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1. The International Consensus Classification of Mature Lymphoid Neoplasms: a report from the Clinical Advisory Committee

Author

Campo, E, Jaffe, ES, Cook, JR, Quintanilla-Martinez, L, Swerdlow, SH, Anderson, KC, Brousset, P, Cerroni, L, de Leval, L, Dirnhofer, S, Dogan, A, Feldman, AL, Fend, F, Friedberg, JW, Gaulard, P, Ghia, P, Horwitz, SM, King, RL, Salles, G, San-Miguel, J, Seymour, JF, Treon, SP, Vose, JM, Zucca, E, Advani, R, Ansell, S, Au, W-Y, Barrionuevo, C, Bergsagel, L, Chan, WC, Cohen, JI, d'Amore, F, Davies, A, Falini, B, Ghobrial, IM, Goodlad, JR, Gribben, JG, Hsi, ED, Kahl, BS, Kim, W-S, Kumar, S, LaCasce, AS, Laurent, C, Lenz, G, Leonard, JP, Link, MP, Lopez-Guillermo, A, Mateos, MV, Macintyre, E, Melnick, AM, Morschhauser, F, Nakamura, S, Narbaitz, M, Pavlovsky, A, Pileri, SA, Piris, M, Pro, B, Rajkumar, V, Rosen, ST, Sander, B, Sehn, L, Shipp, MA, Smith, SM, Staudt, LM, Thieblemont, C, Tousseyn, T, Wilson, WH, Yoshino, T, Zinzani, P-L, Dreyling, M, Scott, DW, Winter, JN, Zelenetz, A, Campo, E, Jaffe, ES, Cook, JR, Quintanilla-Martinez, L, Swerdlow, SH, Anderson, KC, Brousset, P, Cerroni, L, de Leval, L, Dirnhofer, S, Dogan, A, Feldman, AL, Fend, F, Friedberg, JW, Gaulard, P, Ghia, P, Horwitz, SM, King, RL, Salles, G, San-Miguel, J, Seymour, JF, Treon, SP, Vose, JM, Zucca, E, Advani, R, Ansell, S, Au, W-Y, Barrionuevo, C, Bergsagel, L, Chan, WC, Cohen, JI, d'Amore, F, Davies, A, Falini, B, Ghobrial, IM, Goodlad, JR, Gribben, JG, Hsi, ED, Kahl, BS, Kim, W-S, Kumar, S, LaCasce, AS, Laurent, C, Lenz, G, Leonard, JP, Link, MP, Lopez-Guillermo, A, Mateos, MV, Macintyre, E, Melnick, AM, Morschhauser, F, Nakamura, S, Narbaitz, M, Pavlovsky, A, Pileri, SA, Piris, M, Pro, B, Rajkumar, V, Rosen, ST, Sander, B, Sehn, L, Shipp, MA, Smith, SM, Staudt, LM, Thieblemont, C, Tousseyn, T, Wilson, WH, Yoshino, T, Zinzani, P-L, Dreyling, M, Scott, DW, Winter, JN, and Zelenetz, A

Abstract

Since the publication of the Revised European-American Classification of Lymphoid Neoplasms in 1994, subsequent updates of the classification of lymphoid neoplasms have been generated through iterative international efforts to achieve broad consensus among hematopathologists, geneticists, molecular scientists, and clinicians. Significant progress has recently been made in the characterization of malignancies of the immune system, with many new insights provided by genomic studies. They have led to this proposal. We have followed the same process that was successfully used for the third and fourth editions of the World Health Organization Classification of Hematologic Neoplasms. The definition, recommended studies, and criteria for the diagnosis of many entities have been extensively refined. Some categories considered provisional have now been upgraded to definite entities. Terminology for some diseases has been revised to adapt nomenclature to the current knowledge of their biology, but these modifications have been restricted to well-justified situations. Major findings from recent genomic studies have impacted the conceptual framework and diagnostic criteria for many disease entities. These changes will have an impact on optimal clinical management. The conclusions of this work are summarized in this report as the proposed International Consensus Classification of mature lymphoid, histiocytic, and dendritic cell tumors.

Published
2022

4. PROGNOSTIC CORRELATION OF CELL-OF-ORIGIN AND MYC, BCL-2 AND BCL-6 STATUS IN HIV-ASSOCIATED DIFFUSE LARGE B-CELL LYMPHOMAS

Author

Rusconi C, Crucitti L, Re A, Bandiera L, Spina M, Gini G, Paulli M, Lucioni M, Facchetti F, Goteri G, Canzonieri V, Lorenzi L, Balzarini P, Fisogni S, Riboni R, Malfitano A, Bonfichi M, Moioli MC, Nichelatti M, Melle F, Motta G, Pileri SA, Cairoli R, Rusconi, C, Crucitti, L, Re, A, Bandiera, L, Spina, M, Gini, G, Paulli, M, Lucioni, M, Facchetti, F, Goteri, G, Canzonieri, V, Lorenzi, L, Balzarini, P, Fisogni, S, Riboni, R, Malfitano, A, Bonfichi, M, Moioli, M, Nichelatti, M, Melle, F, Motta, G, Pileri, S, and Cairoli, R

Subjects
Hematology
Published
2019

5. PROGNOSTIC CORRELATION OF CELL-OF-ORIGIN AND MYC, BCL-2 AND BCL-6 STATUS IN HIV-ASSOCIATED DIFFUSE LARGE B-CELL LYMPHOMAS

Author

Rusconi, C, Crucitti, L, Re, A, Bandiera, L, Spina, M, Gini, G, Paulli, M, Lucioni, M, Facchetti, F, Goteri, G, Canzonieri, V, Lorenzi, L, Balzarini, P, Fisogni, S, Riboni, R, Malfitano, A, Bonfichi, M, Moioli, M, Nichelatti, M, Melle, F, Motta, G, Pileri, S, Cairoli, R, Rusconi C, Crucitti L, Re A, Bandiera L, Spina M, Gini G, Paulli M, Lucioni M, Facchetti F, Goteri G, Canzonieri V, Lorenzi L, Balzarini P, Fisogni S, Riboni R, Malfitano A, Bonfichi M, Moioli MC, Nichelatti M, Melle F, Motta G, Pileri SA, Cairoli R, Rusconi, C, Crucitti, L, Re, A, Bandiera, L, Spina, M, Gini, G, Paulli, M, Lucioni, M, Facchetti, F, Goteri, G, Canzonieri, V, Lorenzi, L, Balzarini, P, Fisogni, S, Riboni, R, Malfitano, A, Bonfichi, M, Moioli, M, Nichelatti, M, Melle, F, Motta, G, Pileri, S, Cairoli, R, Rusconi C, Crucitti L, Re A, Bandiera L, Spina M, Gini G, Paulli M, Lucioni M, Facchetti F, Goteri G, Canzonieri V, Lorenzi L, Balzarini P, Fisogni S, Riboni R, Malfitano A, Bonfichi M, Moioli MC, Nichelatti M, Melle F, Motta G, Pileri SA, and Cairoli R

Published
2019

6. Bone marrow stroma CD40 expression correlates with inflammatory mast cell infiltration and disease progression in splenic marginal zone lymphoma

Author

FRANCO, Giovanni, GUARNOTTA, Carla, Piccaluga, PP, Boveri, E, GULINO, Alessandro, Fuligni, F, Rigoni, A, Porcasi, R, Buffa, S, Betto, E, FLORENA, Ada Maria, FRANCO, Vito, Iannitto, E, Arcaini, L, Pileri, SA, Pucillo, C, Colombo, MP, Sangaletti, S, TRIPODO, Claudio, Frossi, B, PORCASI, Rossana, Franco, G, Guarnotta, C, Frossi, Piccaluga, PP, Boveri, E, Gulino, A, Fuligni, F, Rigoni, A, Porcasi, R, Buffa, S, Betto, E, Florena, AM, Franco, V, Iannitto, E, Arcaini, L, Pileri, SA, Pucillo, C, Colombo, MP, Sangaletti, S, Tripodo, C, Franco, Giovanni, Guarnotta, Carla, Frossi, Barbara, Piccaluga, Pier Paolo, Boveri, Emanuela, Gulino, Alessandro, Fuligni, Fabio, Rigoni, Alice, Porcasi, Rossana, Buffa, Salvatore, Betto, Elena, Florena, Ada Maria, Franco, Vito, Iannitto, Emilio, Arcaini, Luca, Pileri, Stefano Aldo, Pucillo, Carlo, Colombo, Mario Paolo, Sangaletti, Sabina, and Tripodo, Claudio

Subjects
Male, Pathology, Biochemistry, Mice, Tumor Microenvironment, Mast Cell, Medicine, Mast Cells, Inflammation Mediator, Aged, 80 and over, Mice, Knockout, B-Lymphocytes, Mice, Inbred BALB C, Mesenchymal Stromal Cell, B-Lymphocyte, CD40 Antigen, Cell Differentiation, Hematology, Middle Aged, Prognosis, medicine.anatomical_structure, Disease Progression, Cytokines, Female, Inflammation Mediators, Clone (B-cell biology), Human, Adult, medicine.medical_specialty, Stromal cell, Prognosi, CD40 Ligand, Immunology, Disease-Free Survival, Animals, Humans, Splenic marginal zone lymphoma, CD40 Antigens, Cytokine, B cell, Aged, Cell Proliferation, Animal, business.industry, Mesenchymal stem cell, Mesenchymal Stem Cells, Lymphoma, B-Cell, Marginal Zone, Cell Biology, Genes, p53, medicine.disease, Lymphoma, Splenic marginal zone lymphoma, bone marrow microenvironment, CD40, Mast cell sarcoma, Bone marrow, business
Abstract

Splenic marginal zone lymphoma (SMZL) is a mature B-cell neoplasm characterized by rather indolent clinical course. However, nearly one third of patients experience a rapidly progressive disease with a dismal outcome. Despite the characterization of clone geneticsandthe recognition of deregulated immunologic stimulation in the pathogenesis of SMZL, little is known about microenvironment dynamics and their potential biological influence on disease outcome. Here we investigate the effect of stroma-intrinsic features on SMZL disease progression by focusing on the microenvironment of the bone marrow (BM), which represents an elective disease localization endorsing diagnostic and prognostic relevance. We show that the quality of the BM stromal meshwork of SMZL infiltrates correlates with time to progression. In particular, we describe the unfavorable prognostic influence of dense CD40 expression by BM stromal cells, which involves the contribution of CD40 ligand (CD40L)-expressing bystander mast cells infiltrating SMZL BM aggregates. The CD40/CD40L-assisted crosstalk between mesenchymal stromal cells and mast cells populating the SMZL microenvironment finds correlation in p53-/- mice developing SMZL and contributes to the engendering of detrimental proinflammatory conditions. Our study highlights a dynamic interaction, playing between nonneoplastic elements within the SMZL niche, toward disease progression. © 2014 by The American Society of Hematology.

Published
2014
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7. Cell-of-Origin Identification and Prognostic Correlation in HIV-Associated Diffuse Large B-Cell Lymphomas: Results of an Italian Multicentric Study

Author

Rusconi, C, Re, A, Bandiera, L, Crucitti, L, Spina, M, Gini, G, Paulli, M, Lucioni, M, Facchetti, F, Goteri, G, Canzonieri, V, Lorenzi, L, Balzarini, P, Fisogni, S, Malfitano, A, Bonfichi, M, Moioli, M, Nichelatti, M, Melle, F, Motta, G, Pileri, S, Cairoli, R, Rusconi C, Re A, Bandiera L, Crucitti L, Spina M, Gini G, Paulli M, Lucioni M, Facchetti F, Goteri G, Canzonieri V, Lorenzi L, Balzarini P, Fisogni S, Malfitano A, Bonfichi M, Moioli MC, Nichelatti M, Melle F, Motta G, Pileri SA, Cairoli R, Rusconi, C, Re, A, Bandiera, L, Crucitti, L, Spina, M, Gini, G, Paulli, M, Lucioni, M, Facchetti, F, Goteri, G, Canzonieri, V, Lorenzi, L, Balzarini, P, Fisogni, S, Malfitano, A, Bonfichi, M, Moioli, M, Nichelatti, M, Melle, F, Motta, G, Pileri, S, Cairoli, R, Rusconi C, Re A, Bandiera L, Crucitti L, Spina M, Gini G, Paulli M, Lucioni M, Facchetti F, Goteri G, Canzonieri V, Lorenzi L, Balzarini P, Fisogni S, Malfitano A, Bonfichi M, Moioli MC, Nichelatti M, Melle F, Motta G, Pileri SA, and Cairoli R

Published
2018

9. Understanding CD30 biology and therapeutic targeting: a historical perspective providing insight into future directions

Author

van der Weyden, CA, Pileri, SA, Feldman, AL, Whisstock, J, Prince, HM, van der Weyden, CA, Pileri, SA, Feldman, AL, Whisstock, J, and Prince, HM

Abstract

CD30 is a member of the tumor necrosis factor receptor superfamily. It is characteristically expressed in certain hematopoietic malignancies, including anaplastic large cell lymphoma and Hodgkin lymphoma, among others. The variable expression of CD30 on both normal and malignant lymphoid cells has focused research efforts on understanding the pathogenesis of CD30 upregulation, its contribution to lymphomagenesis through anti-apoptotic mechanisms, and its effect on cell survival. Given the restriction of CD30 to certain tumor types, the logical extension of this has been to attempt to exploit it as a therapeutic target. The efficacy of naked anti-CD30 antibodies in practice was, however, modest. Moreover, combinations with bacterial toxins and radioimmunoconjugates have also had limited success. The development of the antibody-drug compound brentuximab vedotin (BV), however, has rejuvenated interest in CD30 as a tumor target. Phase I and II clinical trials in Hodgkin lymphoma, peripheral T-cell lymphoma, cutaneous T cell lymphoma, and even CD30-expressing B-cell lymphomas, have shown the compound is well tolerated, but more importantly, able to deliver meaningful disease control even in patients with multiply relapsed or refractory disease. FDA approval has been granted for its use in relapsed Hodgkin lymphoma and systemic anaplastic large cell lymphoma. A recent phase III trial of BV in cutaneous T-cell lymphoma has confirmed its superiority to standard of care therapies. In this manuscript, we explore the history of CD30 as a tumor marker and as a therapeutic target, both in the laboratory and in the clinic, with a view to understanding future avenues for further study.

Published
2017

10. Gene expression signatures delineate biological and prognostic subgroups in peripheral T-cell lymphoma

Author

Iqbal J, Wright G, Wang C, Rosenwald A, Gascoyne RD, Weisenburger DD, Greiner TC, Smith L, Guo S, Wilcox RA, Teh BT, Lim ST, Tan SY, Rimsza LM, Jaffe ES, Campo E, Martinez A, Delabie J, Braziel RM, Cook JR, Tubbs RR, Ott G, Geissinger E, Gaulard P, PICCALUGA P., Pileri SA, Au WY, Nakamura S, Seto M, Berger F, de Leval L, Connors JM, Armitage J, Vose J, Chan WC, Staudt LM, Lymphoma Leukemia Molecular Profiling Project, the International Peripheral T. cell Lymphoma Project, Iqbal J, Wright G, Wang C, Rosenwald A, Gascoyne RD, Weisenburger DD, Greiner TC, Smith L, Guo S, Wilcox RA, Teh BT, Lim ST, Tan SY, Rimsza LM, Jaffe ES, Campo E, Martinez A, Delabie J, Braziel RM, Cook JR, Tubbs RR, Ott G, Geissinger E, Gaulard P, PICCALUGA P., Pileri SA, Au WY, Nakamura S, Seto M, Berger F, de Leval L, Connors JM, Armitage J, Vose J, Chan WC, Staudt LM, and Lymphoma Leukemia Molecular Profiling Project and the International Peripheral T-cell Lymphoma Project

Subjects
Adult, Male, Pathology, medicine.medical_specialty, Immunology, Gene expression signature, lymphoma, Peripheral T-cell lymphoma not otherwise specified, Biology, Biochemistry, Young Adult, hemic and lymphatic diseases, medicine, Biomarkers, Tumor, Anaplastic lymphoma kinase, Humans, Anaplastic large-cell lymphoma, Survival analysis, Aged, Oligonucleotide Array Sequence Analysis, Aged, 80 and over, Tumor microenvironment, Gene Expression Profiling, Lymphoma, T-Cell, Peripheral, Cell Biology, Hematology, Middle Aged, medicine.disease, Prognosis, Immunohistochemistry, Survival Analysis, Peripheral T-cell lymphoma, Lymphoma, Gene Expression Regulation, Neoplastic, Leukemia, Cancer research, Female
Abstract

Peripheral T-cell lymphoma (PTCL) encompasses a heterogeneous group of neoplasms with generally poor clinical outcome. Currently 50% of PTCL cases are not classifiable: PTCL-not otherwise specified (NOS). Gene-expression profiles on 372 PTCL cases were analyzed and robust molecular classifiers and oncogenic pathways that reflect the pathobiology of tumor cells and their microenvironment were identified for major PTCL-entities, including 114 angioimmunoblastic T-cell lymphoma (AITL), 31 anaplastic lymphoma kinase (ALK)-positive and 48 ALK-negative anaplastic large cell lymphoma, 14 adult T-cell leukemia/lymphoma and 44 extranodal NK/T-cell lymphoma that were further separated into NK-cell and gdT-cell lymphomas. Thirty-seven percent of morphologically diagnosed PTCL-NOS cases were reclassified into other specific subtypes by molecular signatures. Reexamination, immunohistochemistry, and IDH2 mutation analysis in reclassified cases supported the validity of the reclassification. Two major molecular subgroups can be identified in the remaining PTCL-NOS cases characterized by high expression of either GATA3 (33%; 40/121) or TBX21 (49%; 59/121). The GATA3 subgroup was significantly associated with poor overall survival (P = .01). High expression of cytotoxic gene-signature within the TBX21 subgroup also showed poor clinical outcome (P = .05). In AITL, high expression of several signatures associated with the tumor microenvironment was significantly associated with outcome. A combined prognostic score was predictive of survival in an independent cohort (P = .004).

Published
2014

11. Tumours of histiocytes and accessory dendritic cells: an immunohistochemical approach to classification from the International Lymphoma Study Group based on 61 cases

Author

Pileri, SA, Grogan, T, Harris, N, Banks, P, Campo, E, Chan, J, Favera, R, Delsol, G, De Wolf-Peeters, C, Falini, B, Gascoyne, R, Gaulard, P, Gatter, K, Isaacson, P, Jaffe, E, Kluin, P, Knowles, D, Mason, D, Mori, S, Müller-Hermelink, H, Piris, M, Ralfkiaer, E, Stein, H, Su, I, and Warnke, R

Abstract

Neoplasms of histiocytes and dendritic cells are rare, and their phenotypic and biological definition is incomplete. Seeking to identify antigens detectable in paraffin-embedded sections that might allow a more complete, rational immunophenotypic classification of histiocytic/dendritic cell neoplasms, the International Lymphoma Study Group (ILSG) stained 61 tumours of suspected histiocytic/dendritic cell type with a panel of 15 antibodies including those reactive with histiocytes (CD68, lysozyme (LYS)), Langerhans cells (CD1a), follicular dendritic cells (FDC: CD21, CD35) and S100 protein. This analysis revealed that 57 cases (93%) fit into four major immunophenotypic groups (one histiocytic and three dendritic cell types) utilizing six markers: CD68, LYS, CD1a, S100, CD21, and CD35. The four (7%) unclassified cases were further classifiable into the above four groups using additional morphological and ultrastructural features. The four groups then included: (i) histiocytic sarcoma (n=18) with the following phenotype: CD68 (100%), LYS (94%), CD1a (0%), S100 (33%), CD21/35 (0%). The median age was 46 years. Presentation was predominantly extranodal (72%) with high mortality (58% dead of disease (DOD)). Three had systemic involvement consistent with 'malignant histiocytosis'; (ii) Langerhans cell tumour (LCT) (n=26) which expressed: CD68 (96%), LYS (42%), CD1a (100%), S100 (100%), CD21/35 (0%). There were two morphological variants: cytologically typical (n=17) designated LCT; and cytologically malignant (n=9) designated Langerhans cell sarcoma (LCS). The LCS were often not easily recognized morphologically as LC-derived, but were diagnosed based on CD1a staining. LCT and LCS differed in median age (33 versus 41 years), male:female ratio (3.7:1 versus 1:2), and death rate (31% versus 50% DOD). Four LCT patients had systemic involvement typical of Letterer-Siwe disease; (iii) follicular dendritic cell tumour/sarcoma (FDCT) (n=13) which expressed: CD68 (54%), LYS (8%), CD1a (0%), S100 (16%), FDC markers CD21/35 (100%), EMA (40%). These patients were adults (median age 65 years) with predominantly localized nodal disease (75%) and low mortality (9% DOD); (iv) interdigitating dendritic cell tumour/sarcoma (IDCT) (n=4) which expressed: CD68 (50%), LYS (25%), CD1a (0%), S100 (100%), CD21/35 (0%). The patients were adults (median 71 years) with localized nodal disease (75%) without mortality (0% DOD). In conclusion, definitive immunophenotypic classification of histiocytic and accessory cell neoplasms into four categories was possible in 93% of the cases using six antigens detected in paraffin-embedded sections. Exceptional cases (7%) were resolvable when added morphological and ultrastructural features were considered. We propose a classification combining immunophenotype and morphology with five categories, including Langerhans cell sarcoma. This simplified scheme is practical for everyday diagnostic use and should provide a framework for additional investigation of these unusual neoplasms.

Published
2016

12. Comparison of different DNA extraction methods from peripheral blood cells: advices from the Fondazione Italiana Linfomi - MRD Network

Author

Mannu C, Gazzola A, Ciabatti E, Fuligni F, Cavalli M, Della Starza I, Genuardi E, Mantoan B, Monitillo L, Del Giudice I, Ladetto M, Gaidano G, Sabattini E, Pileri SA, Galimberti S, PICCALUGA P., on behalf of Fondazione Italiana Linfomi MrdNetwork, Mannu C, Gazzola A, Ciabatti E, Fuligni F, Cavalli M, Della Starza I, Genuardi E, Mantoan B, Monitillo L, Del Giudice I, Ladetto M, Gaidano G, Sabattini E, Pileri SA, Galimberti S, PICCALUGA P., and on behalf of Fondazione Italiana Linfomi - MrdNetwork.

Subjects
Minimal Residual Disease, DNA extraction
Abstract

Genomic DNA extraction is a primary component of genomic research and diagnostic routine analysis. Recently, the importance of this process has been highlighted by the necessity to standardize the diagnostic procedure. In this regard, the Minimal Residual Disease (MRD) Network of the Fondazione Italiana Linfomi (FIL MRD Network) has performed a comparative study of four different commercially available kits for DNA extraction, applying them on a panel of cellular pellets, with the aim of defining possible technical recommendations in order to harmonize and standardize diagnostic procedures in the clinical setting. Overall, all four kits usually allowed the recovery of a significant quantity of high-quality DNA (in most conditions), although specific indications could be addressed for cellular pellets of different sizes.

Published
2014

13. IRTA1 is selectively expressed in nodal and extranodal marginal zone lymphomas

Author

Falini B, Agostinelli C, Bigerna B, Pucciarini A, Pacini R, Tabarrini A, Falcinelli F, Piccioli M, Paulli M, Gambacorta M, Tiacci E, Ascani S, Martelli MP, Favera RD, Stein H, Pileri SA, PONZONI , MAURILIO, Falini B., Agostinelli C., Bigerna B., Pucciarini A., Pacini R., Tabarrini A., Falcinelli F., Piccioli M., Paulli M., Gambacorta M., Ponzoni M., Tiacci E., Ascani S., Martelli M.P., Favera RD., Stein H., Pileri S.A., Falini, B, Agostinelli, C, Bigerna, B, Pucciarini, A, Pacini, R, Tabarrini, A, Falcinelli, F, Piccioli, M, Paulli, M, Gambacorta, M, Ponzoni, Maurilio, Tiacci, E, Ascani, S, Martelli, Mp, Favera, Rd, Stein, H, and Pileri, Sa

Subjects
B-Lymphocytes, Lymphoma, B-Cell, Lymphoma, B-Cell, Marginal Zone, Receptors, Fc, IRTA1, Translocation, Genetic, immunohistochemistry, marginal zone lymphomas, monoclonal antibodies, Biomarkers, Tumor, Humans, Lymph Nodes, immunohistochemistry, IRTA1, marginal zone lymphomas, monoclonal antibodies, In Situ Hybridization, Fluorescence, Spleen
Abstract

Aims: The aim of this study was to search for a molecule selectively expressed by marginal zone (MZ) lymphomas (MZLs), whose diagnosis is currently based on morphological criteria and negativity for markers detectable in other B-cell lymphomas. Methods and results: Two thousand one hundred and four peripheral lymphomas of various types were immunostained with a monoclonal antibody against immunoglobulin superfamily receptor translocation-associated 1 (IRTA1), which recognizes the equivalents of MZ in human lymphoid tissues other than spleen. IRTA1 expression was restricted to extranodal (93%) and nodal MZLs (73%) and to lymphomas with MZ differentiation. Extranodal MZL cells with the strongest IRTA1 expression were usually located adjacent to epithelia, mimicking the IRTA1 expression pattern of normal and acquired mucosa-associated lymphoid tissue (MALT). The cytological features, growth pattern and IRTA1 positivity in nodal MZLs suggest they may derive from IRTA1(+) perifollicular B cells or monocytoid B cells detectable in reactive lymph nodes. Double immunostaining for IRTA1/bcl-6 tracked the colonization of B-cell follicles by MZL cells, and showed modulation of their phenotype (e.g. acquisition of bcl-6) during recirculation through germinal centres. MZL cells differentiating into plasma cells usually lost IRTA1. Conclusions: These results further expand our knowledge of the biology of MZLs, and highlight IRTA1 as the first positive marker for MZLs, enabling more accurate diagnosis of these neoplasms

Published
2012

15. Intravascular large B-cell lymphoma (IVLBCL): International consensus on diagnostic and therapeutic issues

Author

PONZONI , MAURILIO, Ferreri AJ, Campo E, Dognini GP, Facchetti F, Kinoshita T, Mazzucchelli L, Yoshino T, Murase T, Seto M, Shimada K, Pileri SA, Doglioni C, Zucca E, Cavalli F, Nakamura S., Ponzoni, Maurilio, Ferreri, Aj, Campo, E, Dognini, Gp, Facchetti, F, Kinoshita, T, Mazzucchelli, L, Yoshino, T, Murase, T, Seto, M, Shimada, K, Pileri, Sa, Doglioni, C, Zucca, E, Cavalli, F, and Nakamura, S.

Published
2008

16. Induction chemotherapy strategies for primary mediastinal large B-cell lymphoma with sclerosis: a retrospective multinational study on 426 previously untreated patients

Author

Zinzani, Pl, Martelli, M, Bertini, M, Gianni, Am, Devizzi, L, Federico, M, Pangalis, G, Michels, J, Zucca, E, Cantonetti, M, Cortelazzo, S, Wotherspoon, A, Ferreri, Aj, Zaja, Francesco, Lauria, F, De Renzo, A, Liberati, Ma, Falini, B, Balzarotti, M, Calderoni, A, Zaccaria, A, Gentilini, P, Fattori, Pp, Pavone, E, Angelopoulou, Mk, Alinari, L, Brugiatelli, M, Di Renzo, N, Bonifazi, F, Pileri, Sa, Cavalli, F, International Extranodal Lymphoma Study Group, Zinzani, Pl, Martelli, M, Bertini, M, Gianni, Am, Devizzi, L, Federico, M, Pangalis, G, Michels, J, Zucca, E, Cantonetti, M, Cortelazzo, S, Wotherspoon, A, Ferreri, Aj, Zaja, Francesco, Lauria, F, De Renzo, A, Liberati, Ma, Falini, B, Balzarotti, M, Calderoni, A, Zaccaria, A, Gentilini, P, Fattori, Pp, Pavone, E, Angelopoulou, Mk, Alinari, L, Brugiatelli, M, Di Renzo, N, Bonifazi, F, Pileri, Sa, Cavalli, F, and International Extranodal Lymphoma Study, Group

Subjects
response rate, Author Keywords:PMLBCL, chemotherapy, radiotherapy, combined modality treatment KeyWords Plus:HIGH-DOSE CHEMOTHERAPY, NON-HODGKINS-LYMPHOMA, MACOP-B, COMBINATION CHEMOTHERAPY, MALIGNANT-LYMPHOMA, RADIATION-THERAPY, CLINICAL-TRIALS, TRANSPLANTATION, CLASSIFICATION, MANAGEMENT
Abstract

BACKGROUND AND OBJECTIVES: This multinational retrospective study compares the outcomes of patients with primary mediastinal large B-cell lymphoma (PMLBCL) with sclerosis after first-generation (dose-intensive regimens), third-generation (alternating regimens) and high-dose chemotherapy strategies, frequently with adjuvant radiation therapy. DESIGN AND METHODS: Between August 1981 and December 1999, a total of 426 previously untreated patients with confirmed diagnosis were enrolled in 20 institutions to receive combination chemotherapy with either first generation (CHOP or CHOP-like) regimens, third generation (MACOP-B, VACOP-B, ProMACE CytaBOM) regimens or high-dose chemotherapy (HDS/ABMT). RESULTS: With chemotherapy, complete response (CR) rates were 49% (50/105), 51% (142/277) and 53% (23/44) with first generation, third generation and high-dose chemotherapy strategies, respectively; partial response (PR) rates were 32%, 36% and 35%, respectively. All patients who achieved CR and 124/142 (84%) with PR had radiation therapy on the mediastinum. The final CR rates became 61% for CHOP/CHOP-like regimens, 79% for MACOP-B and other regimens, and 75% for HDS/ABMT. After median follow-ups from attaining CR of 48.5 months for CHOP/CHOP-like regimens, 51.7 months for MACOP-B type regimens and 32.4 months for HDS/ABMT, relapses occurred in 15/64 (23%), 27/218 (12%) and 0/33 (0%) patients, respectively. Projected 10-year progression-free survival rates were 35%, 67% and 78%, respectively (p=0.0000). Projected 10-year overall survival rates were 44%, 71% and 77%, respectively (p=0.0000), after median follow-ups from diagnosis of 52.3 months, 54.9 months and 35.8 months, respectively. INTERPRETATION AND CONCLUSIONS: In patients with PMLBCL with sclerosis, MACOP-B plus radiation therapy may be a better strategy than other treatments; these retrospective data need to be confirmed by prospective studies. The encouraging survival results after high dose chemotherapy require confirmation in selected high-risk patients.

Published
2002

19. Molecular profiling of blastic plasmacytoid dendritic cell neoplasm reveals a unique pattern and suggests selective sensitivity to NF-kB pathway inhibition

Author

Sapienza, Mr, Fuligni, F, Agostinelli, C, Tripodo, C, Righi, S, Laginestra, Ma, Pileri, A, Mancini, M, Rossi, M, Ricci, F, Gazzola, A, Melle, F, Mannu, C, Ulbar, F, Arpinati, M, Paulli, M, Maeda, T, Gibellini, D, Pagano, Livio, Pimpinelli, N, Santucci, M, Cerroni, L, Croce, Cm, Facchetti, F, Piccaluga, Pp, Pileri, Sa, Pagano, Livio (ORCID:0000-0001-8287-928X), Sapienza, Mr, Fuligni, F, Agostinelli, C, Tripodo, C, Righi, S, Laginestra, Ma, Pileri, A, Mancini, M, Rossi, M, Ricci, F, Gazzola, A, Melle, F, Mannu, C, Ulbar, F, Arpinati, M, Paulli, M, Maeda, T, Gibellini, D, Pagano, Livio, Pimpinelli, N, Santucci, M, Cerroni, L, Croce, Cm, Facchetti, F, Piccaluga, Pp, Pileri, Sa, and Pagano, Livio (ORCID:0000-0001-8287-928X)

Abstract

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare disease of controversial origin recently recognized as a neoplasm deriving from plasmacytoid dendritic cells (pDCs). Nevertheless, it remains an orphan tumor with obscure biology and dismal prognosis. To better understand the pathobiology of BPDCN and discover new targets for effective therapies, the gene expression profile (GEP) of 25 BPDCN samples was analyzed and compared with that of pDCs, their postulated normal counterpart. Validation was performed by immunohistochemistry (IHC), whereas functional experiments were carried out ex vivo. For the first time at the molecular level, we definitely recognized the cellular derivation of BPDCN that proved to originate from the myeloid lineage and in particular, from resting pDCs. Furthermore, thanks to an integrated bioinformatic approach we discovered aberrant activation of the NF-kB pathway and suggested it as a novel therapeutic target. We tested the efficacy of anti-NF-kB-treatment on the BPDCN cell line CAL-1, and successfully demonstrated by GEP and IHC the molecular shutoff of the NF-kB pathway. In conclusion, we identified a molecular signature representative of the transcriptional abnormalities of BPDCN and developed a cellular model proposing a novel therapeutic approach in the setting of this otherwise incurable disease.

Published
2014

24. Tumours of histiocytes and accessory dendritic cells: an immunohistochemical approach to classification from the International Lymphoma Study Group based on 61 cases

Author

Pileri, SA, Grogan, TM, Harris, NL, Banks, P, Campo, E, Chan, JK, Favera, RD, Delsol, G, De Wolf-Peeters, C, Falini, B, Gascoyne, RD, Gaulard, P, Gatter, KC, Isaacson, PG, Jaffe, ES, Kluin, P, Knowles, DM, Mason, DY, Mori, S, Müller-Hermelink, HK, Piris, MA, Ralfkiaer, E, Stein, H, Su, IJ, Warnke, RA, and Weiss, LM

Subjects
Adult, Histiocytic Disorders, Malignant, Male, Lymphoma, Histiocytes, Dendritic Cells, Middle Aged, Immunohistochemistry, Immunophenotyping, Microscopy, Electron, Biomarkers, Tumor, Humans, Female, Aged
Abstract

Neoplasms of histiocytes and dendritic cells are rare, and their phenotypic and biological definition is incomplete. Seeking to identify antigens detectable in paraffin-embedded sections that might allow a more complete, rational immunophenotypic classification of histiocytic/dendritic cell neoplasms, the International Lymphoma Study Group (ILSG) stained 61 tumours of suspected histiocytic/dendritic cell type with a panel of 15 antibodies including those reactive with histiocytes (CD68, lysozyme (LYS)), Langerhans cells (CD1a), follicular dendritic cells (FDC: CD21, CD35) and S100 protein. This analysis revealed that 57 cases (93%) fit into four major immunophenotypic groups (one histiocytic and three dendritic cell types) utilizing six markers: CD68, LYS, CD1a, S100, CD21, and CD35. The four (7%) unclassified cases were further classifiable into the above four groups using additional morphological and ultrastructural features. The four groups then included: (i) histiocytic sarcoma (n=18) with the following phenotype: CD68 (100%), LYS (94%), CD1a (0%), S100 (33%), CD21/35 (0%). The median age was 46 years. Presentation was predominantly extranodal (72%) with high mortality (58% dead of disease (DOD)). Three had systemic involvement consistent with 'malignant histiocytosis'; (ii) Langerhans cell tumour (LCT) (n=26) which expressed: CD68 (96%), LYS (42%), CD1a (100%), S100 (100%), CD21/35 (0%). There were two morphological variants: cytologically typical (n=17) designated LCT; and cytologically malignant (n=9) designated Langerhans cell sarcoma (LCS). The LCS were often not easily recognized morphologically as LC-derived, but were diagnosed based on CD1a staining. LCT and LCS differed in median age (33 versus 41 years), male:female ratio (3.7:1 versus 1:2), and death rate (31% versus 50% DOD). Four LCT patients had systemic involvement typical of Letterer-Siwe disease; (iii) follicular dendritic cell tumour/sarcoma (FDCT) (n=13) which expressed: CD68 (54%), LYS (8%), CD1a (0%), S100 (16%), FDC markers CD21/35 (100%), EMA (40%). These patients were adults (median age 65 years) with predominantly localized nodal disease (75%) and low mortality (9% DOD); (iv) interdigitating dendritic cell tumour/sarcoma (IDCT) (n=4) which expressed: CD68 (50%), LYS (25%), CD1a (0%), S100 (100%), CD21/35 (0%). The patients were adults (median 71 years) with localized nodal disease (75%) without mortality (0% DOD). In conclusion, definitive immunophenotypic classification of histiocytic and accessory cell neoplasms into four categories was possible in 93% of the cases using six antigens detected in paraffin-embedded sections. Exceptional cases (7%) were resolvable when added morphological and ultrastructural features were considered. We propose a classification combining immunophenotype and morphology with five categories, including Langerhans cell sarcoma. This simplified scheme is practical for everyday diagnostic use and should provide a framework for additional investigation of these unusual neoplasms.

Published
2002

29. Anaplastic lymphoma kinase expression as a marker of malignancy. Application to a case of anaplastic large cell lymphoma with huge granulomatous reaction

Author

Piccaluga, Pp, Ascani, S., Orcioni, Gf, MILENA PICCIOLI, Pileri, A., Falini, B., and Pileri, Sa

Subjects
Granuloma, chromosomal aberration, Insect Bites and Stings, Receptor Protein-Tyrosine Kinases, Protein-Tyrosine Kinases, chemotherapy, immunophenotype, Neoplasm Proteins, Diagnosis, Differential, Ticks, anaplastic large cell lymphoma, Biomarkers, Tumor, Animals, Humans, Lymphoma, Large-Cell, Anaplastic, Anaplastic Lymphoma Kinase, Female, Child
Abstract

Anaplastic large cell lymphoma (ALCL) shows a wide morphologic spectrum, including the occurrence of reactive components obscuring the neoplastic population. This makes its distinction from hyperimmune reaction difficult. The authors describe an ALCL in a girl wha had a tick bite 20 days prior to clinical presentation. She developed a huge epithelioid reaction (an unprecedented finding for this tumor). The diagnostic controversies were solved by applying the ALKc antibody against anaplastic large cell lymphoma kinase (ALK), in conjunction with reagents anti-nucleophosmin (NPM), which showed the typical staining pattern observed in ALCL carrying t(2;5). Comprised within the epithelioid component there were large anaplastic cells and small-medium sized atypical elements displaying strong nuclear and cytoplasmic positivity for ALK and NPM (N-terminal region). This pattern, never observed in normal lymphocytes, corresponds to the presence of the product of the hybrid gene NPM/ALK produced by t(2;5). Following the diagnosis, the patient - whose general conditions were critical - underwent aggressive chemotherapy, achieving complete remission.

Published
2000

32. The genetics of Richter syndrome reveals disease heterogeneity and predicts survival after transformation

Author

Rossi, D, Spina, V, Deambrogi, C, Rasi, S, Laurenti, Luca, Stamatopoulos, K, Arcaini, L, Lucioni, M, Rocque, Gb, Xu Monette, Zy, Visco, C, Chang, J, Chigrinova, E, Forconi, F, Marasca, R, Besson, C, Papadaki, T, Paulli, M, Larocca, Luigi Maria, Pileri, Sa, Gattei, V, Bertoni, Francesco, Foà, R, Young, Kh, Gaidano, G., Laurenti, Luca (ORCID:0000-0002-8327-1396), Larocca, Luigi Maria (ORCID:0000-0003-1739-4758), Rossi, D, Spina, V, Deambrogi, C, Rasi, S, Laurenti, Luca, Stamatopoulos, K, Arcaini, L, Lucioni, M, Rocque, Gb, Xu Monette, Zy, Visco, C, Chang, J, Chigrinova, E, Forconi, F, Marasca, R, Besson, C, Papadaki, T, Paulli, M, Larocca, Luigi Maria, Pileri, Sa, Gattei, V, Bertoni, Francesco, Foà, R, Young, Kh, Gaidano, G., Laurenti, Luca (ORCID:0000-0002-8327-1396), and Larocca, Luigi Maria (ORCID:0000-0003-1739-4758)

Abstract

Richter syndrome (RS) represents the development of diffuse large B-cell lymphoma in the context of chronic lymphocytic leukemia. The scarcity of biologic information about RS has hampered the identification of molecular predictors of RS outcome. We addressed this issue by performing a comprehensive molecular characterization of 86 pathologically proven RS. TP53 disruption (47.1%) and c-MYC abnormalities (26.2%) were the most frequent alterations, whereas common genetic lesions of de novo diffuse large B-cell lymphoma were rare or absent. By multivariate analysis, lack of TP53 disruption (hazard ratio, 0.43; P = .003) translated into significant survival advantage with 57% reduction in risk of death. An algorithm based on TP53 disruption, response to RS treatment, and Eastern Cooperative Oncology Group performance status had 80.9% probability of correctly discriminating RS survival (c-index = .809). RS that were clonally unrelated to the paired chronic lymphocytic leukemia phase were clinically and biologically different from clonally related RS because of significantly longer survival (median, 62.5 months vs 14.2 months; P = .017) and lower prevalence of TP53 disruption (23.1% vs 60.0%; P = .018) and B-cell receptor stereotypy (7.6% vs 50.0%; P = .009). The molecular dissection of RS into biologically distinct categories highlights the genetic heterogeneity of this disorder and provides clinically relevant information for refining the prognostic stratification of patients.

Published
2011

33. Anaplastic large cell lymphoma: a concept reviewed

Author

Pileri, Sa, Milani, M, Ascani, Stefano, Fraternali Orcioni, G, Piccioli, M, Poggi, S, Sabattini, E, and Falini, B.

Abstract

The development of the concept of anaplastic large cell lymphoma is reviewed. The subtypes of the tumor proposed in the literature, including the so-called Hodgkin's-like variant, are discussed both on morphological and clinical grounds. The more recent information on the genetic and molecular characteristics of the tumor (i.e. 2;5 translocation, formation of the NPM/ALK hybrid gene, and production of a specific protein) are presented: their possible implications in the future classification and clinical management of the neoplasm are discussed.

Published
1999

35. Tumours of histiocytes and accessory dendritic cells: an immunohistochemical approach to classification from the International Lymphoma Study Group based on 61 cases

Author

UCL, Pileri, SA., UCL, and Pileri, SA.

Abstract

Neoplasms of histiocytes and dendritic cells are rare, and their phenotypic and biological definition is incomplete. Seeking to identify antigens detectable in paraffin-embedded sections that might allow a more complete, rational immunophenotypic classification of histiocytic/dendritic cell neoplasms, the International Lymphoma Study Group (ILSG) stained 61 tumours of suspected histiocytic/dendritic cell type with a panel of 15 antibodies including those reactive with histiocytes (CD68, lysozyme (LYS)), Langerhans cells (CD1a), follicular dendritic cells (FDC: CD21, CD35) and S100 protein. This analysis revealed that 57 cases (93%) fit into four major immunophenotypic groups (one histiocytic and three dendritic cell types) utilizing six markers: CD68, LYS, CD1a, S100, CD21, and CD35. The four (7%) unclassified cases were further classifiable into the above four groups using additional morphological and ultrastructural features. The four groups then included: (i) histiocytic sarcoma (n =18) with the following phenotype: CD68 (100%), LYS (94%), CD1a (0%), S100 (33%), CD21/35 (0%). The median age was 46 years. Presentation was predominantly extranodal (72%) with high mortality (58% dead of disease (DOD)). Three had systemic involvement consistent with `malignant histiocytosis'; (ii) Langerhans cell tumour (LCT) (n =26) which expressed: CD68 (96%), LYS (42%), CD1a (100%), S100 (100%), CD21/35 (0%). There were two morphological variants: cytologically typical (n =17) designated LCT; and cytologically malignant (n =9) designated Langerhans cell sarcoma (LCS). The LCS were often not easily recognized morphologically as LC-derived, but were diagnosed based on CD1a staining. LCT and LCS differed in median age (33 versus 41 years), male:female ratio (3.7:1 versus 1:2), and death rate (31% versus 50% DOD). Four LCT patients had systemic involvement typical of Letterer-Siwe disease; (iii) follicular dendritic cell tumour/sarcoma (FDCT) (n =13) which expressed: CD68 (54%), LYS (

Published
2002

36. A20deletion is associated with copy number gain at theTNFA/B/Clocus and occurs preferentially in translocation-negative MALT lymphoma of the ocular adnexa and salivary glands

Author

Chanudet, E, primary, Ye, H, additional, Ferry, J, additional, Bacon, CM, additional, Adam, P, additional, Müller-Hermelink, HK, additional, Radford, J, additional, Pileri, SA, additional, Ichimura, K, additional, Collins, VP, additional, Hamoudi, RA, additional, Nicholson, AG, additional, Wotherspoon, AC, additional, Isaacson, PG, additional, and Du, MQ, additional

Published
2009
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37. Selective loss of B-cell phenotype in lymphocyte predominant Hodgkin lymphoma

Author

Tedoldi, S, primary, Mottok, A, additional, Ying, J, additional, Paterson, JC, additional, Cui, Y, additional, Facchetti, F, additional, van Krieken, JHJM, additional, Ponzoni, M, additional, Özkal, S, additional, Masir, N, additional, Natkunam, Y, additional, Pileri, SA, additional, Hansmann, M-L, additional, Mason, DY, additional, Tao, Q, additional, and Marafioti, T, additional

Published
2007
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39. Jaw1/LRMP, a germinal centre‐associated marker for the immunohistological study of B‐cell lymphomas

Author

Tedoldi, S, primary, Paterson, JC, additional, Cordell, J, additional, Tan, S‐Y, additional, Jones, M, additional, Manek, S, additional, Dei Tos, AP, additional, Roberton, H, additional, Masir, N, additional, Natkunam, Y, additional, Pileri, SA, additional, Facchetti, F, additional, Hansmann, M‐L, additional, Mason, DY, additional, and Marafioti, T, additional

Published
2006
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40. Chlamydia psittaci is variably associated with ocular adnexal MALT lymphoma in different geographical regions

Author

Chanudet, E, primary, Zhou, Y, additional, Bacon, CM, additional, Wotherspoon, AC, additional, Müller-Hermelink, H-K, additional, Adam, P, additional, Dong, HY, additional, de Jong, D, additional, Li, Y, additional, Wei, R, additional, Gong, X, additional, Wu, Q, additional, Ranaldi, R, additional, Goteri, G, additional, Pileri, SA, additional, Ye, H, additional, Hamoudi, RA, additional, Liu, H, additional, Radford, J, additional, and Du, M-Q, additional

Published
2006
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42. Lymphoma Classification Proposal - Clarification

Author

UCL, Harris, NL., Jaffe, ES., Stein, H., Banks, PM., Chan, JKC., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Isaacson, PG., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., Warnke, RA., UCL, Harris, NL., Jaffe, ES., Stein, H., Banks, PM., Chan, JKC., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Isaacson, PG., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., and Warnke, RA.

Published
1995

43. A Revised European-american Classification of Lymphoid Neoplasms Proposed By the International Lymphoma Study-group - a Summary Version

Author

UCL, Chan, JKC., Banks, PM., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Harris, NL., Isaacson, PG., Jaffe, ES., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., Stein, H., Warnke, RA., UCL, Chan, JKC., Banks, PM., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Harris, NL., Isaacson, PG., Jaffe, ES., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., Stein, H., and Warnke, RA.

Published
1995

44. A Revised European-american Classification of Lymphoid Neoplasms - a Proposal From the International Lymphoma Study-group

Author

UCL, Harris, NL., Jaffe, ES., Stein, H., Banks, PM., Chan, JKC., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Isaacson, PG., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., Warnke, RA., UCL, Harris, NL., Jaffe, ES., Stein, H., Banks, PM., Chan, JKC., Cleary, ML., Delsol, G., Dewolfpeeters, C., Falini, B., Gatter, KC., Grogan, TM., Isaacson, PG., Knowles, DM., Mason, DY., Mullerhermelink, HK., Pileri, SA., Piris, MA., Ralfkiaer, E., and Warnke, RA.

Published
1994

45. New molecular insights into peripheral T cell lymphomas.

Author

Pileri SA, Piccaluga PP, Pileri, Stefano A, and Piccaluga, Pier Paolo

Abstract

Peripheral T cell lymphomas (PTCLs) are heterogeneous neoplasms and represent about 12% of all lymphoid malignancies. They are often regarded as "orphan diseases," a designation that does not reflect their real incidence but rather signifies the difficulties encountered in their classification, diagnosis, and treatment. Here we revise the current understanding of the pathobiological characteristics of the most common nodal PTCLs by focusing on the contribution given by high-throughput technologies and the identification of potential therapeutic targets proposed by translational studies. [ABSTRACT FROM AUTHOR]

Published
2012
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48. Aberrant promoter methylation of multiple genes throughout the clinico-pathologic spectrum of B-cell neoplasia

Author

Gaidano, G., Carbone, A., Esteller, M., Pileri, Sa, Vitolo, U., Saglio, G., Bhatia, K., Paulli, M., Franceschetti, S., Annunziata Gloghini, Capello, D., and Rossi, D.

Subjects
Limfomes, B cells, Leukemia, Cèl·lules B, ADN, Leucèmia, DNA, Methylation, hemic and lymphatic diseases, Genetics, Lymphomas, Metilació, neoplasms, Genètica
Abstract

Background and objectives: aberrant promoter methylation targets CpG islands causing gene silencing. We explored aberrant promoter methylation of genes potentially involved in B-cell malignancies and encoding proteins implicated in DNA repair (O6-methylguanine-DNA methyltransferase, MGMT), detoxification of environmental xenobiotics (glutathione S-transferase P1, GSTP1), apoptosis regulation (death associated protein kinase, DAP-k and caspase 8, CASP8) and cell cycle control (p73). Design and methods: three hundred and seventeen B-cell malignancies were investigated by methylation-specific polymerase chain reaction (MSP) of MGMT, GSTP1, DAP-k, CASP8 and p73 genes. In selected cases, MSP results were matched to protein expression studies by immunohistochemistry or Western blotting. Results: DAP-k promoter methylation occurred at highest frequency in follicular lymphoma (85.0%) and MALT-lymphoma (72.2%). MGMT methylation targeted both precursor B-cell neoplasia (23.8%) and mature B-cell tumors (27.6%). GSTP1 methylation was commonest in hairy cell leukemia (75.0%), follicular lymphoma (55.5%), Burkitt s lymphoma (52.0%), and MALT lymphoma (50.0%). Methylation of p73 and CASP8 was rare or absent. DAP-k and MGMT methylation caused absent protein expression. Interpretation and conclusions: methylation of MGMT, DAP-k and GSTP1 represents a major pathogenetic event in several B-cell malignancies. In follicular lymphoma and MALT lymphoma, frequent inactivation of the apoptosis extrinsic pathway through DAP-k methylation may reinforce the survival advantage already conferred by deregulation of the intrinsic apoptotic pathway. Inactivation of GSTP1 in gastric MALT lymphoma represents an additional mechanism favoring accumulation of reactive oxygen species and lymphomagenesis. Finally, the frequency of GSTP1 aberrant methylation in diffuse large B-cell lymphoma prompts studies aimed at verifying the prognostic impact of this epigenetic lesion in these lymphomas.

49. The pathologist's view point. Part II - Aggressive lymphomas

Author

Pileri, Sa, Ascani, S., Sabattini, E., Fraternali-Orcioni, G., Poggi, S., Piccoli, M., Piccaluga, Pp, Gamberi, B., Zinzani, Pl, Lorenzo LEONCINI, and Falini, B.

Subjects
Humans, Immunophenotyping, Lymphoma, Lymphoma, B-Cell, Lymphoma, T-Cell, Practice Guidelines as Topic, large cell lymphoma, lymphoblastoma, practice guideline, disease classification, mantle cell lymphoma, B-Cell, Burkitt lymphoma, B cell lymphoma, follicular lymphoma, histopathology, immunophenotyping, lymphoma, T cell lymphoma, T-Cell
Abstract

The REAL/WHO classification constitutes a new tool for the better understanding and treatment of malignant lymphomas. The authors focus on the key features of aggressive B- and T-cell lymphomas, aiming to contribute to the cross-talk between pathologists and clinicians.Each lymphoma entity is analyzed on the basis of the most representative contributions in the literature and the authors' experience gained in studying more than 20,000 lymphoid tumors over a 20-year period.Guidelines for diagnosis and areas of interest for future clinico-pathologic studies are identified and discussed. Within this context, selected data obtained by the application of novel markers are presented.The present know- ledge and organization of malignant lymphomas now make the development of tailored therapies a feasible goal.

50. The alteration of lipid metabolism in burkitt lymphoma identifies a novel marker: adipophilin

Author

Monica Onorati, Stefano Pileri, Claudio Doglioni, Maria Raffaella Ambrosio, Pier Paolo Piccaluga, Martin D. Ogwang, Maurilio Ponzoni, Valeria Malagnino, Kikkeri N. Naresh, Valeria Calbi, Giulia De Falco, Lorenzo Leoncini, Stefano Lazzi, Bruno Jim Rocca, Ambrosio MR, Piccaluga PP, Ponzoni M, Rocca BJ, Malagnino V, Onorati M, De Falco G, Calbi V, Ogwang M, Naresh KN, Pileri SA, Doglioni C, Leoncini L, Lazzi S, Ambrosio, Mr, Piccaluga, Pp, Ponzoni, Maurilio, Rocca, Bj, Malagnino, V, Onorati, M, De Falco, G, Calbi, V, Ogwang, M, Naresh, Kn, Pileri, Sa, Doglioni, Claudio, Leoncini, L, and Lazzi, S.

Subjects
Genetics and Molecular Biology (all), Pathology, Anatomy and Physiology, Lymphoma, lcsh:Medicine, Biochemistry, immune system diseases, Immune Physiology, hemic and lymphatic diseases, Lipid droplet, lcsh:Science, Hematopathology, Multidisciplinary, Tumor, medicine.diagnostic_test, Medicine (all), Burkitt Lymphoma, Diffuse, BCL10, Gene Expression Regulation, Neoplastic, Oncology, Medicine, Oncology Agents, lipids (amino acids, peptides, and proteins), Lymphoma, Large B-Cell, Diffuse, Molecular Pathology, Research Article, medicine.medical_specialty, Clinical Pathology, Perilipin 2, Histopathology, Biology, Biomarkers, Tumor, Humans, Membrane Proteins, Perilipin-2, Staining and Labeling, Lipid Metabolism, Biochemistry, Genetics and Molecular Biology (all), Agricultural and Biological Sciences (all), Molecular Genetics, Diagnostic Medicine, Biopsy, medicine, Large B-Cell, Neoplastic, lcsh:R, Lipid metabolism, medicine.disease, Gene Expression Regulation, Anatomical Pathology, Cytoplasm, Surgical Pathology, biology.protein, lcsh:Q, Burkitt's lymphoma, Biomarkers, General Pathology
Abstract

BACKGROUND: Recent evidence suggests that lipid pathway is altered in many human tumours. In Burkitt lymphoma this is reflected by the presence of lipid droplets which are visible in the cytoplasm of neoplastic cells in cytological preparations. These vacuoles are not identifiable in biopsy section as lipids are "lost" during tissue processing. METHODS AND RESULTS: In this study we investigated the expression of genes involved in lipid metabolism, at both RNA and protein level in Burkitt lymphoma and in other B-cell aggressive lymphoma cases. Gene expression profile indicated a significant over-expression of the adipophilin gene and marked up-regulation of other genes involved in lipid metabolism in Burkitt lymphoma. These findings were confirmed by immunohistochemistry on a series od additional histological samples: 45 out of 47 BL cases showed strong adipophilin expression, while only 3 cases of the 33 of the not-Burkitt lymphoma category showed weak adipophilin expression (p

Published
2012

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