ABSTRACT
Introduction 315 Pathobiology and diagnosis 317 Interface between classical Hodgkin lymphoma 317
and large B cell lymphomas Hodgkin lymphoma and mediastinal large B cell 317
lymphoma Hodgkin lymphoma and T cell/histiocyte-rich large B cell 318
lymphoma Hodgkin lymphoma and EBV-positive lymphoproliferative 318
disorders Interface between classical Hodgkin lymphoma and 318
anaplastic large cell lymphoma Synchronous lymphomas 319 Hodgkin and B cell non-Hodgkin lymphomas 319 Metachronous lymphomas 319
Non-Hodgkin lymphoma following Hodgkin lymphoma 320 Hodgkin lymphoma following non-Hodgkin lymphoma 320 Hodgkin lymphoma and chronic lymphocytic leukemia 320 Hodgkin lymphoma and T cell lymphomas 321 Nodular lymphocyte-predominant Hodgkin lymphoma 322
and diffuse large B cell lymphoma Nodular lymphocyte-predominant Hodgkin lymphoma 322
and T cell/histiocyte-rich large B cell lymphoma Clinical management 322 Gray zone lymphomas 323 Synchronous lymphomas 324 Metachronous lymphomas 324 Conclusion 324 Key points 324 References 325
Considerable progress has been made regarding the origin of the neoplastic cell in the lymphomas, both classical Hodgkin lymphoma (CHL) and the non-Hodgkin lymphomas (NHL). Regarding the Reed-Sternberg cell (RS) and mononuclear Hodgkin (H) cells, the neoplastic cells of CHL, recent evidence has indicated a B cell derivation in all or nearly all cases. If CHL is derived from an altered B lymphocyte, it is not surprising that areas of overlap with B cell NHL should occur both biologically and clinically (Fig. 19.1).1 The HRS cell is a crippled B cell, incapable of immunoglobulin secretion.2 Many other aspects of the B cell program are also suppressed in HRS cells.3-5 The biological and molecular events leading to this state are complex, and not fully resolved.6,7 These events may occur in the context of a relatively normal immune system as seen in most patients with CHL, or in the setting of immunodeficiency.8-12 In addition, cells resembling RS cells and variants may be observed disease states not meeting all
in the transformation to CHL.11,13 The study of lymphomas at the interface of CHL and NHL may provide insight into the pathogenesis of de novo CHL, and the molecular and cellular events distinguishing it from NHL.
