Instability of dinucleotide repeats in Hodgkin's disease

Abstract

Tumorigenesis has been shown to proceed through a series of genetic alterations involving protooncogenes and tumor suppressor genes. However, the investigation of genomic instability of microsatellites has disclosed a new mechanism for human carcinogenesis, which is involved not only in hereditary nonpolyposis colon cancer (HNPCC) but in a number of other malignancies as well. To determine whether microsatellite instability is involved in Hodgkin's disease, we screened 16 such tumors using 7 microsatellite marker loci on 6 chromosome arms 4, 5, 9p, 9q, 11, 14, and 17. Using the polymerase chain reaction method, DNA samples from the tumors and from normal peripheral blood leukocytes from each patient were compared for the allelic pattern produced at each locus. Five cases of genomic instability were identified, suggesting that this mechanism is relevant to the pathogenesis of HD. Am.

Proficient mismatch repair protein expression in Hodgkin and Reed Sternberg cells

“…There has been an attempt to determine MSI in cHD by analyzing lymph nodes affected by HD by performing whole tissue PCR, but the results unlikely reflect the biology of H/RS cells. 32 Hasse and colleagues, 33 in contrast, have analyzed 7 cases of cHD for the presence of MSI by pooling 10 single H/RS cells of each case. No extra microsatellite bands were detected in this study.…”

Involvement of Sp1 and Microsatellite Repressor Sequences in the Transcriptional Control of the Human CD30 Gene

“…Microsatellite instability has been identified in adult T-cell leukemia, childhood T-cell acute lymphoblastic leukemia, Hodgkin's disease, and some B-cell non-Hodgkin's lymphomas. [52][53][54][55][56][57] Whether the degenerate microsatellite within the CD30 promoter is specifically affected by microsatellite instability in vivo remains to be investigated. However, as the microsatellite in CD30 is a strong repressor, it is possible that deletion of the CD30 microsatellite may lead to relief of transcriptional repression, resulting in the overexpression of CD30 in Hodgkin's and non-Hodgkin's lymphomas.…”

Natural Resistance Against Brucellosis: A Review

“…In humans, instability in DNA dinucleotide and trinucleotide repeats is associated with several neurodegenerative and tumorigenic diseases. Genome wide instability of dinucleotide repeats is observed in tumors isolated from patients suffering from Hodgkin's disease and hereditary nonpolyposis colon cancer [95,96]. The archetypal triplet repeat disease, Huntington's disease, is categorized as a translated polyglutamine (polyQ) repeat disease, with its functionally associated unstable trinucleotide repeat (CAG), located in the first exon of the huntington (Htt) gene, laying down an expanded tract of glutamines within the expressed sequence of the gene [95].…”