Hodgkin-like anaplastic large cell lymphoma (previously designated in the REAL classification) has same immunophenotypic features to classical Hodgkin lymphoma

In the WHO classification, the majority of Hodgkin-like ALCL cases as defined by the REAL classification are considered to be CHL. However, establishing a histological diagnosis for the gray zone between CHL and ALCL is often confusing. In this study, we re-evaluated such cases by performing immunohistochemistry with antibodies against PAX-5/BSAP, Oct.2, and BOB.1/OBF.1. Expression of PAX-5/BSAP was observed in 88% (76/87) of CHL specimens and none (0/11) of ALK-positive ALCL specimens. Among specimens of Hodgkin-like ALCL and ALK-negative ALCL, expression of PAX-5/BSAP was observed in 77% (20/26) and 18% (3/17), respectively. Most of the PAX-5/BSAP-positive specimens were negative for Oct.2 and/or BOB.1/OBF.1 except for four CHL specimens. Our results may support the WHO classification in which most cases of Hodgkin-like ALCL are classified as CHL. However, the patients with Hodgkin-like ALCL with CHL-immunophenotype (PAX-5/BSAP-positive and negative for Oct.2 and/or BOB.1) did not have a favorable outcome, with a 5-year OS rate of 58%.

[1]  C. de Wolf‐Peeters,et al.  Relationship between classic Hodgkin lymphoma and overlapping large cell lymphoma investigated by comparative expressed sequence hybridization expression profiling , 2006, The Journal of pathology.

[2]  A. Mikata,et al.  Reciprocal/dichotomic expression of vimentin and B cell differentiation antigens in Reed-Sternberg's cells , 2005, Virchows Archiv A.

[3]  Juan F. García,et al.  Analysis of transcription factor OCT.1, OCT.2 and BOB.1 expression using tissue arrays in classical Hodgkin's lymphoma , 2004, Modern Pathology.

[4]  G. Rassidakis,et al.  Absence of Epstein-Barr virus in anaplastic large cell lymphoma: a study of 64 cases classified according to World Health Organization criteria. , 2004, Human pathology.

[5]  H. Stein,et al.  Differential Eµ enhancer activity and expression of BOB.1/OBF.1, Oct2, PU.1, and immunoglobulin in reactive B‐cell populations, B‐cell non‐Hodgkin lymphomas, and Hodgkin lymphomas , 2004, The Journal of pathology.

[6]  T. Golub,et al.  The molecular signature of mediastinal large B-cell lymphoma differs from that of other diffuse large B-cell lymphomas and shares features with classical Hodgkin lymphoma. , 2003, Blood.

[7]  J. A. Chan,et al.  The B-cell transcription factors BSAP, Oct-2, and BOB.1 and the pan-B-cell markers CD20, CD22, and CD79a are useful in the differential diagnosis of classic Hodgkin lymphoma. , 2003, American journal of clinical pathology.

[8]  L. Staudt,et al.  Molecular Diagnosis of Primary Mediastinal B Cell Lymphoma Identifies a Clinically Favorable Subgroup of Diffuse Large B Cell Lymphoma Related to Hodgkin Lymphoma , 2003, The Journal of experimental medicine.

[9]  C. Fellbaum,et al.  Expression patterns of transcription factors in progressively transformed germinal centers and Hodgkin lymphoma , 2003, Virchows Archiv.

[10]  J. Delabie,et al.  The Value of Anti-Pax-5 Immunostaining in Routinely Fixed and Paraffin-Embedded Sections: A Novel Pan Pre-B and B-Cell Marker , 2002, The American journal of surgical pathology.

[11]  A. van den Berg,et al.  Clonal relation in a case of CLL, ALCL, and Hodgkin composite lymphoma. , 2002, Blood.

[12]  P. Vyas,et al.  Pathology and genetics: Tumours of haematopoietic and lymphoid tissues , 2001 .

[13]  J. Delabie,et al.  The transcription factor PU.1, necessary for B-cell development is expressed in lymphocyte predominance, but not classical Hodgkin's disease. , 2001, The American journal of pathology.

[14]  P. Gaulard,et al.  Pathologic and Clinical Features of 77 Hodgkin's Lymphoma Patients Treated in a Lymphoma Protocol (LNH87): A GELA Study , 2001, The American journal of surgical pathology.

[15]  E. Jaffe Anaplastic Large Cell Lymphoma: The Shifting Sands of Diagnostic Hematopathology , 2001, Modern Pathology.

[16]  H. Stein,et al.  Down-regulation of BOB.1/OBF.1 and Oct2 in classical Hodgkin disease but not in lymphocyte predominant Hodgkin disease correlates with immunoglobulin transcription. , 2001, Blood.

[17]  S. Pileri,et al.  CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. , 2000, Blood.

[18]  H. Stein,et al.  Detection of clonal T-cell receptor gamma-chain gene rearrangements in Reed-Sternberg cells of classic Hodgkin disease. , 2000, Blood.

[19]  H. Stein,et al.  Hodgkin and reed-sternberg cells represent an expansion of a single clone originating from a germinal center B-cell with functional immunoglobulin gene rearrangements but defective immunoglobulin transcription. , 2000, Blood.

[20]  G Flandrin,et al.  World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues: report of the Clinical Advisory Committee meeting-Airlie House, Virginia, November 1997. , 1999, Journal of clinical oncology : official journal of the American Society of Clinical Oncology.

[21]  K. Rajewsky,et al.  Cellular origin of human B-cell lymphomas. , 1999, The New England journal of medicine.

[22]  G. Lenz,et al.  Frequent expression of the B-cell-specific activator protein in Reed-Sternberg cells of classical Hodgkin's disease provides further evidence for its B-cell origin. , 1999, Blood.

[23]  S. Pileri,et al.  Anaplastic large cell lymphoma Hodgkin's-like: a randomized trial of ABVD versus MACOP-B with and without radiation therapy. , 1998, Blood.

[24]  S. Pileri,et al.  Origin of nodular lymphocyte-predominant Hodgkin's disease from a clonal expansion of highly mutated germinal-center B cells. , 1997, The New England journal of medicine.

[25]  E. Jaffe,et al.  Cytotoxic cell antigen expression in anaplastic large cell lymphomas of T- and null-cell type and Hodgkin's disease: evidence for distinct cellular origin. , 1997, Blood.

[26]  S. Mori,et al.  Anaplastic large cell lymphomas expressing the novel chimeric protein p80NPM/ALK: a distinct clinicopathologic entity. , 1995, Leukemia.

[27]  H. Stein,et al.  Anaplastic large-cell lymphomas of T-cell and null-cell phenotype express cytotoxic molecules. , 1996, Blood.

[28]  K. Oka,et al.  Poor correlation between clonal immunoglobulin gene rearrangement and immunoglobulin gene transcription in Hodgkin's disease. , 1996, The American journal of pathology.

[29]  K. Rajewsky,et al.  Hodgkin and Reed-Sternberg cells in Hodgkin's disease represent the outgrowth of a dominant tumor clone derived from (crippled) germinal center B cells , 1996, The Journal of experimental medicine.

[30]  H Stein,et al.  A revised European-American classification of lymphoid neoplasms: a proposal from the International Lymphoma Study Group. , 1994, Blood.

[31]  H. Stein,et al.  Hodgkin's disease with a B-cell phenotype often shows a VDJ rearrangement and somatic mutations in the VH genes. , 1994, Blood.

[32]  G. Delsol,et al.  High incidence of Epstein–Barr virus detection in Hodgkin's disease and absence of detection in anaplastic large‐cell lymphoma in children , 1993, Histopathology.

[33]  G. Pinkus,et al.  Hodgkin's disease, lymphocyte predominance type, nodular--further evidence for a B cell derivation. L & H variants of Reed-Sternberg cells express L26, a pan B cell marker. , 1988, The American journal of pathology.

[34]  K. Lennert,et al.  The expression of the Hodgkin's disease associated antigen Ki-1 in reactive and neoplastic lymphoid tissue: evidence that Reed-Sternberg cells and histiocytic malignancies are derived from activated lymphoid cells. , 1985, Blood.

[35]  H. Stein,et al.  Hodgkin and sternberg‐reed cells contain antigens specific to late cells of granulopoiesis , 1982, International journal of cancer.

[36]  E. Kaplan,et al.  Nonparametric Estimation from Incomplete Observations , 1958 .