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 JournalArticleAcademicpeer-review


    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 languageEnglish
    Pages (from-to)28-39
    JournalJournal of Pathology
    Issue number1
    Publication statusPublished - 2012


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