ReviewBritish journal of cancer2005
Role of netrin-1 and netrin-1 dependence receptors in colorectal cancers.
Review in British journal of cancer, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 53 citations in OpenAlex.
- Netrin-1-UNC5B/neogenin axis enhances the stemness of colorectal cancer cells.Cell communication and signaling : CCS · 2025Article
- "Netrin-slaying nanoparticles: A new frontier in cancer therapy".BBA advances · 2025Review
- Netrin-1-CD146 and netrin-1-S100A9 are associated with early stage of lymph node metastasis in colorectal cancer.BMC gastroenterology · 2024Article
- Increased Expression Levels of Netrin-1 in Visceral Adipose Tissue during Obesity Favour Colon Cancer Cell Migration.Cancers · 2023Article
- Inactivation of axon guidance molecule netrin-1 in human colorectal cancer by an epigenetic mechanism.Biochemical and biophysical research communications · 2022Article
- Promoter methylation-mediated repression of UNC5 receptors and the associated clinical significance in human colorectal cancer.Clinical epigenetics · 2021Article
- Using BioPAX-Parser (BiP) to enrich lists of genes or proteins with pathway data.BMC bioinformatics · 2021Article
- Netrin1 deficiency activates MST1 via UNC5B receptor, promoting dopaminergic apoptosis in Parkinson's disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Dependence and Guidance Receptors-DCC and Neogenin-In Partial EMT and the Actions of Serine Proteases.Frontiers in oncology · 2020Review
- A Transcriptomic Insight into the Impact of Colon Cancer Cells on Mast Cells.International journal of molecular sciences · 2019Article
- Serine protease modulation of Dependence Receptors and EMT protein expression.Cancer biology & therapy · 2019Article
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- Epidermal Growth Factor Receptor-Dependent Mutual Amplification between Netrin-1 and the Hepatitis C Virus.PLoS biology · 2016Article
- Genetic and epigenetic alterations of netrin-1 receptors in gastric cancer with chromosomal instability.Clinical epigenetics · 2015Article
- Context is everything for dependence receptors in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- TNF-α mediates macrophage-induced bystander effects through Netrin-1.Cancer research · 2012Article
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- Overexpression of netrin-1 improves neurological outcomes in mice following transient middle cerebral artery occlusion.Frontiers of medicine · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although cancer is a multifaceted disease, all cancer types share identical molecular and cellular mechanisms. These mechanisms involve a collection of alterations critical to the normal physiological functioning of cells, such as alterations of growth factor signalling pathways, angiogenesis, cell adhesion signals, DNA replication and apoptotic cell death. Many genes involved in the processes enumerated above are functionally inactive in tumour cells, designating them as putative 'tumour suppressor genes'. Back in the early 1990s, Vogelstein and colleagues suggested that a gene called DCC (for Deleted in Colorectal Cancer) could be a tumour suppressor gene because it was found to be deleted in more than 70% of colorectal cancers, as well as in many other cancers. During the last 15 years, controversial data have failed to firmly establish whether DCC is indeed a tumour suppressor gene. However, the recent observations that DCC triggers cell death and is a receptor for netrin-1, a molecule recently implicated in colorectal tumorigenesis, have prompted a renewal of interest in the role of DCC in tumorigenesis and suggest that the netrin-1/receptor pairs act as novel negative regulators of tumour development.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.