Research Topics
| Riccardo FoddeSummaryAffiliation: Erasmus MC Country: The Netherlands Publications
| Collaborators
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Detail Information
Publications
Adenomatous polyposis coli-mediated control of beta-catenin is essential for both chondrogenic and osteogenic differentiation of skeletal precursorsRazvan L Miclea
Department of Tissue Regeneration, Institute for Biomedical Technology, University of Twente, Enschede, The Netherlands
BMC Dev Biol 9:26. 2009..Adenomatous polyposis coli (Apc) is a key controller of beta-catenin turnover by down-regulating intracellular levels of beta-catenin...
Smad4 haploinsufficiency: a matter of dosagePaola Alberici
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
Pathogenetics 1:2. 2008..To date, the molecular and cellular consequences of SMAD4 haploinsufficiency on TGF-beta and BMP signaling and on genome-wide gene expression have not been investigated...
The stem of cancerRiccardo Fodde
Department of Pathology, Josephine Nefkens Institute, Erasmus Medical Center, Rotterdam, The Netherlands
Cancer Cell 15:87-9. 2009..Two recent publications provide experimental evidence that normal intestinal stem cells are the cells of origin of intestinal cancer in the mouse...
Nuclear beta-catenin expression and Wnt signalling: in defence of the dogmaRiccardo Fodde
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
J Pathol 221:239-41. 2010....
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...
Stem cells and metastatic cancer: fatal attraction?Riccardo Fodde
Department of Pathology, Josephine Nefkens Institute, Erasmus Medical Center, Rotterdam, The Netherlands
PLoS Med 3:e482. 2006
Cross-species comparison of human and mouse intestinal polyps reveals conserved mechanisms in adenomatous polyposis coli (APC)-driven tumorigenesisClaudia Gaspar
Dept of Pathology, Erasmus MC, PO Box 2040, 3000CA Rotterdam, The Netherlands
Am J Pathol 172:1363-80. 2008....
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...
A targeted constitutive mutation in the APC tumor suppressor gene underlies mammary but not intestinal tumorigenesisClaudia Gaspar
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
PLoS Genet 5:e1000547. 2009..The striking phenotype of Apc(+/1572T) mice suggests that specific dosages of Wnt/beta-catenin signaling activity differentially affect tissue homeostasis and initiate tumorigenesis in an organ-specific fashion...
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....
Quiescent stem cells in intestinal homeostasis and cancerSabrina Roth
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
Cell Commun Adhes 18:33-44. 2011..Because of their infrequent cycling, quiescent CSCs are refractory to chemo- and radiotherapy and are likely to play a role in tumour dissemination, dormancy and recurrence...
Loss of APC function in mesenchymal cells surrounding the Müllerian duct leads to myometrial defects in adult miceYongyi Wang
Department of Obstetrics and Gynaecology, Erasmus University Medical Center, Rotterdam, The Netherlands
Mol Cell Endocrinol 341:48-54. 2011....
Barrett's oesophageal adenocarcinoma encompasses tumour-initiating cells that do not express common cancer stem cell markersBrechtje A Grotenhuis
Department of Surgery, Josephine Nefkens Institute, Erasmus Medical Centre, Rotterdam, The Netherlands
J Pathol 221:379-89. 2010..However, antibodies directed against novel surface antigens are needed to detect subpopulations enriched for CSCs in EA by transplantation assays...
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...
?-catenin tyrosine 654 phosphorylation increases Wnt signalling and intestinal tumorigenesisWendy Van Veelen
Department of Gastroenterology and Hepatology, Erasmus MC University Medical Centre, room L 63, s Gravendijkwal 230, 3015 CE, Rotterdam, The Netherlands
Gut 60:1204-12. 2011..In addition, in contrast to the current belief that ?-catenin Y654 phosphorylation increases tumour progression to a more invasive phenotype, these results show that it rather increases tumour initiation by enhancing Wnt signalling...
Generation of a tightly regulated doxycycline-inducible model for studying mouse intestinal biologySabrina Roth
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
Genesis 47:7-13. 2009..Thus, we have generated a novel doxycycline-inducible mouse model, providing a valuable tool to study the effect of different gene dosages on intestinal physiology and pathology...
Cancer stemness and metastasis: therapeutic consequences and perspectivesJoana Monteiro
Department of Pathology, Josephine Nefkens Institute, Erasmus MC, Rotterdam, The Netherlands
Eur J Cancer 46:1198-203. 2010....
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....
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...
cAMP/PKA pathway activation in human mesenchymal stem cells in vitro results in robust bone formation in vivoRamakrishnaiah Siddappa
Department of Tissue Regeneration, Institute for Biomedical Technology, University of Twente, 7500 AE, Enschede, The Netherlands
Proc Natl Acad Sci U S A 105:7281-6. 2008..As a consequence, PKA activation results in robust in vivo bone formation by hMSCs derived from orthopedic patients...
SET-CAN, the product of the t(9;9) in acute undifferentiated leukemia, causes expansion of early hematopoietic progenitors and hyperproliferation of stomach mucosa in transgenic miceUgur Ozbek
Department of Genetics and Tumor Cell Biology, St Jude Children s Research Hospital, Memphis, Tennessee 38105, USA
Am J Pathol 171:654-66. 2007....
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...
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...
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....
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...
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...
Cancer biology. A matter of dosageRiccardo Fodde
Center for Human and Clinical Genetics, Leiden University Medical Center, Leiden, Netherlands
Science 298:761-3. 2002
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...
