R Fodde

Summary

Affiliation: Leiden University Medical Center
Country: The Netherlands

Publications

  1. ncbi request reprint APC, signal transduction and genetic instability in colorectal cancer
    R Fodde
    Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, The Netherlands
    Nat Rev Cancer 1:55-67. 2001
  2. ncbi request reprint Cancer biology. A matter of dosage
    Riccardo Fodde
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands
    Science 298:761-3. 2002
  3. ncbi request reprint Disease model: familial adenomatous polyposis
    R Fodde
    Dept of Human and Clinical Genetics, Leiden University Medical Center, Sylvius Laboratories, Wassenaarseweg 72, 2333 AL, Leiden, The Netherlands
    Trends Mol Med 7:369-73. 2001
  4. ncbi request reprint Mutations in the APC tumour suppressor gene cause chromosomal instability
    R Fodde
    Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, PO Box 9503, 2300 RA Leiden, The Netherlands
    Nat Cell Biol 3:433-8. 2001
  5. ncbi request reprint Somatic Apc mutations are selected upon their capacity to inactivate the beta-catenin downregulating activity
    R Smits
    MGC Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 29:229-39. 2000
  6. ncbi request reprint E-cadherin and adenomatous polyposis coli mutations are synergistic in intestinal tumor initiation in mice
    R Smits
    Medical Genetics Center, Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Gastroenterology 119:1045-53. 2000
  7. ncbi request reprint Mechanisms of APC-driven tumorigenesis: lessons from mouse models
    R Fodde
    MGC Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Cytogenet Cell Genet 86:105-11. 1999
  8. pmc Apc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development
    R Smits
    Medical Genetics Center MGC Department of Human Genetics, Leiden University Medical Center, 2300 RA Leiden, The Netherlands
    Genes Dev 13:1309-21. 1999
  9. ncbi request reprint A targeted mouse Brca1 mutation removing the last BRCT repeat results in apoptosis and embryonic lethality at the headfold stage
    P Hohenstein
    Department of Human and Clinical Genetics, Leiden University Medical Center, P O Box 9503, 2300 RA, The Netherlands
    Oncogene 20:2544-50. 2001
  10. ncbi request reprint Dynamic expression and nuclear accumulation of beta-catenin during the development of hair follicle-derived structures
    M Ridanpaa
    Department of Human and Clinical Genetics, Leiden University Medical Center LUMC, 72, 2333 AL, Wassenaarseweg, The Netherlands
    Mech Dev 109:173-81. 2001

Collaborators

Detail Information

Publications42

  1. ncbi request reprint APC, signal transduction and genetic instability in colorectal cancer
    R Fodde
    Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, The Netherlands
    Nat Rev Cancer 1:55-67. 2001
    ..Inactivation of APC--the gene responsible for most cases of colorectal cancer--might fulfil both requirements...
  2. ncbi request reprint Cancer biology. A matter of dosage
    Riccardo Fodde
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands
    Science 298:761-3. 2002
  3. ncbi request reprint Disease model: familial adenomatous polyposis
    R Fodde
    Dept of Human and Clinical Genetics, Leiden University Medical Center, Sylvius Laboratories, Wassenaarseweg 72, 2333 AL, Leiden, The Netherlands
    Trends Mol Med 7:369-73. 2001
    ..Also, the close phenotypic resemblance to the human disease makes these mice unique preclinical models to test chemopreventive and therapeutic interventions...
  4. ncbi request reprint Mutations in the APC tumour suppressor gene cause chromosomal instability
    R Fodde
    Department of Human and Clinical Genetics, and Center for Biomedical Genetics, Leiden University Medical Center, PO Box 9503, 2300 RA Leiden, The Netherlands
    Nat Cell Biol 3:433-8. 2001
    ..We conclude that loss of APC sequences that lie C-terminal to the beta-catenin regulatory domain contributes to chromosomal instability in colorectal cancer...
  5. ncbi request reprint Somatic Apc mutations are selected upon their capacity to inactivate the beta-catenin downregulating activity
    R Smits
    MGC Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 29:229-39. 2000
    ..These results indicate that somatic Apc mutations are selected during intestinal tumorigenesis and that inactivation of the beta-catenin downregulating function of APC is likely to represent the main selective factor...
  6. ncbi request reprint E-cadherin and adenomatous polyposis coli mutations are synergistic in intestinal tumor initiation in mice
    R Smits
    Medical Genetics Center, Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Gastroenterology 119:1045-53. 2000
    ..In addition, loss or haploinsufficiency of E-cadherin may affect tumorigenesis by altering its cell-adhesive and associated functions...
  7. ncbi request reprint Mechanisms of APC-driven tumorigenesis: lessons from mouse models
    R Fodde
    MGC Department of Human Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Cytogenet Cell Genet 86:105-11. 1999
    ..Here we review the major features of the available animal models for FAP and attempt the formulation of a hypothetical model for APC-driven tumorigenesis based on the observed genetic and phenotypic variability in mouse and man...
  8. pmc Apc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development
    R Smits
    Medical Genetics Center MGC Department of Human Genetics, Leiden University Medical Center, 2300 RA Leiden, The Netherlands
    Genes Dev 13:1309-21. 1999
    ....
  9. ncbi request reprint A targeted mouse Brca1 mutation removing the last BRCT repeat results in apoptosis and embryonic lethality at the headfold stage
    P Hohenstein
    Department of Human and Clinical Genetics, Leiden University Medical Center, P O Box 9503, 2300 RA, The Netherlands
    Oncogene 20:2544-50. 2001
    ..5 dpc due to massive apoptosis throughout the embryo. These results indicate that a C-terminal truncating Brca1 mutation removing the last BRCT repeat has a different effect on normal cell function than does the complete absence of Brca1...
  10. ncbi request reprint Dynamic expression and nuclear accumulation of beta-catenin during the development of hair follicle-derived structures
    M Ridanpaa
    Department of Human and Clinical Genetics, Leiden University Medical Center LUMC, 72, 2333 AL, Wassenaarseweg, The Netherlands
    Mech Dev 109:173-81. 2001
    ..These results further elucidate the role of the Wnt signal transduction pathway during hair follicle related development and tumorigenesis and illustrate the dynamic role of beta-catenin in signal transduction and cell-adhesion...
  11. ncbi request reprint Clinical findings with implications for genetic testing in families with clustering of colorectal cancer
    J T Wijnen
    Department of Human Genetics, Leiden University Medical Center, The Netherlands
    N Engl J Med 339:511-8. 1998
    ..We assessed the prevalence of MSH2 and MLH1 mutations in families suspected of having hereditary nonpolyposis colorectal cancer and evaluated whether clinical findings can predict the outcome of genetic testing...
  12. ncbi request reprint The APC gene in colorectal cancer
    R Fodde
    Department of Human and Clinical Genetics, LUMC, Sylvius Laboratories, Leiden, The Netherlands
    Eur J Cancer 38:867-71. 2002
    ....
  13. ncbi request reprint Radiation induces different changes in expression profiles of normal rectal tissue compared with rectal carcinoma
    I D Nagtegaal
    Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
    Virchows Arch 446:127-35. 2005
    ..In the current study, we analyzed the effects of irradiation on gene expression in normal and tumor tissue of rectal cancer patients...
  14. ncbi request reprint Molecular analysis of the APC gene in 105 Dutch kindreds with familial adenomatous polyposis: 67 germline mutations identified by DGGE, PTT, and southern analysis
    R B Van der Luijt
    MGC Department of Human Genetics, Sylvius Laboratories, Medical Faculty, Leiden University, The Netherlands
    Hum Mutat 9:7-16. 1997
    ..We found that the combined use of the currently available molecular approaches still fails to identify the underlying genetic defect in a significant subset of the FAP families. The possible causes for this limitation are discussed...
  15. ncbi request reprint Cancer risk in hereditary nonpolyposis colorectal cancer due to MSH6 mutations: impact on counseling and surveillance
    Yvonne M C Hendriks
    Center of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Gastroenterology 127:17-25. 2004
    ..Hereditary nonpolyposis colorectal carcinoma (HNPCC) is caused by a mutated mismatch repair (MMR) gene. The aim of our study was to determine the cumulative risk of developing cancer in a large series of MSH6 mutation carriers...
  16. ncbi request reprint Spectrum of genetic alterations in Muir-Torre syndrome is the same as in HNPCC
    Daniela Barana
    Am J Med Genet A 125:318-9. 2004
  17. ncbi request reprint TGFBR1*6A may contribute to hereditary colorectal cancer
    Yansong Bian
    Cancer Genetics Program, Division of Hematology Oncology, Department of Medicine, Robert H Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, 676 N St Clair St, Suite 880, Chicago, IL 60611, USA
    J Clin Oncol 23:3074-8. 2005
    ..To test this hypothesis, we determined whether TGFBR16A contributes to a proportion of mismatch repair (MMR) gene mutation-negative hereditary nonpolyposis colorectal cancer (HNPCC) patients...
  18. ncbi request reprint Molecular characterization of the spectrum of genomic deletions in the mismatch repair genes MSH2, MLH1, MSH6, and PMS2 responsible for hereditary nonpolyposis colorectal cancer (HNPCC)
    Heleen van der Klift
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 44:123-38. 2005
    ..The characterization of these genomic rearrangements underlines the importance of genomic deletions in the etiology of HNPCC and will facilitate the development of PCR-based tests for their detection in diagnostic laboratories...
  19. ncbi request reprint Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrum
    Claudio Soravia
    Clinic of Digestive Surgery, Geneva University Hospital, Geneva, Switzerland
    Am J Med Genet A 121:159-62. 2003
    ..Hence, prostate cancer should be included in the HNPCC tumor spectrum...
  20. pmc Automated acquisition of stained tissue microarrays for high-throughput evaluation of molecular targets
    Hans Vrolijk
    Laboratory for Cytochemistry and Cytometry, Leiden University Medical Center, Leiden, The Netherlands
    J Mol Diagn 5:160-7. 2003
    ..Performance of the system was compared to manual classification for a representative set of arrays containing colorectal tumors stained with different markers...
  21. pmc The CHEK2 1100delC mutation identifies families with a hereditary breast and colorectal cancer phenotype
    Hanne Meijers-Heijboer
    Department of Clinical Genetics, Erasmus MC, Rotterdam, The Netherlands
    Am J Hum Genet 72:1308-14. 2003
    ..The unequivocal definition of the HBCC phenotype opens new avenues to search for this putative HBCC-susceptibility gene...
  22. pmc Prevalence of adenomas and hyperplastic polyps in mismatch repair mutation carriers among CAPP2 participants: report by the colorectal adenoma/carcinoma prevention programme 2
    Annelie Liljegren
    The Oncology Unit of Radiumhemmet at Karolinska University Hospital, Stockholm, Sweden
    J Clin Oncol 26:3434-9. 2008
    ..These prevalences have been estimated previously in smaller studies, and the results have been found to be variable...
  23. ncbi request reprint Apc modulates embryonic stem-cell differentiation by controlling the dosage of beta-catenin signaling
    Menno F Kielman
    Center for Human and Clinical Genetics, Leiden University Medical Center, Sylvius Laboratory, Wassenaarseweg 72, 2333 RA Leiden, The Netherlands
    Nat Genet 32:594-605. 2002
    ..Our results imply that constitutive activation of the Apc/beta-catenin signaling pathway results in differentiation defects in tissue homeostasis, and possibly underlies tumorigenesis in the colon and other self-renewing tissues...
  24. pmc Molecular analysis of hereditary nonpolyposis colorectal cancer in the United States: high mutation detection rate among clinically selected families and characterization of an American founder genomic deletion of the MSH2 gene
    Anja Wagner
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Am J Hum Genet 72:1088-100. 2003
    ..Genealogical, molecular, and haplotype studies showed that this deletion represents a North American founder mutation that could be traced back to the 19th century...
  25. pmc Conventional and tissue microarray immunohistochemical expression analysis of mismatch repair in hereditary colorectal tumors
    Yvonne Hendriks
    Center for Human and Clinical Genetics, Leiden, The Netherlands
    Am J Pathol 162:469-77. 2003
    ..This study therefore shows that IHC-TMA can be reliably used to simultaneously screen a large number of tumors from (suspected) HNPCC patients, at first in a research setting...
  26. ncbi request reprint Chromosomal instability in MYH- and APC-mutant adenomatous polyps
    Joana Cardoso
    Department of Pathology, Josephine Nefkens Institute, Rotterdam, The Netherlands
    Cancer Res 66:2514-9. 2006
    ..The aneuploid changes detected at early stages of MYH-driven tumorigenesis may underlie accelerated tumor progression, increased cancer risk, and poor prognosis in MAP...
  27. ncbi request reprint Multiple primary cancer, including transitional cell carcinoma of the upper uroepithelial tract in a multigeneration HNPCC family: molecular genetic, diagnostic, and management implications
    Henry T Lynch
    Department of Preventive Medicine and Public Health, Creighton University School of Medicine, Omaha, Nebraska 68178, USA
    Am J Gastroenterol 98:664-70. 2003
    ..We report a multigeneration family where colorectal cancer and cancer of multiple diverse anatomic sites, inclusive of transitional cell carcinoma of the upper uroepithelial tract, were manifested in several relatives...
  28. ncbi request reprint Somatic acquisition and signaling of TGFBR1*6A in cancer
    Boris Pasche
    Cancer Genetics Program, Division of Hematology Oncology, Department of Medicine, The Feinberg School of Medicine, Northwestern, University, Chicago, Ill 60611, USA
    JAMA 294:1634-46. 2005
    ..Epidemiological studies suggest that TGFBR1*6A may act as a tumor susceptibility allele. How TGFBR1*6A contributes to cancer development is largely unknown...
  29. pmc Aneuploidy arises at early stages of Apc-driven intestinal tumorigenesis and pinpoints conserved chromosomal loci of allelic imbalance between mouse and human
    Paola Alberici
    Department of Pathology, Josephine Nefkens Institute, Erasmus University Medical Center, PO Box 2040, 3000 CA Rotterdam, The Netherlands
    Am J Pathol 170:377-87. 2007
    ....
  30. ncbi request reprint Wnt/beta-catenin signaling in cancer stemness and malignant behavior
    Riccardo Fodde
    Department of Pathology, Josephine Nefkens Institute, Erasmus MC, PO Box 2040, 3000 CA Rotterdam, The Netherlands
    Curr Opin Cell Biol 19:150-8. 2007
    ..Several intrinsic (cell-autonomous and/or autocrine) and extrinsic (paracrine, derived from the tumor microenvironment) factors may explain this heterogeneity of Wnt/beta-catenin signaling activity within the tumor mass...
  31. ncbi request reprint Morphological changes in tumour type after radiotherapy are accompanied by changes in gene expression profile but not in clinical behaviour
    Iris Nagtegaal
    Department of Pathology, Leiden University Medical Center, Leiden, The Netherlands
    J Pathol 204:183-92. 2004
    ..It is concluded that tumour morphology equates to expression profile, but that external factors might influence both, leading to sub-optimal prognostication...
  32. ncbi request reprint American founder mutation for Lynch syndrome. Prevalence estimates and implications
    Henry T Lynch
    Department of Preventive Medicine and Public Health, Creighton University, Omaha, Nebraska 68178, USA
    Cancer 106:448-52. 2006
    ..This test might serve as first-line screening for Lynch syndrome mutations, provided AFM was prevalent, which is assessed in the current study...
  33. pmc Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGH
    Joana Cardoso
    Department of Pathology, Josephine Nefkens Institute, Erasmus University Medical Center, Rotterdam, The Netherlands
    Nucleic Acids Res 32:e146. 2004
    ....
  34. ncbi request reprint APC dosage effects in tumorigenesis and stem cell differentiation
    Claudia Gaspar
    Dept of Pathology, Josephine Nefkens Institute, Erasmus University Medical Center, 3000 DR Rotterdam, The Netherlands
    Int J Dev Biol 48:377-86. 2004
    ..Hence, beta-catenin dosage-dependent effects may not only explain how a single pathway is involved in the development and homeostasis of different tissues, but also its pleiotrophic role in tumorigenesis...
  35. ncbi request reprint A founder mutation of the MSH2 gene and hereditary nonpolyposis colorectal cancer in the United States
    Henry T Lynch
    Department of Preventive Medicine, Creighton University School of Medicine, Omaha, Neb 68178, USA
    JAMA 291:718-24. 2004
    ..However, while carriers of these mutations should be identified, counseled, and offered clinical surveillance, at present the mutations are not tested for in mutation analyses...
  36. ncbi request reprint Genetic deletion of receptor for hyaluronan-mediated motility (Rhamm) attenuates the formation of aggressive fibromatosis (desmoid tumor)
    Cornelia Tolg
    Departments of Oncology and Biochemistry, The University of Western Ontario, Canada
    Oncogene 22:6873-82. 2003
    ....
  37. ncbi request reprint Premature chromosome condensation revisited: a novel chemical approach permits efficient cytogenetic analysis of cancers
    Vladimir Bezrookove
    Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 38:177-86. 2003
    ....
  38. ncbi request reprint EXO1 variants occur commonly in normal population: evidence against a role in hereditary nonpolyposis colorectal cancer
    Shantie Jagmohan-Changur
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands 2333
    Cancer Res 63:154-8. 2003
    ..Thus, little evidence was obtained to support a major causative role of EXO1 in HNPCC, although we cannot exclude a role for EXO1 as a low penetrance cancer susceptibility or modifying gene...
  39. ncbi request reprint The multiple functions of tumour suppressors: it's all in APC
    Riccardo Fodde
    Nat Cell Biol 5:190-2. 2003
  40. ncbi request reprint Serrated adenomas and mixed polyposis caused by a splice acceptor deletion in the mouse Smad4 gene
    Peter Hohenstein
    Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 36:273-82. 2003
    ..Identification of a Smad4 mutation in the Sad mouse model provides further support for the involvement of the Smad genes, and thus the TGFB pathway, in the serrated/hyperplastic route to colorectal cancer...
  41. ncbi request reprint A 10-Mb paracentric inversion of chromosome arm 2p inactivates MSH2 and is responsible for hereditary nonpolyposis colorectal cancer in a North-American kindred
    Anja Wagner
    MGC Department of Human and Clinical Genetics, Leiden University Medical Center, Leiden, The Netherlands
    Genes Chromosomes Cancer 35:49-57. 2002
    ..Moreover, monoallelic expression analysis represents an attractive approach to demonstrate pathogenicity of unusual mutations in autosomal dominant hereditary conditions...
  42. ncbi request reprint The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascade
    Cristina Albuquerque
    Centro de Investigacao de Patobiologia Molecular CIPM, Instituto Portugues de Oncologia Francisco Gentil, 1093 Lisbon, Portugal
    Hum Mol Genet 11:1549-60. 2002
    ..We propose that this selection process is aimed at a specific degree of beta-catenin signaling optimal for tumor formation, rather than at its constitutive activation by deletion of all of the beta-catenin downregulating motifs in APC...