Lack of Oncogenic Effect of the H-Viruses for Hamsters

Toolan, Helene Wallace

doi:10.1038/2141036a0

Cited by 43 publications

(17 citation statements)

References 1 publication

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“…The use of parvoviruses as therapeutic agents to limit the spread or even to completely remove already existing, extended neoplasms has also been tested [122]. The results, however, were disappointing.…”

Section: Parvoviruses and Tumorsmentioning

confidence: 99%

Parvoviruses: agents of distinct pathogenic and molecular potential

Siegl

Tratschin

1987

FEMS Microbiology Letters

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Parvoviruses are small, spherical and extremely stable particles with a genome of linear single‐stranded DNA. They are widespread in nature and thus have been in virtually every animal species and in man. Many parvoviruses were initially isolated by chance and could not be associated with clinical disease. Today, however, a considerable number of these agents are known to cause a broad spectrum of syndromes including fetal death, malformations, dwarfism, cerebellar hypolasia and ataxia, enteritis, panleukopenia, aplastic anemia, and immunologic disorders. Biological, pathological, and molecular studies revealed that all these syndromes are explainable on the basis of two predominant requirements for productive cytolytic parvovirus replication: the availability of cellular helper function(s) provided exclusively by mitotically active cells in the phase of cellular DNA replication, and by apparently specific, yet so far undefined cellular functions

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Section: Parvoviruses and Tumorsmentioning

confidence: 99%

Parvoviruses: agents of distinct pathogenic and molecular potential

Siegl

Tratschin

1987

FEMS Microbiology Letters

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“…The rodent parvoviruses are also markedly oncoselective, displaying enhanced fitness and toxicity in many human cancer cell lines compared to their untransformed counterparts, although they show variable tropism between tumor types (Chen et al, 1986; Chen et al, 1989; Cornelis et al, 2004; Dupont et al, 2000; Guetta et al, 1990; Legrand et al, 1992; Mousset et al, 1994; Rommelaere and Cornelis, 1991; Van Hille et al, 1989). They show potent oncosuppressive properties in many in vivo models, including syngeneic mouse tumor models and human xenografts transplanted into immunocompromised animals (Dupressoir et al, 1989; Faisst et al, 1998; Raykov et al, 2007; Rommelaere and Cornelis, 1991; Shi et al, 1997; Toolan, 1967; Toolan et al, 1982), and can also induce both curative and protective immune responses in some immunocompetent rodent tumor models (Guetta et al, 1986; Geletneky et al, 2010). Importantly for the prospective use of these agents in virotherapy of human cancer, there is no human disease associated with any known member of this genus (Dupont, 2003; Rommelaere and Cornelis, 1991; Siegl, 1984).…”

Section: Introductionmentioning

confidence: 99%

The parvoviral capsid controls an intracellular phase of infection essential for efficient killing of stepwise-transformed human fibroblasts

Paglino

Tattersall

2011

Virology

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Members of the rodent subgroup of the genus Parvovirus exhibit lytic replication and spread in many human tumor cells and are therefore attractive candidates for oncolytic virotherapy. However, the significant variation in tumor tropism observed for these viruses remains largely unexplained. We report here that LuIII kills BJ-ELR ‘stepwise-transformed’ human fibroblasts efficiently, while MVM does not. Using viral chimeras, we mapped this property to the LuIII capsid gene, VP2, which is necessary and sufficient to confer the killer phenotype on MVM. LuIII VP2 facilitates a post-entry, pre-DNA-amplification step early in the life cycle, suggesting the existence of an intracellular moiety whose efficient interaction with the incoming capsid shell is critical to infection. Thus targeting of human cancers of different tissue-type origins will require use of parvoviruses with capsids that effectively make this critical interaction.

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“…This possibility, so far, has been almost entirely ignored because of the unavailability of proper biological models. Our initial hypothesis (4, 5) that the H-1 parvovirus selects for revertant cells was based on experiments demonstrating that it preferentially kills tumor cells while sparing their normal counterparts (6,7).…”

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confidence: 99%

Biological models and genes of tumor reversion: Cellular reprogramming through tpt1 /TCTP and SIAH-1

Tuynder

Susini

Prieur

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

241

268

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Tumor reversion is the process by which some cancer cells lose their malignant phenotype. This study was aimed at defining some of the molecular and phenotypic properties of this process. Biological models of tumor reversion were isolated from human leukemia and breast cancer cell lines by using the H-1 parvovirus as a selective agent. Differential gene expression analysis was performed between the parental malignant cells and their revertants or alternatively between these parental cells and their SIAH-1 transfectant counterparts. These SIAH-1 transfectants have a suppressed malignant phenotype and were used as a control for a viral-free system. Two hundred sixty-three genes were found to be either activated or inhibited during the reversion process, as confirmed by Northern blot analysis or quantitative PCR. Of these, 32% were differentially expressed in all systems, irrespective of whether parvovirus-selected, SIAH-1 overexpressing, or p53 mutant or wild-type cell lines were used, suggesting the existence of a universal mechanism underlying tumor reversion. Translationally Controlled Tumor Protein (tpt1͞TCTP) has the strongest differential expression, down-regulated in the reversion of U937-and SIAH-1-overexpressing cells. Inhibition of TCTP expression by anti-sense cDNA or small interfering RNA molecules results in suppression of the malignant phenotype and in cellular reorganization, similar to the effect of SIAH-1. Hence, tumor reversion can be defined at the molecular level, not just as the reversal of malignant transformation, but as a biological process in its own right involving a cellular reprogramming mechanism, overriding genetic changes in cancer, by triggering an alternative pathway leading to suppression of tumorigenicity.

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Lack of Oncogenic Effect of the H-Viruses for Hamsters

Cited by 43 publications

References 1 publication

Parvoviruses: agents of distinct pathogenic and molecular potential

Parvoviruses: agents of distinct pathogenic and molecular potential

The parvoviral capsid controls an intracellular phase of infection essential for efficient killing of stepwise-transformed human fibroblasts

Biological models and genes of tumor reversion: Cellular reprogramming through tpt1 /TCTP and SIAH-1

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