Skip Navigation

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 ISI Web of Science
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 Search for citing articles in:
ISI Web of Science (2)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Callén, E.
Right arrow Articles by Surrallés, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Callén, E.
Right arrow Articles by Surrallés, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Carcinogenesis, Vol. 23, No. 8, 1267-1271, August 2002
© 2002 Oxford University Press

CANCER BIOLOGY

The clastogenic response of the 1q12 heterochromatic region to DNA cross-linking agents is independent of the Fanconi anaemia pathway

E. Callén1, M.J. Ramírez, A. Creus1, R. Marcos1, S. Frias2, B. Molina1, I. Badell3, T. Olivé4, J.J. Ortega4 and J. Surrallés1,5

1 Group of Mutagenesis, Department of Genetics and Microbiology, Universitat Autònoma de Barcelona, Barcelona, Spain,
2 Cytogenetics Laboratory, Instituto Nacional de Pediatría, México D.F., Mexico,
3 Bone Marrow Transplantation Unit, Department of Paediatrics, Sant Pau Hospital, Barcelona, Spain and
4 Bone Marrow Transplantation Unit, Service of Paediatric Hematology-Oncology, Vall d’Hebron Hospital, Barcelona, Spain

Fanconi anaemia (FA) is a rare genetic syndrome of cancer susceptibility characterized by spontaneous and induced chromosome fragility, especially after treatment with cross-linking agents. Recent investigations showed interactions between FA proteins and chromatin remodelling factors. To investigate a potential uneven distribution of the FA pathway through the human genome depending on chromatin conformation, we have analysed chromosome breakage in the largest constitutively heterochromatic region in the human genome, the 1q12 band, in lymphocytes from FA patients, carriers and healthy controls after treatment with the cross-linking agents mitomycin-C (MMC) and diepoxybutane (DEB). As expected, a higher level of MMC-induced cytotoxicity and chromosome breakage was observed in cells from FA patients when compared with normal controls and carriers. However, the increase in 1q12 breakage after increasing concentrations of MMC was of a similar magnitude in FA patients, carriers and controls. Similarly, DEB induced a high level of overall genome chromosome fragility in cells from FA patients when compared with controls with no parallel increase in chromosome breaks specifically involving the heterochromatic band 1q12. We therefore conclude that, unlike the overall genome, the sensitivity of chromosome 1 constitutive heterochromatin to the chromosome breaking activity of cross-linking agents is independent of a functional FA pathway, indicating that the action of the FA pathway is unevenly distributed through the human genome.


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
E. Callen, J. A. Casado, M. D. Tischkowitz, J. A. Bueren, A. Creus, R. Marcos, A. Dasi, J. M. Estella, A. Munoz, J. J. Ortega, et al.
A common founder mutation in FANCA underlies the world's highest prevalence of Fanconi anemia in Gypsy families from Spain
Blood, March 1, 2005; 105(5): 1946 - 1949.
[Abstract] [Full Text] [PDF]

Home page
 MutagenesisHome page
M. Bogliolo, O. Cabre, E. Callen, V. Castillo, A. Creus, R. Marcos, and J. Surralles
The Fanconi anaemia genome stability and tumour suppressor network
Mutagenesis, November 1, 2002; 17(6): 529 - 538.
[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.