The Chinese hamster cell mutant V-H4 is homologous to Fanconi anemia (complementation group A)

Arwert, Fré; Rooimans, Martin A.; Westerveld, A.; Simons, J.W.I.M.; Zdzienicka, M. Z.

doi:10.1159/000133038

Cited by 21 publications

(12 citation statements)

References 11 publications

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“…It is considered to be a rodent equivalent of human Fanconi anaemia cells and is in the same complementation group as FA group A cells [24,25] which lack the FANCA protein. In the mouse FANCA is a 161 kDa protein which complements the cross-linking sensitive phenotype [26].…”

Section: Methodsmentioning

confidence: 99%

The relationship between the RBE of alpha particles and the radiosensitivity of different mutations of Chinese hamster cells

Zyuzikov

Prise

Zdzienicka

et al. 2001

Radiation and Environmental Biophysics

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The RBE of alpha-particles in different mutations of Chinese hamster cells was determined with the aim of identifying differences in the sensitivity to x-ray and alpha-particle-induced DNA damage. Two parental lines of Chinese hamster cells and four radiosensitive mutants were irradiated with different single doses of x-rays and alpha-particles and clonogenic cell survival was determined. Radiosensitivity to x-rays varied by a factor of 5 between the cell strains whereas sensitivity to alpha-particle irradiation was almost identical among all strains. The RBE is only determined by the sensitivity of the cells towards x-rays. Since cells with different defects of repair or cell cycle control have different radiosensitivities, we conclude that the effects of x-ray irradiation and the RBE are mostly determined by the activity of repair processes.

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Section: Methodsmentioning

confidence: 99%

The relationship between the RBE of alpha particles and the radiosensitivity of different mutations of Chinese hamster cells

Zyuzikov

Prise

Zdzienicka

et al. 2001

Radiation and Environmental Biophysics

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“…Since it was previously shown by genetic complementation, that V-H4 cells are homologous to FA-A cells (Arwert et al, 1991), we examined FANCA protein levels in wild-type V79 and mutant V-H4 cells by immunoblot analysis. Only very low levels of FANCA protein were detected in V-H4 cells, whereas parental V79 cells significantly expressed FANCA (Fig.…”

Section: Expression Of Fanca Protein Is Defective In V-h4 Cellsmentioning

confidence: 99%

Impairment of homologous recombination control in a Fanconi anemia‐like Chinese Hamster Cell mutant

Larminat

Germanier

Papouli

et al. 2004

Biology of the Cell

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DNA interstrand cross-links (ICL)-inducing agents such as cisplatin, mitomycin C (MMC) and nitrogen mustards are widely used as potent antitumor drugs. Although ICL repair mechanism is not yet well characterized in mammalian cells, this pathway is thought to involve a sequential action of nucleotide excision repair (NER) and homologous recombination (HR). The importance of unraveling ICL repair pathways is highlighted by the hypersensitivity to ICL-inducing agents in cells of patients with the genetic disease Fanconi anemia (FA) and in cells mutated in the Breast Cancer susceptibility genes BRCA1 and BRCA2. To better characterize the involvement of HR in the sensitivity to ICL-inducing agents, we examined spontaneous and ICL-induced HR in rodent FA-like V-H4 cells. In this report, we show that MMC-hypersensitive V-H4 cells exhibit an increased spontaneous homology-directed repair (HDR) activity compared to the resistant V79 parental cells. Elevated HDR activity results mainly in increased conservative Rad51-dependent recombination, without affecting nonconservative single-strand annealing process (SSA). We also show that HDR activity is enhanced following MMC treatment in parental cells, but not in rodent FA-like V-H4 cells. Moreover, our data indicate that Rad51 foci formation is significantly delayed in these FA-like cells in response to crosslinking agent. These findings provide evidence for an impairment of HR control in V-H4 cells and emphasize the involvement of the FA pathway in HR-mediated repair.

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“…However, the MMC-sensitive Chinese hamster cell mutant VH-4 TOR can be used to determine whether an unclassified fibroblast strain belongs to the FA complementation group A or not [Arwert et al, 1991]. Figure 5 shows MMC sensitivity of a hybrid cell population obtained after fusion of VH-4 TOR with fibroblasts obtained from patient 1.…”

Section: Resultsmentioning

confidence: 99%

An atypical case of Fanconi anemia in elderly sibs

Kwee

Kleij²,

Essen

et al. 1997

Am. J. Med. Genet.

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We describe a 56-year-old woman suspected of Fanconi anemia on the basis of the following clinical findings: microcephaly, short stature, congenital deafness, and the clinical findings in her deceased brother. Hematologic or other signs of malignancy were absent. The diagnosis was confirmed by demonstrating hypersensitivity of her lymphocytes to mitomycin C (MMC). Cell fusion experiments indicated that the patient belongs to complementation group A. The patient's brother died at the age of 50 of heart and renal failure, and anemia. He had clinical findings similar to those of his sister, and a horseshoe kidney. From 31 years on he had thrombocytopenia and leucopenia. Both patients had insulin-dependent diabetes mellitus. A chromosomal breakage test carried out elsewhere before his death failed to demonstrate MMC hypersensitivity of his lymphocytes, which led to the investigation of his sister. To our knowledge these two cases are the oldest Fanconi anemia patients reported thus far.

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The Chinese hamster cell mutant V-H4 is homologous to Fanconi anemia (complementation group A)

Cited by 21 publications

References 11 publications

The relationship between the RBE of alpha particles and the radiosensitivity of different mutations of Chinese hamster cells

The relationship between the RBE of alpha particles and the radiosensitivity of different mutations of Chinese hamster cells

Impairment of homologous recombination control in a Fanconi anemia‐like Chinese Hamster Cell mutant

An atypical case of Fanconi anemia in elderly sibs

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