Skip Navigation

This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Küppers, R.
Right arrow Articles by Rajewsky, K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Küppers, R.
Right arrow Articles by Rajewsky, K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Annals of Oncology 9:S17-S20, 1998
© 1998 European Society for Medical Oncology

Reviews

Clonality and germinal centre B-cell derivation of Hodgkin/Reed-Sternberg cells in Hodgkin's disease

R. Küppers1, M. L. Hansmann2 and K. Rajewsky1

1 Institute for Genetics, University of Cologne Cologne
2 Department of Pathology, University of Frankfurt Frankfurt, Germany

Correspondence to: R. Küppers, University of Cologne, LFI-Building. E4 R706, Joseph-Stelzmann-Str. 9, 50931 Cologne, Germany

Molecular single-cell studies of Hodgkin and Reed-Sternberg (HRS) cells in Hodgkin's disease (HD) have revealed the clonal nature of these peculiar tumour cells. HRS cells in classical HD as well as lymphocyte predominant (LP) HD originate from germinal center (GC) B cells in most cases, if not all. Whereas HRS cells in LP HD represent transformed antigen-selected GC B cells with evidence of ongoing immu-noglobulin (Ig) V gene mutation, HRS cells in classical HD appear to often or always derive from GC B cells that have lost the capacity to express a functional antigen receptor. Using Iggene rearrangements amplified from HRS cells as clonal markers for the tumour cells, it could be shown that the same HRS cell clone can disseminate in the patient and persist throughout the course of the disease. A common derivation of the tumour cells was recently demonstrated in two cases representing combinations of HD and non-Hodgkin's lymphoma. Finally, V-gene analysis showed that viable cells enriched by magnetic cell sorting from HD patients as HRS cells indeed represent the HRS-cell population of the patient.

Hodgkin's diseaseg, Ig gene rearrangements, micro-manipulation, Reed-Sternberg cell, single-cell PCR


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 BloodHome page
A. Sanchez-Aguilera, J. Delgado, F. I. Camacho, M. Sanchez-Beato, L. Sanchez, C. Montalban, M. F. Fresno, C. Martin, M. A. Piris, and J. F. Garcia
Silencing of the p18INK4c gene by promoter hypermethylation in Reed-Sternberg cells in Hodgkin lymphomas
Blood, March 15, 2004; 103(6): 2351 - 2357.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
J. F. Garcia, F. I. Camacho, M. Morente, M. Fraga, C. Montalban, T. A. C. Bellas, A. Castano, A. Diez, T. Flores, C. Martin, et al.
Hodgkin and Reed-Sternberg cells harbor alterations in the major tumor suppressor pathways and cell-cycle checkpoints: analyses using tissue microarrays
Blood, January 15, 2003; 101(2): 681 - 689.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.