Hodgkin lymphoma: 2011 update on diagnosis, risk‐stratification, and management

Abstract

Disease overview: Hodgkin lymphoma (HL) is an uncommon B‐cell lymphoid malignancy affecting 8,500 new patients annually and representing ∼11% of all lymphomas in the United States. Diagnosis: HL is composed of two distinct disease entities; the more commonly diagnosed classical HL and the rare nodular lymphocyte predominant HL. Nodular sclerosis, mixed cellularity, lymphocyte depletion, and lymphocyte‐rich HL are subgroups under the designation of classical HL. Risk stratification: An accurate assessment of the stage of disease in patients with HL is critical for the selection of the appropriate therapy. Prognostic models that identify patients at low or high risk for recurrence are used to optimize therapy for patients with limited or advanced stage disease. Risk‐adapted therapy: Initial therapy for HL patients is based on the histology of the disease, the anatomical stage, and the presence of poor prognostic features. Patients with early stage disease are treated with combined modality strategies using abbreviated courses of combination chemotherapy followed by involved‐field radiation therapy, while those with advanced stage disease receive a longer course of chemotherapy often without radiation therapy. Management of relapsed/refractory disease: High‐dose chemotherapy (HDCT) followed by an autologous stem‐cell transplant (ASCT) is the standard of care for most patients who relapse following initial therapy. For patients who fail HDCT with ASCT, palliative chemotherapy, nonmyeloablative allogeneic transplant, or participation in a clinical trial should be considered. Am. J. Hematol. 86:852–858, 2011. © 2011 Wiley‐Liss, Inc.

TerraFlow, A New High Parameter Data Analysis Tool, Reveals Systemic T-cell Exhaustion and Dysfunctional Cytokine Production in Classical Hodgkin Lymphoma

“…Specifically, are immune perturbations in cHL global or local, and what influence does TME exert on systemic immunity? A number of studies suggest systemic immune dysregulation in early and advanced stage cHL, as demonstrated by poor responses to recall antigens in delayed-type hypersensitivity testing 9 and systemic elevations of a variety of immune modulators, including CCL17 (TARC) 8-10 , IL6 11 , IL2R 11 , galectin-1 12 , and soluble CD30 13 . Importantly, these studies did not detail the particular cell subsets that are altered in cHL.…”