SINCE Hodgkin's disease was last considered in detail in this journal1 impressive progress has been made in understanding discrete aspects of the disease. Evidence has accumulated in support of a monocyte-macrophage origin for the malignant cell, while immune suppression has been implicated in the disturbed cellular immunity that characterizes Hodgkin's disease. Some evidence from these immunologic studies, together with genetic and family surveys, hints at a genetic proclivity for immune suppression that may predispose to Hodgkin's disease, but the pathogenesis of the disease remains unknown. The newer strategies for staging and treatment can now be evaluated, and the earlier optimistic.
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