanelli, Valentina, Laginestra, Maria Antonella, Pileri, Alessandro, Motta, Giovanna, Rossi, Maura, Agostinelli, Claudio, Sabattini, Elena, Pimpinelli, Nicola, Truni, Mauro, Falini, Brunangelo, Cerroni, Lorenzo, Talarico, Giovanna, Piccioni, Rossana, Amente, Stefano, Indio, Valentina, Tarantino, Giuseppe, Brundu, Francesco, Paulli, Marco, Berti, Emilio, Facchetti, Fabio, Dellino, Gaetano Ivan, Bertolini, Francesco, Tripodo, Claudio, Rabadan, Raul, and Pileri, Stefano A
- Subjects
Acute Myeloid Leukemia ,Blastic plasmacytoid dendritic cell neoplasm, epigenetic mutations ,Skin Neoplasms ,Azacitidine ,Decitabine ,Plasmacytoid dendritic cell ,Gene mutation ,Biology ,BPDCN ,Article ,Epigenesis, Genetic ,03 medical and health sciences ,0302 clinical medicine ,Histone methylation ,5-Azacytidine ,WES ,medicine ,Humans ,Epigenetics ,Exome sequencing ,Regulation of gene expression ,Myeloproliferative Disorders ,Dendritic Cells ,Genomics ,Hematology ,5 -Azacytidine ,Myeloid Neoplasms ,Cancer research ,030215 immunology ,medicine.drug - Abstract
Blastic Plasmacytoid Dendritic Cell Neoplasm is a rare and aggressive hematological malignancy currently lacking an effective therapy. To possibly identify genetic alterations useful for a new treatment design, we analyzed by whole-exome sequencing fourteen Blastic Plasmacytoid Dendritic Cell Neoplasm patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program as the most significantly undermined (P
- Published
- 2018
5. A targeted gene signature stratifying mediastinal gray zone lymphoma into classical HL-like or PMBL-like subtypes.
- Author
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Gargano G, Vegliante MC, Esposito F, Pappagallo SA, Sabattini E, Agostinelli C, Pileri SA, Tabanelli V, Ponzoni M, Lorenzi L, Facchetti F, Di Napoli A, Lucioni M, Paulli M, Leoncini L, Lazzi S, Ascani S, Opinto G, Zaccaria GM, Volpe G, Mondelli P, Bucci A, Selicato L, Negri A, Loseto G, Clemente F, Scattone A, Zito AF, Nassi L, Del Buono N, Guarini A, and Ciavarella S
- Abstract
Not available.
- Published
- 2024
- Full Text
- View/download PDF
6. Massive parallel sequencing unveils homologous recombination deficiency in follicular dendritic cell sarcoma.
- Author
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Lorenzi L, Haferlach T, Mori L, Simbeni M, Walter W, Balzarini P, Meggendorfer M, Döring C, Lonardi S, Bugatti M, Agostinelli C, Mehta J, Borges A, Agaimy A, Simonitsch-Klupp I, Cabeçadas J, Campo E, Pileri SA, Facchetti F, Leo Hansmann M, and Hartmann S
- Subjects
- Humans, Male, Middle Aged, Female, Aged, Exome Sequencing, Homologous Recombination, Adult, Whole Genome Sequencing, Biomarkers, Tumor genetics, Dendritic Cell Sarcoma, Follicular genetics, Dendritic Cell Sarcoma, Follicular pathology, Dendritic Cell Sarcoma, Follicular diagnosis, Mutation, High-Throughput Nucleotide Sequencing
- Abstract
Standardized treatment options are lacking for patients with unresectable or multifocal follicular dendritic cell sarcoma (FDCS) and disease-related mortality is as high as 20%. Applying whole-genome sequencing (WGS) in one case and whole-exome sequencing (WES) in additional twelve cases, this study adds information on the molecular landscape of FDCS, expanding knowledge on pathobiological mechanisms and identifying novel markers of potential theragnostic significance. Massive parallel sequencing showed high frequency of mutations on oncosuppressor genes, particularly in RB1, CARS and BRCA2 and unveiled alterations on homologous recombination DNA damage repair-related genes in 70% (9/13) of cases. This indicates that patients with high-stage FDCS may be eligible for poly ADP ribose polymerase inhibition protocols. Low tumor mutational burden was confirmed in this study despite common PDL1 expression in FDCS arguing on the efficacy of immune checkpoint inhibitors. CDKN2A deletion, detected by WGS and confirmed by fluorescence in situ hybridization in 41% of cases (9/22) indicates that impairment of cell cycle regulation may sustain oncogenesis in FDCS. Absence of mutations in the RAS/RAF/MAPK pathway and lack of clonal hematopoiesis-related mutations in FDCS sanction its differences from dendritic cell-derived neoplasms of hematopoietic derivation. WGS and WES in FDCS provides additional information on the molecular landscape of this rare tumor, proposing novel candidate genes for innovative therapeutical approaches to improve survival of patients with multifocal disease.
- Published
- 2024
- Full Text
- View/download PDF
7. A three-gene signature based on MYC , BCL-2 and NFKBIA improves risk stratification in diffuse large B-cell lymphoma.
- Author
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Derenzini E, Mazzara S, Melle F, Motta G, Fabbri M, Bruna R, Agostinelli C, Cesano A, Corsini CA, Chen N, Righi S, Sabattini E, Chiappella A, Calleri A, Fiori S, Tabanelli V, Cabras A, Pruneri G, Vitolo U, Gianni AM, Rambaldi A, Corradini P, Zinzani PL, Tarella C, and Pileri S
- Subjects
- Gene Expression Profiling, Humans, NF-KappaB Inhibitor alpha, Prognosis, Proto-Oncogene Proteins c-bcl-2 genetics, Proto-Oncogene Proteins c-bcl-6 genetics, Proto-Oncogene Proteins c-myc genetics, Risk Assessment, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Lymphoma, Large B-Cell, Diffuse diagnosis, Lymphoma, Large B-Cell, Diffuse drug therapy, Lymphoma, Large B-Cell, Diffuse genetics
- Abstract
Recent randomized trials focused on gene expression-based determination of the cell of origin in diffuse large B-cell lymphoma could not show significant improvements by adding novel agents to standard chemoimmunotherapy. The aim of this study was the identification of a gene signature able to refine current prognostication algorithms and applicable to clinical practice. Here we used a targeted gene expression profiling panel combining the Lymph2Cx signature for cell of origin classification with additional targets including MYC, BCL-2 and NFKBIA, in 186 patients from 2 randomized trials (discovery cohort) (NCT00355199 and NCT00499018). Data were validated in 3 independent series (2 large public datasets and a real-life cohort). By integrating the cell of origin, MYC/BCL-2 double expressor status and NFKBIA expression, we defined a 3-gene signature combining MYC, BCL-2 and NFKBIA (MBN-signature), which outperformed the MYC/BCL-2 double expressor status in multivariate analysis, and allowed further risk stratification within the germinal center B-cell/unclassified subset. The high-risk (MBN Sig-high) subgroup identified the vast majority of double hit cases and a significant fraction of Activated B-Cell-derived diffuse large B-cell lymphomas. These results were validated in 3 independent series including a cohort from the REMoDL-B trial, where, in an exploratory ad hoc analysis, the addition of bortezomib in the MBN Sig-high subgroup provided a progression free survival advantage compared with standard chemoimmunotherapy. These data indicate that a simple 3-gene signature based on MYC, BCL-2 and NFKBIA could refine the prognostic stratification in diffuse large B-cell lymphoma, and might be the basis for future precision-therapy approaches.
- Published
- 2021
- Full Text
- View/download PDF
8. Blastic plasmacytoid dendritic cell neoplasm: genomics mark epigenetic dysregulation as a primary therapeutic target.
- Author
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Sapienza MR, Abate F, Melle F, Orecchioni S, Fuligni F, Etebari M, Tabanelli V, Laginestra MA, Pileri A, Motta G, Rossi M, Agostinelli C, Sabattini E, Pimpinelli N, Truni M, Falini B, Cerroni L, Talarico G, Piccioni R, Amente S, Indio V, Tarantino G, Brundu F, Paulli M, Berti E, Facchetti F, Dellino GI, Bertolini F, Tripodo C, Rabadan R, and Pileri SA
- Subjects
- Aged, Animals, Cell Line, Tumor, Female, Humans, Male, Mice, Mice, Inbred NOD, Mice, SCID, Middle Aged, Xenograft Model Antitumor Assays, Azacitidine pharmacology, Decitabine pharmacology, Epigenesis, Genetic drug effects, Gene Expression Regulation, Neoplastic drug effects, Hematologic Neoplasms drug therapy, Hematologic Neoplasms genetics, Hematologic Neoplasms metabolism, Hematologic Neoplasms pathology, Myeloproliferative Disorders drug therapy, Myeloproliferative Disorders genetics, Myeloproliferative Disorders metabolism, Myeloproliferative Disorders pathology, Neoplasm Proteins biosynthesis, Neoplasm Proteins genetics, Skin Neoplasms drug therapy, Skin Neoplasms genetics, Skin Neoplasms metabolism
- Abstract
Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and aggressive hematologic malignancy for which there is still no effective therapy. In order to identify genetic alterations useful for a new treatment design, we used whole-exome sequencing to analyze 14 BPDCN patients and the patient-derived CAL-1 cell line. The functional enrichment analysis of mutational data reported the epigenetic regulatory program to be the most significantly undermined ( P <0.0001). In particular, twenty-five epigenetic modifiers were found mutated (e.g. ASXL1, TET2, SUZ12, ARID1A, PHF2, CHD8); ASXL1 was the most frequently affected (28.6% of cases). To evaluate the impact of the identified epigenetic mutations at the gene-expression and Histone H3 lysine 27 trimethylation/acetylation levels, we performed additional RNA and pathology tissue-chromatin immunoprecipitation sequencing experiments. The patients displayed enrichment in gene signatures regulated by methylation and modifiable by decitabine administration, shared common H3K27-acetylated regions, and had a set of cell-cycle genes aberrantly up-regulated and marked by promoter acetylation. Collectively, the integration of sequencing data showed the potential of a therapy based on epigenetic agents. Through the adoption of a preclinical BPDCN mouse model, established by CAL-1 cell line xenografting, we demonstrated the efficacy of the combination of the epigenetic drugs 5'-azacytidine and decitabine in controlling disease progression in vivo ., (Copyright© 2019 Ferrata Storti Foundation.)
- Published
- 2019
- Full Text
- View/download PDF
9. CD30 expression in peripheral T-cell lymphomas.
- Author
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Sabattini E, Pizzi M, Tabanelli V, Baldin P, Sacchetti CS, Agostinelli C, Zinzani PL, and Pileri SA
- Subjects
- Animals, Edetic Acid, Humans, Ki-1 Antigen genetics, Gene Expression Regulation, Neoplastic immunology, Ki-1 Antigen biosynthesis, Lymphoma, T-Cell, Peripheral immunology, Lymphoma, T-Cell, Peripheral metabolism
- Published
- 2013
- Full Text
- View/download PDF
10. The pre-B-cell receptor associated protein VpreB3 is a useful diagnostic marker for identifying c-MYC translocated lymphomas.
- Author
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Rodig SJ, Kutok JL, Paterson JC, Nitta H, Zhang W, Chapuy B, Tumwine LK, Montes-Moreno S, Agostinelli C, Johnson NA, Ben-Neriah S, Farinha P, Shipp MA, Piris MA, Grogan TM, Pileri SA, Gascoyne RD, and Marafioti T
- Subjects
- B-Lymphocytes metabolism, B-Lymphocytes pathology, Biomarkers, Tumor genetics, Blotting, Western, Burkitt Lymphoma genetics, Burkitt Lymphoma metabolism, Burkitt Lymphoma pathology, Cell Line, Tumor, Gene Expression Profiling, Germinal Center metabolism, Humans, Immunohistochemistry, Lymphoma, B-Cell genetics, Lymphoma, B-Cell pathology, Lymphoma, Large B-Cell, Diffuse genetics, Lymphoma, Large B-Cell, Diffuse metabolism, Lymphoma, Large B-Cell, Diffuse pathology, Pre-B Cell Receptors genetics, Proto-Oncogene Proteins c-myc genetics, Survival Analysis, Biomarkers, Tumor metabolism, Lymphoma, B-Cell metabolism, Pre-B Cell Receptors metabolism, Proto-Oncogene Proteins c-myc metabolism
- Abstract
Background: During B-cell development, precursor B cells transiently express the pre-B-cell receptor composed of μ heavy chain complexed with VpreB and λ5 surrogate light chain polypeptides. Recent profiling studies unexpectedly revealed abundant transcripts of one member of the VpreB family, VpreB3, in a subset of mature B cells and Burkitt lymphoma., Design and Methods: Here we used a novel antibody to investigate the normal expression pattern of VpreB3 protein in human hematopoietic and lymphoid tissues, and to determine whether VpreB3 could serve as a useful diagnostic biomarker for select B-cell lymphomas., Results: We found that VpreB3 protein is normally expressed by precursor B cells in bone marrow and by a subset of normal germinal center B cells in secondary lymphoid organs. Among lymphoid malignancies, we found an association between VpreB3 expression and B-cell tumors with c-MYC abnormalities. VpreB3 was highly expressed in all cases of Burkitt lymphoma, whether of endemic or sporadic origin (44/44 cases, 100%), all cases of B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma (5/5 cases, 100%), and the majority of diffuse large B-cell lymphomas harboring a c-MYC translocation (15/18 cases, 83%). The expression of VpreB3 in diffuse large B-cell lymphomas without a c-MYC translocation was associated with c-MYC polysomy in 25/75 cases (33%) but only rarely observed in diffuse large B-cell lymphomas lacking a c-MYC abnormality (9/98 cases, 9%)., Conclusions: We conclude that for B-cell tumors with features suggesting a possible c-MYC translocation, such as intermediate to large cell size and high proliferation rate, the presence of VpreB3 should prompt subsequent confirmatory genetic testing, whereas the absence of VpreB3 is virtually always associated with wild-type c-MYC alleles.
- Published
- 2010
- Full Text
- View/download PDF
11. Physiological PTEN expression in peripheral T-cell lymphoma not otherwise specified.
- Author
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Gazzola A, Bertuzzi C, Agostinelli C, Righi S, Pileri SA, and Piccaluga PP
- Subjects
- DNA Primers chemistry, Gene Expression Profiling, Humans, Models, Biological, Oligonucleotide Array Sequence Analysis, PTEN Phosphohydrolase genetics, Polymerase Chain Reaction methods, Sequence Analysis, DNA, Transcription, Genetic, Gene Expression Regulation, Neoplastic, Lymphoma, T-Cell genetics, Lymphoma, T-Cell metabolism, PTEN Phosphohydrolase biosynthesis
- Published
- 2009
- Full Text
- View/download PDF
12. Cytoplasmic nucleophosmin is not detected in blastic plasmacytoid dendritic cell neoplasm.
- Author
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Facchetti F, Pileri SA, Agostinelli C, Martelli MP, Paulli M, Venditti A, Martelli MF, and Falini B
- Subjects
- Blast Crisis, Classification, Diagnosis, Differential, Humans, Nucleophosmin, World Health Organization, Cytoplasm chemistry, Dendritic Cells pathology, Leukemia, Myeloid, Acute diagnosis, Myeloproliferative Disorders diagnosis, Nuclear Proteins analysis
- Abstract
Acute myeloid leukemia carrying cytoplasmic mutated nucleophosmin (NPMc(+) AML) and blastic plasmacytoid dendritic cell neoplasm have been included as new entities in the 4(th) edition (2008) WHO classification of myeloid neoplasms. These conditions may show clinical and pathological overlapping features (leukemic and skin involvement, and expression of macrophage markers). In this study, we provide evidence that aberrant cytoplasmic dislocation of nucleophosmin - the immunohistochemical surrogate for NPM1 mutations - allows the two entities to be genetically separated. In fact, nucleophosmin is consistently cytoplasmic in NPMc(+) AML (because of the presence of NPM1 mutations), whilst it is nucleus-restricted (predictive of a germline NPM1 gene) in blastic plasmacytoid dendritic cell neoplasm. Our results clearly point cytoplasmic nucleophosmin (a full predictor of NPM1 mutations) as a new marker for distinguishing NPMc(+) AML and blastic plasmacytoid dendritic cell neoplasm, further clarify the cell of origin of NPMc(+) AML, and justify the inclusion of these pathological conditions as separate entities in the new WHO classification.
- Published
- 2009
- Full Text
- View/download PDF
13. Gene expression analysis provides a potential rationale for revising the histological grading of follicular lymphomas.
- Author
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Piccaluga PP, Califano A, Klein U, Agostinelli C, Bellosillo B, Gimeno E, Serrano S, Solè F, Zang Y, Falini B, Zinzani PL, and Pileri SA
- Subjects
- Adult, Aged, Cluster Analysis, Female, Genome, Human, Humans, Lymphoma, B-Cell diagnosis, Lymphoma, Follicular classification, Lymphoma, Non-Hodgkin diagnosis, Male, Middle Aged, Neoplasm Staging, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Gene Expression Regulation, Neoplastic, Lymphoma, B-Cell genetics, Lymphoma, Follicular diagnosis, Lymphoma, Follicular genetics, Lymphoma, Non-Hodgkin genetics
- Abstract
Background: Follicular lymphomas are currently subdivided into grades I, II, IIIa and IIIb. This distinction is, however, questioned., Design and Methods: We studied the gene expression profile of 43 follicular lymphomas, 50 B-cell non-Hodgkin's lymphomas of different histotype, and 20 samples of normal B-lymphocytes in order to assess: (i) the relationship of follicular lymphoma with normal B cells and other B-cell non-Hodgkin's lymphomas; (ii) whether follicular lymphoma is a unique disease; and (iii) whether follicular lymphoma grade IIIb is closer to follicular lymphoma or diffuse large B-cell lymphoma of the germinal center B-cell type., Results: First, we found that the molecular profile of follicular lymphoma is intimately related to that of normal germinal center B cells, irrespectively of the histological grade. Secondly, we observed that follicular lymphoma has a relatively homogeneous gene expression profile that is distinct from that of other B-cell non-Hodgkin's lymphoma and does not include discrete molecular subgroups. However, by further clustering samples according to signatures differentially expressed among follicular lymphomas or in follicular lymphomas versus diffuse large B-cell lymphoma, we showed that grade I-IIIa tumors tend to cluster together, while grade IIIb follicular lymphoma constitutes a distinct subgroup, whose molecular signature is closer to that of the remaining follicular lymphomas than to that of diffuse large B-cell lymphoma of the germinal center B-cell type., Conclusions: These data support the hypothesis that grade IIIb follicular lymphoma does indeed belong to the group of follicular lymphomas rather than diffuse large B-cell lymphomas, and also suggests a possible revision of the histological grading of follicular lymphomas, with their simple distinction into follicular lymphoma (grade I-IIIa) and follicular lymphoma/large cell (grade IIIb).
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- 2008
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14. Expression of CD52 in peripheral T-cell lymphoma.
- Author
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Piccaluga PP, Agostinelli C, Righi S, Zinzani PL, and Pileri SA
- Subjects
- Alemtuzumab, Antibodies, Monoclonal immunology, Antibodies, Monoclonal therapeutic use, Antibodies, Monoclonal, Humanized, Antibodies, Neoplasm immunology, Antibodies, Neoplasm therapeutic use, Antigens, CD genetics, Antigens, CD immunology, Antigens, Neoplasm genetics, Antigens, Neoplasm immunology, CD52 Antigen, Gene Expression Profiling, Glycoproteins genetics, Glycoproteins immunology, Humans, Lymphoma, T-Cell, Peripheral pathology, Oligonucleotide Array Sequence Analysis, Paraffin Embedding, RNA, Messenger biosynthesis, RNA, Messenger genetics, RNA, Neoplasm biosynthesis, RNA, Neoplasm genetics, T-Lymphocytes pathology, Antigens, CD biosynthesis, Antigens, Neoplasm biosynthesis, Glycoproteins biosynthesis, Lymphoma, T-Cell, Peripheral metabolism, T-Lymphocytes metabolism
- Abstract
Peripheral T-cell lymphoma unspecified (PTCL/U) is a rare tumor characterized by poor treatment response and a dismal prognosis. We studied CD52 expression in 97 PTCL/U cases by immunohistochemistry on tissue-microarrays. Furthermore, CD52 gene expression was studied in 28 cases for which RNA was available. We found that CD52 is expressed in approximately 40% of PTCLs/U at the same level as in normal T-lymphocytes. Although other factors may play a role in the in vivo response to alemtuzumab, an anti-CD52 monoclonal antibody, the estimation of CD52 expression may provide a rationale for the selection of patients with a higher probability of treatment response.
- Published
- 2007
- Full Text
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15. Erythrophagocytosis by neoplastic cells in a patient with myelodysplastic syndrome.
- Author
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Ascani S, Sabattini E, Agostinelli C, Piccaluga PP, Zinzani PL, and Pileri SA
- Subjects
- Aged, Bone Marrow Examination, Erythrocytes, Humans, Male, Myelodysplastic Syndromes diagnosis, Neoplasms pathology, Pancytopenia etiology, Myelodysplastic Syndromes pathology, Neoplasms physiopathology, Phagocytosis
- Published
- 2004
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