As cells age, the ends of their chromosomes, the telomeres, become shortened. The chromosomal length eventually shortens to a critical point, which is thought to lead to chromosomal instability and/or cell death. Neoplastic cells have increased amounts of telomerase, an enzyme that prevents this shortening; this may be one mechanism by which tumor cells grow. Due to the scarcity of neoplastic Reed-Sternberg cells in tissues of Hodgkin Lymphoma, studies of telomere length and telomerase expression have been difficult and few. These few studies have tended to show an increase in telomerase expression in tissues from Hodgkin Lymphoma. In order to determine telomere length in Reed-Sternberg cells, we performed an immunofluorescence/FISH assay using a PNA pantelomeric probe and a CD30 antibody with which to identify the Reed-Sternberg cells (Am J Pathol 160:1259–68, 2002). Six cases were studied, with patient ages ranging from 18– 51 years. Telomere length was assessed on a semiquantitative scale. Of the six cases, five had evaluable hybridization signal. In these five cases, 53 CD30-positive cells (between 3–20 per case) were studied. In forty cells, the hybridization signal (telomere length) was less than that of surrounding cells, and in 13 it was the same; in no case was telomere length greater in the Reed-Sternberg cell than in surrounding lymphocytes (p< 0.001, Wilcoxon signed ranks test). There was no correlation between the age of the patient or the age of the sample and telomere probe signal intensity/quantity. Similar to epithelial and soft tissue tumors, it appears that the neoplastic cells in Hodgkin Lymphoma have shortened telomere length as compared to the surrounding normal cells.
Disclosure: No relevant conflicts of interest to declare.