Skip Navigation

JNCI Journal of the National Cancer Institute 1999 91(18):1581-1583; doi:10.1093/jnci/91.18.1581
© 1999 by Oxford University Press
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
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 arrow Request Permissions
Google Scholar
Right arrow Articles by Hasse, U.
Right arrow Articles by Fey, M. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hasse, U.
Right arrow Articles by Fey, M. F.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Journal of the National Cancer Institute, Vol. 91, No. 18, 1581-1583, September 15, 1999
© 1999 Oxford University Press

BRIEF COMMUNICATION

Clonal Loss of Heterozygosity in Microdissected Hodgkin and Reed-Sternberg Cells

Urs Hasse, Marianne Tinguely, Elisabeth Oppliger Leibundgut, Jean-François Cajot, Alex M. Garvin, Andreas Tobler, Bettina Borisch, Martin F. Fey

Affiliations of authors: U. Hasse, M. F. Fey (Institute of Medical Oncology), E. O. Leibundgut, J.-F. Cajot, A. Tobler (Central Haematology Laboratory), Inselspital and Department of Clinical Research, University of Berne, Switzerland; M. Tinguely, B. Borisch, Department of Clinical Pathology, University of Geneva, Switzerland; A. M. Garvin, Department of Obstetrics and Gynaecology, Laboratory for Prenatal Medicine, University of Basel, Switzerland.

Correspondence to: Martin F. Fey, M.D., Institute of Medical Oncology, Inselspital, CH-3010 Berne, Switzerland (e-mail: martin.fey@insel.ch).

The typical Hodgkin and Reed-Sternberg (HRS) cells are thought to represent the malignant cellular elements of Hodgkin's disease (HD). The detection of immunoglobulin gene rearrangements in HRS cells indicates that they are clonally derived from B cells (1-8), but immunogenotyping, as such, does not provide any information on specific gene alterations possibly involved in the molecular pathology of HD. In many tumors, highly informative polymorphic DNA markers may identify loci harboring clonal loss of heterozygosity (LOH) and thus help to trace tumor suppressor genes (9,10). Although in HD, cytogenetic data suggest that nonrandom chromosomal deletions may occur at several loci, including 1q42, 4q26, and others, very little (if anything) is known about clonal LOH in HRS cells at the molecular level (11-15). We, therefore, set out to study microdissected HRS cells from classical types of HD at candidate . . . [Full Text of this Article]

NOTES

REFERENCES


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
 Cancer Res.Home page
D. Re, P. Starostik, N. Massoudi, A. Staratschek-Jox, V. Dries, R. K. Thomas, V. Diehl, and J. Wolf
Allelic Losses on Chromosome 6q25 in Hodgkin and Reed Sternberg Cells
Cancer Res., May 15, 2003; 63(10): 2606 - 2609.
[Abstract] [Full Text] [PDF]