HIV-associated Hodgkin's iymphoma. Antiapoptotic pathways and mechanisms for immune escape by tumor cells in the setting of improved immunity

摘要

Although Reed-Sternberg (RS) cells of classical Hodgkin's Iymphoma (cHL) are usually transformed B cells, gene expression analysis of RS cell lines using microarrays revealed that the RS cells have lost the expression of most B-cell markers (1). The alterations involved in the pathogenesis of Hodgkin's Iymphoma are still largely unknown. Escape from apoptosis is an important event in tumor-cell pathogenesis and this applies especially to RS cells. As RS cells are likely derived from preapoptotic germinal-center B cells (2), the rescue from apoptosis is a key event in the transformation process, leading to RS cell generation. Several aberrantly activated signaling pathways contribute to the survival of RS cells, nuclear factor kappa B (NFkB) being perhaps the most important one (3).