Parvovirus H‐1 inhibits growth of short‐term tumor‐derived but not normal mammary tissue cultures

Pachterbeke, C. Van; Tuynder, Marcel; Rommelaere, Jean; Cosyn, J. P.; Lespagnard, Laurence; Larsimont, Denis

doi:10.1002/ijc.2910550427

Cited by 32 publications

(19 citation statements)

References 25 publications

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“…13 It may be argued that long -time culturing of the tumor-derived cells may have caused a drift to a greater permissivity of those tumor cells to parvovirus infection. However, freshly isolated breast and gastric tumor cells from different patients could be better infected by H1 virus than the corresponding normal cells, 27,28 suggesting that these tumor cells were susceptible to H1 virus infection before their establishment as permanent lines. Similarly, simian virus 40 ±transformed human fibroblasts became sensitive to H1 infection before or after their immortalization.…”

Section: Discussionmentioning

confidence: 99%

“…26 So far, only a few studies have investigated the susceptibility of a series of human tumor cells deriving from the same tissue to H1 virus ± induced toxicity. 24,27,28 As parvovirus replication is not restricted to tumors in the natural hosts ( rodents ), studies are needed to identify human tumor cells susceptible to parvovirus replication from which the normal parental cells resist such infection, apoptotic cell killing, and parvovirus -based gene transduction. Susceptibility of normal human cells to parvovirus infection would be considered as a drawback for the use of parvovirus vectors as antitumor agents as it may cause damage to healthy tissue.…”

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confidence: 99%

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Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vectors

Moehler¹,

Blechacz

Weiskopf³

et al. 2001

Cancer Gene Ther

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Autonomous parvoviruses preferentially replicate in and kill in vitro ± transformed cells and reduce the incidence of spontaneous and implanted tumors in animals. Because of these natural oncotropic and oncolytic properties, parvoviruses deserve to be considered as potential antitumor vectors. Here, we assessed whether parvovirus H1 is able to kill human hepatoma cells by induction of apoptosis but spares primary human liver cells, and whether the former cells can efficiently be transduced by H1 virus ± based vectors. Cell death, infectivity, and transgene transduction were investigated in Hep3B, HepG2, and Huh7 cells and in primary human hepatocytes with natural and recombinant H1 virus. All hepatoma cells were susceptible to H1 virus ± induced cytolyis. Cell death correlated with H1 virus DNA replication, nonstructural protein expression, and with morphological features of apoptosis. H1 virus ± induced apoptosis was more pronounced in p53 -deleted Hep3B and p53 -mutated Huh7 cells than in HepG2 cells which express wild -type p53. In Hep3B cells, apoptosis was partially inhibited by DEVD -CHO, a caspase -3 inhibitor. In contrast, H1 virus ± infected primary hepatocytes were neither positive for nonstructural protein expression nor susceptible to H1 virus ± induced killing. Infection with a recombinant parvovirus vector carrying the luciferase gene under control of parvovirus promoter P38 led to higher transgene activities in hepatoma cells than in the hepatocytes. Taken together, H1 virus kills human hepatoma cells at low virus multiplicity but not primary hepatocytes. Thus, recombinant H1 viruses carrying antitumor transgenes may be considered as potential therapeutic options for the treatment of hepatocellular carcinomas. Cancer Gene Therapy ( 2001 ) 8, 158 ± 167

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vectors

Moehler¹,

Blechacz

Weiskopf³

et al. 2001

Cancer Gene Ther

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“…Recent molecular studies on parvovirus pathogenicity suggest that the viral non-structural (NS) protein, which is highly conserved among parvoviruses, may be cytotoxic (Caillet-Fauquet et al, 1990 ;Van Pachterbeke et al, 1993 ;Momoeda et al, 1994). This is consistent with the observation that oncogenically transformed cells show increases in sensitivity to the killing effect of minute virus of mice (MVM) and in the capacity for virus NS protein synthesis (Mousset et al, 1994).…”

Section: Observations Made In Vivo Revealed That the Number Of Apoptomentioning

confidence: 99%

Induction of apoptosis in vitro and in vivo by H-1 parvovirus infection.

Ohshima

Iwama

Ueno

et al. 1998

Journal of General Virology

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Apoptosis induced by H-1 parvovirus infection was investigated in C6 rat glioblastoma cells and in newborn rats. Apoptotic changes, such as chromatin condensation, the appearance of apoptotic nuclear bodies and oligonucleosomal DNA ladders, were observed in infected C6 cells 2 days after infection. Inhibitor assay results suggest that a caspase-3-dependent apoptosis activation pathway is induced by H-1 virus infection in C6 cells. Observations made in vivo revealed that the number of apoptotic cells increased in the infected cerebellum, coinciding with known virus infection sites.

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“…In this paper, we used spheroids for analysis of CRAds, but the model should be applicable to any type of replicating agent. Replication competent viruses currently undergoing preclinical or clinical evaluation for cancer treatment include herpes simplex virus, 65,66 vaccinia, 67 Newcastle disease virus, 68 parvovirus, 69 reovirus, 70 measles virus, 71 retrovirus, 72 influenza virus, 73 poliovirus, 74 vesicular stomatitis virus, 75 and avian sarcoma leucosis virus. 76 Therefore, replication competent viruses represent a dynamic field desperate for practical substrates for primary tumor specimen analyses.…”

Section: Discussionmentioning

confidence: 99%

Replication of an integrin targeted conditionally replicating adenovirus on primary ovarian cancer spheroids

et al. 2003

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Replication competent viruses hold promise for treatment of advanced cancers resistant to available therapeutic modalities. Although preliminary clinical results have substantiated their efficacy, preclinical development of these novel approaches is limited by assay substrates. The evaluation of candidate agents could be confounded by differences between primary tumor cells and tumor cell lines, as discordance in the levels of surface receptors relevant for viral entry has been reported. Since primary tumor cells are difficult to analyze ex vivo for longitudinal observation of virus replication, we developed three-dimensional aggregates or spheroids of unpassaged and purified ovarian cancer cells as a means for prolonging primary tumor cell viability and as a threedimensional in vitro model for replicative viral infection. Ovarian cancer cells purified from ascites samples were sustained for 30 days while retaining the infection profile with tropism modified and unmodified adenoviruses (Ads). Cell line and primary cell spheroids were used to quantitate the replication and oncolytic potency of replicative Ads in preclinical testing for human ovarian cancer trials. Therefore, spheroids provide a method to sustain purified unpassaged primary ovarian cancer cells for extended periods and to allow evaluation of replicative viruses in a three-dimensional model.

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Parvovirus H‐1 inhibits growth of short‐term tumor‐derived but not normal mammary tissue cultures

Cited by 32 publications

References 25 publications

Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vectors

Effective infection, apoptotic cell killing and gene transfer of human hepatoma cells but not primary hepatocytes by parvovirus H1 and derived vectors

Induction of apoptosis in vitro and in vivo by H-1 parvovirus infection.

Replication of an integrin targeted conditionally replicating adenovirus on primary ovarian cancer spheroids

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