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Critical Reviews™ in Oncogenesis
SJR: 0.631 SNIP: 0.503 CiteScore™: 2.2

ISSN Druckformat: 0893-9675
ISSN Online: 2162-6448

Critical Reviews™ in Oncogenesis

DOI: 10.1615/CritRevOncog.v5.i2-3.60
pages 213-245

The Nature of Reed-Sternberg Cells: Phenotype, Genotype, and Other Properties

Su-Ming Hsu
Department of Pathology, University of Arkansas for Medical Sciences, Arkansas Cancer Research Center, and John L. McClellan Veterans Memorial Hospital, Little Rock, Arkansas
Pei-Ling Hsu
Department of Pathology, University of Arkansas for Medical Sciences, Arkansas Cancer Research Center, and John L. McClellan Veterans Memorial Hospital, Little Rock, Arkansas

ABSTRAKT

The most recent sophisticated investigations have provided new and revealing but also contradictory and controversial information on the biological nature and the cellular origin of Hodgkin and Reed-Sternberg (H-RS) cells. Immunophenotypic analyses have shown consistent expression of CD 15, CD30, CD74, and HLA-Dr antigens, but generally lack of T- or B cell-associated markers in H-RS cells. The H-RS cells are also devoid of many monocyte/macrophage-associated antigens. Molecular genetic studies have demonstrated heterogeneous findings with respect to rearrangements of T-cell receptor and immunoglobulin genes. Only a small percentage of the cases have rearrangements; this cannot always be attributed to the threshold of sensitivity of the method and/ or the scarcity of the malignant cells in tissues examined. The H-RS cells do not express transcription factors such as BSAP, TCF-1, and GATA-3, known to be associated with lymphoid cells. It appears that evidence to support a lymphoid origin for H-RS cells is still lacking. On the contrary, the mechanism responsible for the unique clinical and histopathologic alterations associated with this disease has become clear. The H-RS cells have been shown to secrete IL-1, IL-5, IL-6, IL-9, TNF-a, M-CSF, and TGF-b, and, less frequently, IL-4 and G-CSF. These cytokines are likely to be responsible for the increased cellular reaction and fibrosis observed in tissues involved by HD and for the immunosuppression in patients with HD. Like most lymphomas, the etiology or pathogenesis of HD remains unknown. The Epstein-Barr virus (EBV) genomes are clonally integrated in the H-RS cells of about half the cases. The significance of these findings, whether EBV is a causative agent or an epiphenomenon, remains to be elucidated.


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