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Prof.dr. R. Fodde

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  • Familial adenomatous polyposis-associated desmoids display significantly more genetic changes than sporadic desmoids (2011)Open access

    Authors:Robanus-Maandag, E.C. (Els); Bosch, C.A.J. (Cathy); Amini-Nik, S. (Saeid); Knijnenburg, J. (Jeroen); Szuhai, K. (Karoly); Cervera, P. (Pascale); Poon, R. (Raymond); Eccles, D. (Diana); Radice, P. (Paolo); Giovannini, M. (Marcello); Alman, B.A. (Benjamin A.); Tejpar, S. (Sabine); Devilee, P. (Peter); Fodde, R. (Riccardo)
    In:PLoS ONE, 6(9). ISSN 1932-6203.

    Abstract:

    Desmoid tumours (also called deep or aggressive fibromatoses) are potentially life-threatening fibromatous lesions. Hereditary desmoid tumours arise in individuals affected by either familial adenomatous polyposis (FAP) or hereditary desmoid disease (HDD) carrying germline mutations in APC. Most spo

  • β-catenin tyrosine 654 phosphorylation increases Wnt signalling and intestinal tumorigenesis (2011)Open access

    Authors:Veelen, van W. (Wendy); Le, N.H. (Ngoc); Helvensteijn, W. (Werner); Blonden, L. (Lau); Theeuwes, J.J.M. (Myrte); Bakker, E. (Elvira); Franken, P.F. (Patrick); Gurp, van L. (Léon); Meijlink, F. (Frits); Valk, van der M.A. (Martin); Kuipers, E.J. (Ernst); Fodde, R. (Riccardo); Smits, R. (Ron)
    In:Gut (English Edition): an international journal of gastroenterology & hepatology. ISSN 0017-5749.

    Abstract:

    Objective: Deregulation of the Wnt signalling pathway by mutations in the Apc or β-catenin genes underlies colorectal carcinogenesis. As a result, β-catenin stabilises, translocates to the nucleus, and activates gene transcription. Intestinal tumours show a heterogeneous pattern of nuclear β-catenin

  • Wnt/Β-Catenin and Sex Hormone Signaling in Endometrial Homeostasis and Cancer (2010)Open access

    Authors:Wang, Y. (Yongyi); Zee, van der M. (Marten); Fodde, R. (Riccardo); Blok, L.J. (Leen)

    Abstract:

    A delicate balance between estrogen and progestagen signaling underlies proper functioning of the female reproductive tract and, in particular, the monthly re- and degenerative phases characteristic of the menstrual cycle. Here, we propose that the canonical Wnt/β-catenin signaling pathway may under

  • A new conditional Apc-mutant mouse model for colorectal cancer (2010)

    Authors:Robanus-Maandag, E.C. (Els); Koelink, P.J. (Pim); Breukel, C. (Cor); Salvatori, D.C.F. (Daniela); Jagmohan-Changur, S.C. (Shantie); Bosch, C.A.J. (Cathy); Verspaget, H.W.; Devilee, P. (Peter); Fodde, R. (Riccardo); Smits, R. (Ron)
    In:Carcinogenesis: integrative cancer research, 31(5), 946 - 952. ISSN 0143-3334.

    Abstract:

    Mutations of the adenomatous polyposis coli (APC) gene predispose individuals to familial adenomatous polyposis (FAP), characterized by multiple tumours in the large intestine. Most mouse models heterozygous for truncating mutant Apc alleles mimic FAP, however, the intestinal tumours occur mainly in

  • Effect of aspirin or resistant starch on colorectal neoplasia in the Lynch syndrome (2008)

    Authors:Burn, J. (John); Bishop, D.T. (D); Mecklin, J.-P. (Jukka-Pekka); Macrae, F.A. (Finlay); Möslein, G. (Gabriela); Olschwang, S. (Sylviane); Bisgaard, M.-L. (Marie-Luise); Ramesar, R.S. (Rajkumar); Eccles, D. (Diana); Maher, E.R. (Eamonn); Bertario, L. (Lucio); Jarvinen, H.J. (Heikki); Lindblom, A. (Annika); Evans, D.G. (Gareth); Lubinski, J. (Jan); Morrison, P.J. (Patrick); Ho, J.W.C. (Judy); Vasen, H. (Hans); Side, L. (Lucy); Thomas, H.J.W. (Huw ); Scott, R.J. (Rodney); Dunlop, M.G. (Malcolm); Barker, G. (Gail); Elliott, F. (Faye); Jass, J.R. (Jeremy ); Fodde, R. (Riccardo); Lynch, H. (Henry); Mathers, J.C. (John )
    In:New England Journal of Medicine, 359(24), 2567 - 2578. ISSN 0028-4793.

    Abstract:

    BACKGROUND: Observational and epidemiologic data indicate that the use of aspirin reduces the risk of colorectal neoplasia; however, the effects of aspirin in the Lynch syndrome (hereditary nonpolyposis colon cancer) are not known. Resistant starch has been associated with an antineoplastic effect o

  • Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGH. (2004)Open access

    Authors:Cardoso, J. (Joana); Molenaar, L. (Lia); Menezes, de R.X. (Renee); Rosenberg, C.; Morreau, H. (Hans); Moslein, G.; Fodde, R. (Riccardo); Boer, J.M. (Judith)
    In:Nucleic Acids Research. ISSN 0305-1048.

    Abstract:

    Comparative genomic hybridization by means of BAC microarrays (array CGH) allows high-resolution profiling of copy-number aberrations in tumor DNA. However, specific genetic lesions associated with small but clinically relevant tumor areas may pass undetected due to intra-tumor het

  • The CHEK2 1100delC mutation identifies families with a hereditary breast and colorectal cancer phenotype (2003)Open access

    Authors:Meijers-Heijboer, E.J. (Hanne); Moslein, G.; Lynch, H.; Wasielewski, M. (Marijke); Fodde, R. (Riccardo); Wagner, A. (Anja); Elstrodt, F. (Fons); Verkuijlen, P.; Tops, C. (Carli); Burn, J. (John); Bos, van den R.R. (Renate); Snoo, de A. (Anja); Schutte, A.E.M. (Mieke); Franken, P.F. (Patrick); Fat, G.T.; Jagmohan, S.; Chapman, P.; Brekelmans, C.T. (Cecile); Wijnen, J. (Juul); Vasen, H. (Hans); Ouweland, van den A.M.W. (Ans); Klijn, J.G.M. (Jan); Hollestelle, A. (Antoinette)
    In:American Journal of Human Genetics. ISSN 0002-9297.

    Abstract:

    Because of genetic heterogeneity, the identification of breast cancer-susceptibility genes has proven to be exceedingly difficult. Here, we define a new subset of families with breast cancer characterized by the presence of colorectal cancer cases. The 1100delC variant of the cell

  • Atypical HNPCC owing to MSH6 germline mutations: analysis of a large Dutch pedigree (2001)Open access

    Authors:Wagner, A. (Anja); Krimpen, van C.; Morreau, H. (Hans); Hofstra, R.; Tops, C. (Carli); Cornelisse, C.J. (Cees); Zwinderman, A.H. (Ailko); Bik, E.; Brocker-Vriends, A.H.; Fodde, R. (Riccardo); Breuning, M.H. (Martijn); Meer, van der C.; Vasen, H.F. (Hans); Niermeijer, M.F. (Martinus); Lindhout, D. (Dick); Hendriks, Y.; Meijers-Heijboer, E.J. (Hanne); Wijnen, J. (Juul); Leeuw, de W.J.
    In:Journal of Medical Genetics. ISSN 0022-2593.

    Abstract:

    Hereditary non-polyposis colorectal cancer (HNPCC) is the most common genetic susceptibility syndrome for colorectal cancer. HNPCC is most frequently caused by germline mutations in the DNA mismatch repair (MMR) genes MSH2 and MLH1. Recently, mutations in another MMR gene, MSH6 (al

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