Viruses, gene therapy and stem cells for the treatment of human glioma

Kyritsis, Anthanassios P.; Sioka, Chrissa; Rao, Jasti S.

doi:10.1038/cgt.2009.52

Cited by 16 publications

(12 citation statements)

References 83 publications

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“…On the other hand, the short half-life of some virus, like retrovirus, also affect their therapeutic capacity. 28,29 Virus diffuse passively once they are administered into the tissue, and their inadequate distribution and propagation within the tumor diminish their therapeutic capacity. 30 Viral vectors are very large compared with chemotherapeutic agents (over 100-fold), causing their distribution within the tumor to be very limited, thus the penetration of these vectors from the site of injection or from the vasculature is severely restricted.…”

Section: Discussionmentioning

confidence: 99%

Lentiviral transfer of an inducible transgene expressing a soluble form of Gas1 causes glioma cell arrest, apoptosis and inhibits tumor growth

et al. 2010

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Gliomas are the most frequent primary tumors of the central nervous system, and their clinical prognosis remains very poor. Because of the characteristics of gliomas, gene therapy appears as a potentially relevant strategy for their treatment. However, the inability of viral vectors to transfer the therapeutic genes to a significantly high number of tumor cells, due to their limited diffusion and distribution, remains a critical obstacle for their application treating gliomas. We have demonstrated that the overexpression of growth arrest specific1 (Gas1) induces cell arrest and apoptosis and eliminates glioma cells in vitro and when implanted in mice. To improve the therapeutic range of Gas1, we generated lentiviral vectors coding for a soluble form of Gas1. Here, we show that cells infected with this virus produce the mutant protein, that acting both in autocrine and paracrine manners, causes death of infected and neighbor cells, thus importantly enhancing the effect of Gas1. Furthermore, the administration of this vector, or cells expressing it, inhibit the growth of tumors inoculated in mice. We present a gene therapy strategy that increases the effect of the therapeutic molecule by eliminating not just the infected cells that express Gas1, but neighbor non-infected cells.

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Section: Discussionmentioning

confidence: 99%

Lentiviral transfer of an inducible transgene expressing a soluble form of Gas1 causes glioma cell arrest, apoptosis and inhibits tumor growth

et al. 2010

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“…On the other hand, the mutant virus can replicate in cells with disrupted Rb cell cycle control, like glioma cells. [15] In 2000, the production of Ad-Δ24 was described for the first time along with a detailed description of its cytopathic effect on different glioma cell-lines. [13] But despite its potent antiglioma effect, it was obvious even from the first studies that Ad-Δ24 would need further improvements for optimal therapeutic effect.…”

Section: Oncolytic Virusesmentioning

confidence: 99%

Targeting glioblastoma with oncolytic adenovirus delta 24

Tsamis¹,

Alexiou²,

Kyritsis³

2015

Neuroimmunol Neuroinflammation

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“…Other potential useful approaches may include use of dendritic cell vaccines [95], and gene therapy, virotherapy or stem cells as adjuncts to conventional therapies for gliomas [96].…”

Section: Future Directionsmentioning

confidence: 99%

“…Replication-incompetent or competent viruses can be used either as gene delivery vehicles to gliomas or to induce oncolysis and avoid damage of the adjacent normal cells [97,96]. …”

Section: Future Directionsmentioning

confidence: 99%

An algorithm for chemotherapy treatment of recurrent glioma patients after temozolomide failure in the general oncology setting

Kyritsis

Levin

2011

Cancer Chemother Pharmacol

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To cite this version:Athanassios P. Kyritsis, Victor A. Levin. An algorithm for chemotherapy treatment of recurrent glioma patients after temozolomide failure in the general oncology setting. Cancer Chemotherapy and Pharmacology, Springer Verlag, 2011, 67 (5) Results. In order to guide practice in the general oncology setting an algorithm was constructed according to the activity of the reported chemotherapies at the time of writing.There are some molecular studies, performed on tumor tissue that may help to guide selection of chemotherapy. Methylated MGMT in tumor tissue correlates with increased sensitivity to alkylating agents such as fotemustine or other nitrosoureas. Depending on MGMT status and bone marrow reserve, treatment with fotemustine, bevacizumab, bevacizumab with irinotecan, or cis-retinoic acid (cRA), might be of value.Conclusion. Unfortunately, progress in the development of new and more effective chemotherapy agents has been very limited and leaves the clinician treating high-grade glioma patients at relapse with few good options. The suggested algorithm is our objective evaluation of the currently existing knowledge. Hopefully, ongoing phase II and III trials will provide us the needed chemotherapy agents in the years to come.3

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Viruses, gene therapy and stem cells for the treatment of human glioma

Cited by 16 publications

References 83 publications

Lentiviral transfer of an inducible transgene expressing a soluble form of Gas1 causes glioma cell arrest, apoptosis and inhibits tumor growth

Lentiviral transfer of an inducible transgene expressing a soluble form of Gas1 causes glioma cell arrest, apoptosis and inhibits tumor growth

Targeting glioblastoma with oncolytic adenovirus delta 24

An algorithm for chemotherapy treatment of recurrent glioma patients after temozolomide failure in the general oncology setting

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