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Deleted in colorectal carcinoma suppresses metastasis in p53-deficient mammary tumours.(RESEARCH: LETTER)(Report)

Since its discovery in the early 1990s the deleted in colorectal cancer (DCC) gene, located on chromosome 18q21, has been proposed as a tumour suppressor gene as its loss is implicated in the majority of advanced colorectal and many other cancers (1). DCC belongs to the family of netrin 1 receptors,... Full description

Journal Title: Nature Feb 23, 2012, Vol.482(7386), p.538(5)
Main Author: Krimpenfort, Paul
Other Authors: Song, Ji-Ying , Proost, Natalie , Zevenhoven, John , Jonkers, Jos , Berns, Anton
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0028-0836 ; DOI: 10.1038/nature10790
Zum Text:
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recordid: gale_ofa282822995
title: Deleted in colorectal carcinoma suppresses metastasis in p53-deficient mammary tumours.(RESEARCH: LETTER)(Report)
format: Article
creator:
  • Krimpenfort, Paul
  • Song, Ji-Ying
  • Proost, Natalie
  • Zevenhoven, John
  • Jonkers, Jos
  • Berns, Anton
subjects:
  • Colorectal Cancer – Genetic Aspects
  • Colorectal Cancer – Risk Factors
  • Colorectal Cancer – Research
  • Tumor Suppressor Genes – Physiological Aspects
  • Tumor Suppressor Genes – Research
  • Gene Mutation – Health Aspects
  • Gene Mutation – Research
ispartof: Nature, Feb 23, 2012, Vol.482(7386), p.538(5)
description: Since its discovery in the early 1990s the deleted in colorectal cancer (DCC) gene, located on chromosome 18q21, has been proposed as a tumour suppressor gene as its loss is implicated in the majority of advanced colorectal and many other cancers (1). DCC belongs to the family of netrin 1 receptors, which function as dependence receptors as they control survival or apoptosis depending on ligand binding. However, the role of DCC as a tumour suppressor remains controversial because of the rarity of DCC-specific mutations and the presence of other tumour suppressor genes in the same chromosomal region. Here we show that in a mouse model of mammary carcinoma based on somatic inactivation of p53, additional loss of DCC promotes metastasis formation without affecting the primary tumour phenotype. Furthermore, we demonstrate that in cell cultures derived from p53-deficient mouse mammary tumours DCC expression controls netrin-1-dependent cell survival, providing a mechanistic basis for the enhanced metastatic capacity of tumour cells lacking DCC. Consistent with this idea, invivotumour-cell survival is enhanced by DCC loss. Together, our data support the function of DCC as a context-dependent tumour suppressor that limits survival of disseminated tumour cells.
language: eng
source:
identifier: ISSN: 0028-0836 ; DOI: 10.1038/nature10790
fulltext: fulltext
issn:
  • 0028-0836
  • 00280836
url: Link


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titleDeleted in colorectal carcinoma suppresses metastasis in p53-deficient mammary tumours.(RESEARCH: LETTER)(Report)
creatorKrimpenfort, Paul ; Song, Ji-Ying ; Proost, Natalie ; Zevenhoven, John ; Jonkers, Jos ; Berns, Anton
ispartofNature, Feb 23, 2012, Vol.482(7386), p.538(5)
identifierISSN: 0028-0836 ; DOI: 10.1038/nature10790
subjectColorectal Cancer – Genetic Aspects ; Colorectal Cancer – Risk Factors ; Colorectal Cancer – Research ; Tumor Suppressor Genes – Physiological Aspects ; Tumor Suppressor Genes – Research ; Gene Mutation – Health Aspects ; Gene Mutation – Research
descriptionSince its discovery in the early 1990s the deleted in colorectal cancer (DCC) gene, located on chromosome 18q21, has been proposed as a tumour suppressor gene as its loss is implicated in the majority of advanced colorectal and many other cancers (1). DCC belongs to the family of netrin 1 receptors, which function as dependence receptors as they control survival or apoptosis depending on ligand binding. However, the role of DCC as a tumour suppressor remains controversial because of the rarity of DCC-specific mutations and the presence of other tumour suppressor genes in the same chromosomal region. Here we show that in a mouse model of mammary carcinoma based on somatic inactivation of p53, additional loss of DCC promotes metastasis formation without affecting the primary tumour phenotype. Furthermore, we demonstrate that in cell cultures derived from p53-deficient mouse mammary tumours DCC expression controls netrin-1-dependent cell survival, providing a mechanistic basis for the enhanced metastatic capacity of tumour cells lacking DCC. Consistent with this idea, invivotumour-cell survival is enhanced by DCC loss. Together, our data support the function of DCC as a context-dependent tumour suppressor that limits survival of disseminated tumour cells.
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titleDeleted in colorectal carcinoma suppresses metastasis in p53-deficient mammary tumours.(RESEARCH: LETTER)(Report)
descriptionSince its discovery in the early 1990s the deleted in colorectal cancer (DCC) gene, located on chromosome 18q21, has been proposed as a tumour suppressor gene as its loss is implicated in the majority of advanced colorectal and many other cancers (1). DCC belongs to the family of netrin 1 receptors, which function as dependence receptors as they control survival or apoptosis depending on ligand binding. However, the role of DCC as a tumour suppressor remains controversial because of the rarity of DCC-specific mutations and the presence of other tumour suppressor genes in the same chromosomal region. Here we show that in a mouse model of mammary carcinoma based on somatic inactivation of p53, additional loss of DCC promotes metastasis formation without affecting the primary tumour phenotype. Furthermore, we demonstrate that in cell cultures derived from p53-deficient mouse mammary tumours DCC expression controls netrin-1-dependent cell survival, providing a mechanistic basis for the enhanced metastatic capacity of tumour cells lacking DCC. Consistent with this idea, invivotumour-cell survival is enhanced by DCC loss. Together, our data support the function of DCC as a context-dependent tumour suppressor that limits survival of disseminated tumour cells.
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abstractSince its discovery in the early 1990s the deleted in colorectal cancer (DCC) gene, located on chromosome 18q21, has been proposed as a tumour suppressor gene as its loss is implicated in the majority of advanced colorectal and many other cancers (1). DCC belongs to the family of netrin 1 receptors, which function as dependence receptors as they control survival or apoptosis depending on ligand binding. However, the role of DCC as a tumour suppressor remains controversial because of the rarity of DCC-specific mutations and the presence of other tumour suppressor genes in the same chromosomal region. Here we show that in a mouse model of mammary carcinoma based on somatic inactivation of p53, additional loss of DCC promotes metastasis formation without affecting the primary tumour phenotype. Furthermore, we demonstrate that in cell cultures derived from p53-deficient mouse mammary tumours DCC expression controls netrin-1-dependent cell survival, providing a mechanistic basis for the enhanced metastatic capacity of tumour cells lacking DCC. Consistent with this idea, invivotumour-cell survival is enhanced by DCC loss. Together, our data support the function of DCC as a context-dependent tumour suppressor that limits survival of disseminated tumour cells.
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date2012-02-23