Author
Listed:
- Eduard Batlle
(Center for Biomedical Genetics
Biomedical Research Institute, Barcelona Science Park
Institució Catalana de Recerca i Estudis Avançats (ICREA))
- Julinor Bacani
(Mount Sinai Hospital)
- Harry Begthel
(Center for Biomedical Genetics)
- Suzanne Jonkeer
(Center for Biomedical Genetics
Biomedical Research Institute, Barcelona Science Park)
- Alexander Gregorieff
(Center for Biomedical Genetics)
- Maaike van de Born
(Center for Biomedical Genetics)
- Núria Malats
(Institut Municipal d'Investigació Mèdica)
- Elena Sancho
(Center for Biomedical Genetics
Biomedical Research Institute, Barcelona Science Park)
- Elles Boon
(Academic Medical Center)
- Tony Pawson
(Mount Sinai Hospital)
- Steven Gallinger
(Mount Sinai Hospital)
- Steven Pals
(Academic Medical Center)
- Hans Clevers
(Center for Biomedical Genetics)
Abstract
Cancer progression The convergence between stem-cell and cancer-cell biology is well illustrated by a new study of colorectal cancer. A genetic program driven by β-catenin and Tcf is known to control stem-cell specification in the intestine and also to initiate colorectal cancer. EphB guidance receptors, widely studied in the context of axon guidance, are Tcf target genes involved in this pathway. The new work shows that most human colorectal cancers lose expression of EphB at the stage of transition between (benign) adenoma and (cancerous) carcinoma. Loss of EphB expression strongly correlates with degree of malignancy and in a mouse model, loss of EphB accelerates tumorigenesis in the colon and rectum. Loss of EphB expression is therefore a critical step in colorectal cancer progression.
Suggested Citation
Eduard Batlle & Julinor Bacani & Harry Begthel & Suzanne Jonkeer & Alexander Gregorieff & Maaike van de Born & Núria Malats & Elena Sancho & Elles Boon & Tony Pawson & Steven Gallinger & Steven Pals &, 2005.
"EphB receptor activity suppresses colorectal cancer progression,"
Nature, Nature, vol. 435(7045), pages 1126-1130, June.
Handle:
RePEc:nat:nature:v:435:y:2005:i:7045:d:10.1038_nature03626
DOI: 10.1038/nature03626
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