Journal
PATHOBIOLOGY
Volume 73, Issue 3, Pages 107-125Publisher
KARGER
DOI: 10.1159/000095558
Keywords
classical Hodgkin lymphoma; Hodgkin and Reed-Sternberg cells; histopathology; immunophenotype; histogenesis; pathogenesis
Categories
Ask authors/readers for more resources
The World Health Organization has acknowledged the malignant nature of classical Hodgkin lymphoma (cHL), which encompasses four histological subtypes. The diagnosis of cHL is based on the detection of malignant Hodgkin and Reed-Sternberg cells (HRSC) confirmed by immunophenotyping and the detection of growth patterns specific to each histological subtype. The pathologic HRSC arise from germinal center or immediate postgerminal cells that lack detectable immunoglobulin/B-cell antigen receptor expression, with a consequent loss of B-cell identity; very few cHL cases are of T-cell origin. To escape apoptosis, which normally occurs in B cells with nonfunctioning antigen receptor machinery, HRSC develop concurrent antiapoptotic mechanisms by activation of nuclear factor-kappa B or are rescued by Epstein-Barr virus infection. HRSC are characterized by a variable and inconstant immunophenotype, with a remarkable loss of lineage-specific cell antigens and expression of antigens of other cell lineages. The master plan of B-cell identity in HRSC is disturbed not only at the immunoglobulin expression level, but also at the transcriptional factor level. HRSC are further characterized by profound cell cycle deregulation with futile replication, multinucleation and poly- and aneuploidy. Here, we review pathobiological aspects of cHL with respect to lymphomagenesis and routine diagnostics. Copyright (c) 2006 S. Karger AG, Basel.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available