Phenotypic and genotypic characterization of Hodgkin's disease

P. R K Koduru, M. Susin, P. Schulman, D. Catell, J. C. Goh, L. Karp, J. D. Broome

Research output: Contribution to journalArticlepeer-review

11 Scopus citations

Abstract

Although a few studies have reported clonal cytogenetic changes in Hodgkin's disease (HD), their correlation with histologic groups is poorly defined. This is because of insufficient numbers of clonally abnormal cases ascertained in each of these studies, an inherent problem associated with the cytogenetic studies of HD. In this report we present results of pathologic, phenotypic, and genetic studies on 29 HD tumors consecutively ascertained by us and the results of a comprehensive analysis of the cytogenetic data available in the literature. In our series 75% of the tumors were positive for Epstein‐Barr virus (EBV) by polymerase chain reaction (PCR) assay. A higher frequency of EBV‐positive tumors showed clonal karyotypic abnormalities than the EBV‐negative tumors. Unlike the case in the previous reports, none of the 24 tumors studied by PCR showed the presence of t(14;18) (q32;q21)‐carrying cells. From the comprehensive analysis of the literature, we identified recurring nonrandom numerical changes, deletions, and chromosome breaks in HD. Some of these are associated either with nodular sclerosis or with mixed cellular histologies. A comparison of the pattern of these nonrandom cytogenetic changes in HD and those reported for non‐Hodgkin's lymphomas (NHL) identified common deletions and breaks between them. These common genetic lesions probably play a role in disease evolution. © 1993 Wiley‐Liss, Inc.

Original languageEnglish (US)
Pages (from-to)117-124
Number of pages8
JournalAmerican Journal of Hematology
Volume44
Issue number2
DOIs
StatePublished - Oct 1993

Keywords

  • Hodgkin's disease
  • cytogenetics
  • histologic correlations
  • molecular genetics

ASJC Scopus subject areas

  • Hematology

Fingerprint

Dive into the research topics of 'Phenotypic and genotypic characterization of Hodgkin's disease'. Together they form a unique fingerprint.

Cite this