Fancf-deficient mice are prone to develop ovarian tumours

S.T. Bakker; H.J. van der Vrugt; J.A. Visser; E. Delzenne-Goette; A. van der Wal; M.A.D. Berns; M. van de Ven; A.B. Oostra; S. de Vries; P. Kramer; F. Arwert; M van de Valk; J.P. de Winter; H.P.J. te Riele

doi:10.1002/path.2992

Fancf-deficient mice are prone to develop ovarian tumours

S.T. Bakker
, H.J. van der Vrugt
, J.A. Visser
, E. Delzenne-Goette
, A. van der Wal
, M.A.D. Berns
, M. van de Ven
, A.B. Oostra
, S. de Vries
, P. Kramer
, F. Arwert
, M van de Valk
, J.P. de Winter
, H.P.J. te Riele

Research output: Contribution to Journal › Article › Academic › peer-review

Abstract

Fanconi anaemia (FA) is a rare recessive disorder marked by developmental abnormalities, bone marrow failure, and a high risk for the development of leukaemia and solid tumours. The inactivation of FA genes, in particular FANCF, has also been documented in sporadic tumours in non-FA patients. To study whether there is a causal relationship between FA pathway defects and tumour development, we have generated a mouse model with a targeted disruption of the FA core complex gene Fancf. Fancf-deficient mouse embryonic fibroblasts displayed a phenotype typical for FA cells: they showed an aberrant response to DNA cross-linking agents as manifested by G

Original language	English
Pages (from-to)	28-39
Journal	The Journal of Pathology
Volume	226
Issue number	1
DOIs	https://doi.org/10.1002/path.2992
Publication status	Published - 2012

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SDG 3 Good Health and Well-being

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Bakker, S. T., van der Vrugt, H. J., Visser, J. A., Delzenne-Goette, E., van der Wal, A., Berns, M. A. D., van de Ven, M., Oostra, A. B., de Vries, S., Kramer, P., Arwert, F., van de Valk, M., de Winter, J. P., & te Riele, H. P. J. (2012). Fancf-deficient mice are prone to develop ovarian tumours. The Journal of Pathology, 226(1), 28-39. https://doi.org/10.1002/path.2992

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abstract = "Fanconi anaemia (FA) is a rare recessive disorder marked by developmental abnormalities, bone marrow failure, and a high risk for the development of leukaemia and solid tumours. The inactivation of FA genes, in particular FANCF, has also been documented in sporadic tumours in non-FA patients. To study whether there is a causal relationship between FA pathway defects and tumour development, we have generated a mouse model with a targeted disruption of the FA core complex gene Fancf. Fancf-deficient mouse embryonic fibroblasts displayed a phenotype typical for FA cells: they showed an aberrant response to DNA cross-linking agents as manifested by G",

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year = "2012",

doi = "10.1002/path.2992",

language = "English",

volume = "226",

pages = "28--39",

journal = "The Journal of Pathology",

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T1 - Fancf-deficient mice are prone to develop ovarian tumours

AU - Bakker, S.T.

AU - van der Vrugt, H.J.

AU - Visser, J.A.

AU - Delzenne-Goette, E.

AU - van der Wal, A.

AU - Berns, M.A.D.

AU - van de Ven, M.

AU - Oostra, A.B.

AU - de Vries, S.

AU - Kramer, P.

AU - Arwert, F.

AU - van de Valk, M

AU - de Winter, J.P.

AU - te Riele, H.P.J.

PY - 2012

Y1 - 2012

N2 - Fanconi anaemia (FA) is a rare recessive disorder marked by developmental abnormalities, bone marrow failure, and a high risk for the development of leukaemia and solid tumours. The inactivation of FA genes, in particular FANCF, has also been documented in sporadic tumours in non-FA patients. To study whether there is a causal relationship between FA pathway defects and tumour development, we have generated a mouse model with a targeted disruption of the FA core complex gene Fancf. Fancf-deficient mouse embryonic fibroblasts displayed a phenotype typical for FA cells: they showed an aberrant response to DNA cross-linking agents as manifested by G

AB - Fanconi anaemia (FA) is a rare recessive disorder marked by developmental abnormalities, bone marrow failure, and a high risk for the development of leukaemia and solid tumours. The inactivation of FA genes, in particular FANCF, has also been documented in sporadic tumours in non-FA patients. To study whether there is a causal relationship between FA pathway defects and tumour development, we have generated a mouse model with a targeted disruption of the FA core complex gene Fancf. Fancf-deficient mouse embryonic fibroblasts displayed a phenotype typical for FA cells: they showed an aberrant response to DNA cross-linking agents as manifested by G

U2 - 10.1002/path.2992

DO - 10.1002/path.2992

M3 - Article

SN - 0022-3417

VL - 226

SP - 28

EP - 39

JO - The Journal of Pathology

JF - The Journal of Pathology

IS - 1

ER -

Fancf-deficient mice are prone to develop ovarian tumours

Abstract

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