ReviewInternational journal of gastrointestinal cancer2002
Cell growth and metastasis in pancreatic cancer: is Vav the Rho'd to activation?
Review in International journal of gastrointestinal cancer, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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
7 citing papers in PubMed, 11 citations in OpenAlex.
- Dynamic Coupling of MAPK Signaling to the Guanine Nucleotide Exchange Factor GEF-H1.OncoTargets and therapy · 2025Review
- Paxillin kinase linker (PKL) regulates Vav2 signaling during cell spreading and migration.Molecular biology of the cell · 2013Article
- Surfing the big WAVE: Insights into the role of WAVE3 as a driving force in cancer progression and metastasis.Seminars in cell & developmental biology · 2013Review
- miR-143 inhibits the metastasis of pancreatic cancer and an associated signaling pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
- Down-regulation of WAVE3, a metastasis promoter gene, inhibits invasion and metastasis of breast cancer cells.The American journal of pathology · 2007Article
- An active form of Vav1 induces migration of mammary epithelial cells by stimulating secretion of an epidermal growth factor receptor ligand.Cell communication and signaling : CCS · 2006Article
- Using RNAi to catch Drosophila genes in a web of interactions: insights into cancer research.Oncogene · 2004Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The best-known family of low molecular weight GTP-binding proteins is Ras, owing to their high incidence of gain of function mutations in a variety of human cancers including pancreatic cancer. Unlike Ras, no activating mutations have been observed thus far for Rho family GTP-binding proteins in cancer, yet there is increasing evidence that overexpression of Rho family members and/or dysregulation of the GDP-->GTP cycle play an important role in cancer development and progression. The activation of Rho family GTPases downstream of cell surface receptors results in the induction of several intracellular signaling cascades that have been shown to impact on such diverse cellular responses as reorganization of the actin cytoskeleton, gene transcription, cell survival, and cell proliferation. One family of guanine nucleotide exchange factors (GEFs) that have the potential to couple the activation of Rho family members to upstream growth factor receptor tyrosine kinases (RTKs) is the Vav family of proto-oncogenes. Recent experimental evidence has implicated Vav in the regulation of numerous Rho-mediated pathways downstream of RTKs and other cell surface receptors. In this review, we will discuss our current understanding of how Vav proteins are regulated, and how Vav and their target GTP-binding proteins participate in tumorigenesis.
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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.