Genomic alterations in Hodgkin's lymphoma.
Cytogenetic analysis of Hodgkin's lymphoma (HL) is hampered by the scarcity of neoplastic cells within a sea of reactive cells. There is accumulating evidence that HL represents 2 disease entities, classic HL (cHL) with its morphologic variants and nodular lymphocyte predominant HL (NLPHL). This subdivision, initially worked out in morphologic and immunohistochemical studies, has been further substantiated by molecular cytogenetic investigations. Two recurrent chromosomal aberrations, namely gains of 2p13-p16 and 9p24, have been found by comparative genomic hybridization analysis in microdissected cells from cHL patients as well as in cHL cell lines, but not in NLPHL cells. The available cHL cell lines are remarkably heterogeneous in their karyotypes, suggesting profound genomic instability leading to numeric chromosomal aberration and multiple chromosomal breaks and translocations. In this article, we review genomic aberrations that may contribute to the development and maintenance of the morphologic and clinical presentation of these beta-cell lymphoma entities. Furthermore, we delineate current data on the genomic changes observed in the neoplastic cells of HL that are created by epigenetic mechanisms, which are alternative mechanisms that regulate the expression of relevant genes.
Weniger
Marc A
MA
Department of Pathology, University of Ulm, Ulm, Germany.
Barth
Thomas F E
TF
Möller
Peter
P
D002869:Chromosome Aberrations; D002889:Chromosomes, Human, Pair 2 / Q000235:genetics; D002899:Chromosomes, Human, Pair 9 / Q000235:genetics; D044127:Epigenesis, Genetic; D015973:Gene Expression Regulation, Leukemic; D042822:Genomic Instability; D006689:Hodgkin Disease / Q000235:genetics*; D006801:Humans; D016393:Lymphoma, B-Cell / Q000235:genetics; D009693:Nucleic Acid Hybridization / Q000379:methods