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Evolving Therapies in Relapsed and Refractory Hodgkin Lymphoma

S. Pukiat,F. Hernandez-Ilizaliturri

Published 2012 in Unknown venue

ABSTRACT

Approximately 20% of Hodgkin Lymphoma (HL) patients do not achieve a durable remission or fail to respond to front-line chemotherapy. Despite the attempt to improve clinical outcomes by using the risk adaptive therapy, a significant number of patients die as a results of relapsed/refractory (rel/ref) disease.1 Advances in understanding the etiology and molecular biology of HL are leading the development of novel therapeutic strategies that could be applied to improve clinical outcome of rel/ref HL patients. The pathologic features of HL reflect a defect in immune responses resulting from various cytokines and chemokines secreted partially by Hodgkin Reed-Sternberg (HRS) cells. HRS cells are unique in the way that they lost typical B cell gene expression pattern but retain the expression of surface molecules involving in antigen presentation (tumor necrosis factor receptor (CD30, CD40), CD80, MHC class II, and CD86). Aberration of Notch signaling pathway may contribute to their reprogramming.2,3 Multiple genetic lesions, deregulated signaling pathway and transcription factors play important role in pathogenesis of HL including constitutive activation of nuclear factor kappa B (NFκB) and the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway.4-6 Moreover, the role of the microenvironment in HL has been increasingly recognized. The majority of the cell population in HL-affected tissue is composition of the inflammatory cellular infiltrate, not the HRS cells that represents only small population (<1%). Understanding the complex relationship between the HRS cells and the microenvironment and chemokines milieu involved in its formation is crucial for the development of new therapeutic strategies.

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