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

P. Johnstone, C. Reifsteck, S. Kohler, P. Worland, Susan Olson, Robb Moses

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)371-377
Number of pages7
JournalSomatic Cell and Molecular Genetics
Volume23
Issue number6
StatePublished - 1998

Fingerprint

Fanconi Anemia
Somatostatin-Secreting Cells
Cell Cycle
Cell Line
Chromosomal Instability
Methyl Methanesulfonate
Chromosome Breakage
DNA Breaks
Hydroxyurea
DNA
Cell Cycle Checkpoints
Caffeine
DNA Repair
Hydrogen Peroxide
Phosphotransferases
Therapeutics

ASJC Scopus subject areas

  • Genetics
  • Cell Biology

Cite this

Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation. / Johnstone, P.; Reifsteck, C.; Kohler, S.; Worland, P.; Olson, Susan; Moses, Robb.

In: Somatic Cell and Molecular Genetics, Vol. 23, No. 6, 1998, p. 371-377.

Research output: Contribution to journalArticle

@article{1b81d09bdd254db598ea3e8ae97a967e,
title = "Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation",
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.",
author = "P. Johnstone and C. Reifsteck and S. Kohler and P. Worland and Susan Olson and Robb Moses",
year = "1998",
language = "English (US)",
volume = "23",
pages = "371--377",
journal = "Somatic Cell and Molecular Genetics",
issn = "0740-7750",
publisher = "Springer GmbH & Co, Auslieferungs-Gesellschaf",
number = "6",

}

TY - JOUR

T1 - Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation

AU - Johnstone, P.

AU - Reifsteck, C.

AU - Kohler, S.

AU - Worland, P.

AU - Olson, Susan

AU - Moses, Robb

PY - 1998

Y1 - 1998

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0031865309&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031865309&partnerID=8YFLogxK

M3 - Article

C2 - 9661700

AN - SCOPUS:0031865309

VL - 23

SP - 371

EP - 377

JO - Somatic Cell and Molecular Genetics

JF - Somatic Cell and Molecular Genetics

SN - 0740-7750

IS - 6

ER -