A concept of essentially secondary factors central to definitive subtype characterization of Hodgkin’s disease

Abstract

Conceptually, Hodgkin’s disease would appear to constitute a neoplasm that integrally incorporates responsive cellular elements in terms strictly of morphologic patterns of interaction resulting especially in a predictable scale of therapeutic and prognostic implications as related particularly to pathobiologic course and response to treatment. In this sense, Hodgkin’s disease might in a real sense constitute a valid point of reference in terms of processes not only in the generation of the neoplastic process but particularly in terms of how such a neoplastic process interacts with host systems in specifically characterizing the very nature of the intrinsic neoplastic process itself. In this manner, therefore, it might be valid to consider the totality of manifestations of Hodgkin’s disease as a fundamental series of processes that integrally determines the genesis and nature of the neoplastic process as a function especially of various host systems in response to that neoplasm. In terms strictly related to a viral or Epstein–Barr virus-related development of Hodgkin’s disease, it might perhaps be true that transcription factor NF-κB might induce the signaling of a CD30 receptor pathway that is intrinsically linked with anti-apoptosis of germinal center lymphocytes. In overall terms, perhaps, the Epstein–Barr viral nuclear antigens such as Latent membrane protein 1 would activate NF-κB as a mechanism that induces anti-apoptotic effect by multiple pathways in the added context particularly of a concerted series of cytokines that secondarily regulate T lymphocyte response. Indeed, in simple terms, Hodgkin’s disease would appear to involve a basic mechanism of induced transcription as an effective anti-apoptotic mechanism as exerted on Reed–Sternberg cells. The Epstein–Barr viral nuclear antigens might be pivotal in orchestrating a full series of cytokine and T lymphocyte responses that would perhaps contribute significantly to the effective perpetuation of such anti-apoptotic effect or effects as exerted on the Reed–Sternberg cells.