ArticleJournal of virology1998
Induction of programmed cell death by parvovirus H-1 in U937 cells: connection with the tumor necrosis factor alpha signalling pathway.
Article in Journal of virology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 100 citations in OpenAlex.
- Delineated domain of VP2 capsid protein in H-1 parvovirus that determines susceptibility to human cancer cells.Journal of microbiology (Seoul, Korea) · 2026Article
- The SIRT1-Mediated p53 Deacetylation Pathway Modulates Apoptosis and Promotes Viral Replication in MVC-Infected Cells.Pathogens (Basel, Switzerland) · 2026Article
- Review
- Parvoviruses NS1 oncolytic attributes: mechanistic insights and synergistic anti-tumor therapeutic strategies.Frontiers in microbiology · 2025Review
- G2/M checkpoint regulation and apoptosis facilitate the nuclear egress of parvoviral capsids.Frontiers in cell and developmental biology · 2022Article
- Molecular Detection of Parvovirus in Manchurian Chipmunks (Tamias sibiricus asiaticus) Captured in Korea.Intervirology · 2022Article
- Review
- Article
- Review: Oncolytic virotherapy, updates and future directions.Oncotarget · 2017Review
- Article
- The SAT Protein of Porcine Parvovirus Accelerates Viral Spreading through Induction of Irreversible Endoplasmic Reticulum Stress.Journal of virology · 2017Article
- VP2 capsid domain of the H-1 parvovirus determines susceptibility of human cancer cells to H-1 viral infection.Cancer gene therapy · 2015Article
- Viral genes as oncolytic agents for cancer therapy.Cellular and molecular life sciences : CMLS · 2015Review
- Oncolytic parvoviruses: from basic virology to clinical applications.Virology journal · 2015Review
- Tumor Selectivity of Oncolytic Parvoviruses: From in vitro and Animal Models to Cancer Patients.Frontiers in bioengineering and biotechnology · 2015Review
- Complementary induction of immunogenic cell death by oncolytic parvovirus H-1PV and gemcitabine in pancreatic cancer.Journal of virology · 2014Article
- Oncolytic effects of parvovirus H-1 in medulloblastoma are associated with repression of master regulators of early neurogenesis.International journal of cancer · 2014Article
- Role of mitochondria in parvovirus pathology.PloS one · 2014Article
- Distinct host cell fates for human malignant melanoma targeted by oncolytic rodent parvoviruses.Virology · 2013Article
- Trial watch: Oncolytic viruses for cancer therapy.Oncoimmunology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The human promonocytic cell line U937 undergoes apoptosis upon treatment with tumor necrosis factor alpha (TNF-alpha). This cell line has previously been shown to be very sensitive to the lytic effect of the autonomous parvovirus H-1. Parvovirus infection leads to the activation of the CPP32 ICE-like cysteine protease which cleaves the enzyme poly(ADP-ribose)polymerase and induces morphologic changes that are characteristic of apoptosis in a way that is similar to TNF-alpha treatment. This effect is also observed when the U937 cells are infected with a recombinant H-1 virus which expresses the nonstructural (NS) proteins but in which the capsid genes are replaced by a reporter gene, indicating that the induction of apoptosis can be assigned to the cytotoxic nonstructural proteins in this cell system. The c-Myc protein, which is overexpressed in U937 cells, is rapidly downregulated during infection, in keeping with a possible role of this product in mediating the apoptotic cell death induced by H-1 virus infection. Interestingly, four clones (designated RU) derived from the U937 cell line and selected for their resistance to H-1 virus (J. A. Lopez-Guerrero et al., Blood 89:1642-1653, 1997) failed to decrease c-Myc expression upon treatment with differentiation agents and also resisted the induction of cell death after TNF-alpha treatment. Our data suggest that the RU clones have developed defense strategies against apoptosis, either by their failure to downregulate c-Myc and/or by activating antiapoptotic factors.
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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 OpenQuestion graph.