Research Topics
Genomes and Genes | R FoddeSummaryAffiliation: Leiden University Medical Center Country: The Netherlands Publications
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Publications
APC, signal transduction and genetic instability in colorectal cancerR 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...- Cancer biology. A matter of dosageRiccardo Fodde
Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands
Science 298:761-3. 2002 - Disease model: familial adenomatous polyposisR 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... - Mutations in the APC tumour suppressor gene cause chromosomal instabilityR 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... - Somatic Apc mutations are selected upon their capacity to inactivate the beta-catenin downregulating activityR 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... - E-cadherin and adenomatous polyposis coli mutations are synergistic in intestinal tumor initiation in miceR 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... - Mechanisms of APC-driven tumorigenesis: lessons from mouse modelsR 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... 
Apc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and developmentR Smits
Medical Genetics Center MGC Department of Human Genetics, Leiden University Medical Center, 2300 RA Leiden, The Netherlands
Genes Dev 13:1309-21. 1999....- A targeted mouse Brca1 mutation removing the last BRCT repeat results in apoptosis and embryonic lethality at the headfold stageP 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... - Dynamic expression and nuclear accumulation of beta-catenin during the development of hair follicle-derived structuresM 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... - Clinical findings with implications for genetic testing in families with clustering of colorectal cancerJ 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... - The APC gene in colorectal cancerR Fodde
Department of Human and Clinical Genetics, LUMC, Sylvius Laboratories, Leiden, The Netherlands
Eur J Cancer 38:867-71. 2002.... - Radiation induces different changes in expression profiles of normal rectal tissue compared with rectal carcinomaI 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... - Molecular analysis of the APC gene in 105 Dutch kindreds with familial adenomatous polyposis: 67 germline mutations identified by DGGE, PTT, and southern analysisR 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... - Cancer risk in hereditary nonpolyposis colorectal cancer due to MSH6 mutations: impact on counseling and surveillanceYvonne 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... - Spectrum of genetic alterations in Muir-Torre syndrome is the same as in HNPCCDaniela Barana
Am J Med Genet A 125:318-9. 2004 - TGFBR1*6A may contribute to hereditary colorectal cancerYansong 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... - 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... - Prostate cancer is part of the hereditary non-polyposis colorectal cancer (HNPCC) tumor spectrumClaudio 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... - Automated acquisition of stained tissue microarrays for high-throughput evaluation of molecular targetsHans 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... - The CHEK2 1100delC mutation identifies families with a hereditary breast and colorectal cancer phenotypeHanne 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... - Prevalence of adenomas and hyperplastic polyps in mismatch repair mutation carriers among CAPP2 participants: report by the colorectal adenoma/carcinoma prevention programme 2Annelie 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... - Apc modulates embryonic stem-cell differentiation by controlling the dosage of beta-catenin signalingMenno 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... - 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 geneAnja 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... - Conventional and tissue microarray immunohistochemical expression analysis of mismatch repair in hereditary colorectal tumorsYvonne 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... - Chromosomal instability in MYH- and APC-mutant adenomatous polypsJoana 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... - Multiple primary cancer, including transitional cell carcinoma of the upper uroepithelial tract in a multigeneration HNPCC family: molecular genetic, diagnostic, and management implicationsHenry 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.... - Somatic acquisition and signaling of TGFBR1*6A in cancerBoris 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... - Aneuploidy arises at early stages of Apc-driven intestinal tumorigenesis and pinpoints conserved chromosomal loci of allelic imbalance between mouse and humanPaola 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.... - Wnt/beta-catenin signaling in cancer stemness and malignant behaviorRiccardo 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... - Morphological changes in tumour type after radiotherapy are accompanied by changes in gene expression profile but not in clinical behaviourIris 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... - American founder mutation for Lynch syndrome. Prevalence estimates and implicationsHenry 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... - Genomic profiling by DNA amplification of laser capture microdissected tissues and array CGHJoana Cardoso
Department of Pathology, Josephine Nefkens Institute, Erasmus University Medical Center, Rotterdam, The Netherlands
Nucleic Acids Res 32:e146. 2004.... - APC dosage effects in tumorigenesis and stem cell differentiationClaudia 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... - A founder mutation of the MSH2 gene and hereditary nonpolyposis colorectal cancer in the United StatesHenry 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... - 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.... - Premature chromosome condensation revisited: a novel chemical approach permits efficient cytogenetic analysis of cancersVladimir Bezrookove
Department of Molecular Cell Biology, Leiden University Medical Center, Leiden, The Netherlands
Genes Chromosomes Cancer 38:177-86. 2003.... - EXO1 variants occur commonly in normal population: evidence against a role in hereditary nonpolyposis colorectal cancerShantie 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... - The multiple functions of tumour suppressors: it's all in APCRiccardo Fodde
Nat Cell Biol 5:190-2. 2003 - Serrated adenomas and mixed polyposis caused by a splice acceptor deletion in the mouse Smad4 genePeter 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... - A 10-Mb paracentric inversion of chromosome arm 2p inactivates MSH2 and is responsible for hereditary nonpolyposis colorectal cancer in a North-American kindredAnja 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... - The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascadeCristina 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...