ReviewVirology2009
Lessons from polyoma middle T antigen on signaling and transformation: A DNA tumor virus contribution to the war on cancer.
Review in Virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 52 citations in OpenAlex.
- Article
- Hijacking of host Src-PI3K-Akt signaling by WSSV IE1 protein suppresses apoptotic and autophagic defenses to facilitate viral proliferation.Journal of virology · 2026Article
- A degradable form of polyoma small T antigen reveals the high specificity of TAZ in regulating gene expression.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- SRC inhibition enables formation of a growth suppressive MAGI1-PP2A complex in isocitrate dehydrogenase-mutant cholangiocarcinoma.Science translational medicine · 2024Article
- Membrane-bound Merkel cell polyomavirus middle T protein constitutively activates PLCγ1 signaling through Src-family kinases.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Investigating the Role of Heparanase in Breast Cancer Development Utilising the MMTV-PyMT Murine Model of Mammary Carcinoma.Cancers · 2023Article
- Coordinated activation of c-Src and FOXM1 drives tumor cell proliferation and breast cancer progression.The Journal of clinical investigation · 2023Article
- Oncoprotein GT198 vaccination delays tumor growth in MMTV-PyMT mice.Cancer letters · 2020Article
- Small size, big impact: how studies of small DNA tumour viruses revolutionized biology.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- The Human Polyomavirus Middle and Alternative T-Antigens; Thoughts on Roles and Relevance to Cancer.Frontiers in microbiology · 2018Review
- A Transformation-Defective Polyomavirus Middle T Antigen with a Novel Defect in PI3 Kinase Signaling.Journal of virology · 2017Article
- Review
- Transformation by Polyomavirus Middle T Antigen Involves a Unique Bimodal Interaction with the Hippo Effector YAP.Journal of virology · 2016Article
- Global Analysis of Mouse Polyomavirus Infection Reveals Dynamic Regulation of Viral and Host Gene Expression and Promiscuous Viral RNA Editing.PLoS pathogens · 2015Article
- The polyomavirus middle T-antigen oncogene activates the Hippo pathway tumor suppressor Lats in a Src-dependent manner.Oncogene · 2015Article
- Article
- Article
- The phosphatidylinositol 3-kinase (PI3K) isoform dependence of tumor formation is determined by the genetic mode of PI3K pathway activation rather than by tissue type.Journal of virology · 2014Article
- Herpes simplex virus protein kinases US3 and UL13 modulate VP11/12 phosphorylation, virion packaging, and phosphatidylinositol 3-kinase/Akt signaling activity.Journal of virology · 2014Article
- Stat3 and gap junctions in normal and lung cancer cells.Cancers · 2014Article
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
Abstract
Middle T antigen (MT) is the principal oncogene of murine polyomavirus. Its study has led to the discovery of the roles of tyrosine kinase and phosphoinositide 3-kinase (PI3K) signaling in mammalian growth control and transformation. MT is necessary for viral transformation in tissue culture cells and tumorigenesis in animals. When expressed alone as a transgene, MT causes tumors in a wide variety of tissues. It has no known catalytic activity, but rather acts by assembling cellular signal transduction molecules. Protein phosphatase 2A, protein tyrosine kinases of the src family, PI3K, phospholipase Cgamma1 as well as the Shc/Grb2 adaptors are all assembled on MT. Their activation sets off a series of signaling cascades. Analyses of virus mutants as well as transgenic animals have demonstrated that the effects of a given signal depend not only tissue type, but on the genetic background of the host animal. There remain many opportunities as we seek a full molecular understanding of MT and apply some of its lessons to human cancer.
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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 Socratic graph.