PMID: 9661700Jul 14, 1998Paper

Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation

Somatic Cell and Molecular Genetics
P JohnstoneR E Moses

Abstract

Cells from patients with Fanconi anemia (FA) show decreased viability and decreased chromosome stability after treatment with DNA cross-linking agents, compared to normal cells. FA cells also show a relative accumulation at the G2/M transition after such treatment. This has suggested a possible checkpoint abnormality. In the studies presented here, treatment with hydroxyurea, caffeine or inhibitors of cell cycle kinases did not reveal abnormalities in survival or chromosome stability in FA-A or FA-D cells. Chromosomal breaks introduced by hydrogen peroxide or methyl methanesulfonate accumulated to the same extent in FA-A or FA-D cells as in normal cells. We conclude that FA-A and FA-D cells respond normally to agents known to alter the cell cycle or introduce DNA strand breaks. FA cells process strand breaks and a variety of DNA monoadducts normally. Our results are compatible with repair of DNA crosslinks being slower in FA than in normal cells and FA cells having normal cell cycle checkpoints.

References

Jun 1, 1992·Nature Genetics·C A StrathdeeM Buchwald
May 1, 1992·The American Journal of Pediatric Hematology/oncology·C A Strathdee, M Buchwald
Nov 3, 1989·Science·L H Hartwell, T A Weinert
Nov 20, 1986·Journal of Immunological Methods·D Gerlier, N Thomasset
Jan 1, 1982·Cytogenetics and Cell Genetics·S A LattM Lalande
Jan 1, 1982·Human Genetics·B DutrillauxM Prieur
Jul 5, 1994·Proceedings of the National Academy of Sciences of the United States of America·T YamashitaA D D'Andrea
Jun 15, 1994·Biochemical and Biophysical Research Communications·M D LosiewiczP J Worland
Aug 16, 1994·Proceedings of the National Academy of Sciences of the United States of America·H Youssoufian
Aug 1, 1993·Biochemical Society Transactions·J KnappeA F Wagner
Nov 1, 1993·British Journal of Haematology·B P AlterV Najfeld
Feb 1, 1994·Experimental Cell Research·N ShinomiyaM Rokutanda
Feb 1, 1996·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·W K Kaufmann, R S Paules
Mar 1, 1996·Somatic Cell and Molecular Genetics·P M JakobsM Grompe
Feb 1, 1996·Current Opinion in Genetics & Development·D Lydall, T Weinert
Nov 1, 1996·Nature Genetics·A D D'Andrea
Nov 1, 1996·Nature Genetics·J R Lo Ten FoeH Joenje
Jun 1, 1997·Human Genetics·W RuppitschM Hirsch-Kauffmann
Jan 1, 1997·Somatic Cell and Molecular Genetics·P M JakobsM Grompe
Oct 23, 1997·American Journal of Human Genetics·H JoenjeF Arwert
Feb 12, 1998·The Journal of Clinical Investigation·Y Li, H Youssoufian
Jan 2, 2003·Nature Reviews. Cancer·Alan D D'Andrea, Markus Grompe

❮ Previous
Next ❯

Citations

Nov 10, 2001·Annual Review of Genomics and Human Genetics·R E Moses
May 17, 2008·Journal of Biomedicine & Biotechnology·Henning WillersSimon N Powell
May 26, 2009·Mutation Research·Kornelia NevelingDetlev Schindler
May 20, 2009·Journal of Cellular Physiology·Kevin M McCabeRobb E Moses

❮ Previous
Next ❯

Related Concepts

Related Feeds

Cell Checkpoints & Regulators

Cell cycle checkpoints are a series of complex checkpoint mechanisms that detect DNA abnormalities and ensure that DNA replication and repair are complete before cell division. They are primarily regulated by cyclins, cyclin-dependent kinases, and the anaphase-promoting complex/cyclosome. Here is the latest research.