Effective Radiovirotherapy for Malignant Gliomas by Using Oncolytic Measles Virus Strains Encoding the Sodium Iodide Symporter (MV-NIS)

Opyrchal, Mateusz; Allen, Cory; Iankov, Ianko; Aderca, Ileana; Schroeder, Mark A.; Sarkaria, Jann N.; Galanis, Evanthia

doi:10.1089/hum.2011.158

Cited by 49 publications

(45 citation statements)

References 30 publications

(36 reference statements)

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“…188 Re/ 131 I exhibit rapid uptake in U87-hNIS cells, and the dynamic uptake pattern of 188 Re/ 131 I was similar to that of previous studies (30,31). 188 Re uptake of U87-hNIS was up to 21.3-times that of the U87-0 control group, whereas 131 I uptake was up to 25.9-fold of that of the control group.…”

supporting

confidence: 87%

“…Radioisotopes exhibit the potential of a bystander effect, which may destroy tumor cells without hNIS expression by radionuclides emitted from surrounding hNIS expression tumor cells (29). The hNIS gene is not expressed in normal cells however is in glioma cells (30), this indicates that it may assist in improving the specificity of tumor therapy and decreasing the damage to normal brain tissue.…”

Section: Discussionmentioning

confidence: 99%

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Human sodium iodide transporter gene-mediated imaging and therapy of mouse glioma, comparison between 188Re and 131I

Guo

Zhang

et al. 2018

Oncol Lett

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supporting

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Human sodium iodide transporter gene-mediated imaging and therapy of mouse glioma, comparison between 188Re and 131I

Guo

Zhang

et al. 2018

Oncol Lett

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“…Possible explanations for this lack of synergy could be the inappropriate dosage of 131 I administration (2 mCi in this study). The glioblastoma 38 and prostate cancer study 39 both used 1 mCi of 131 I, whereas the pancreatic cancer study 40 used 3 mCi. Absence of synergy could also be the result of lack of a bystander effect from 131 I in certain tumor regions, particularly at the tumor periphery and in newly developing tumor nodules, which were not infected; and the possibility that KTC-3 cells are not sensitive to radiation at these dose levels.…”

Section: Treatment With Mv-nis Results In Ectopic Nis Expression In Vmentioning

confidence: 99%

Preclinical efficacy of the oncolytic measles virus expressing the sodium iodide symporter in iodine non-avid anaplastic thyroid cancer: a novel therapeutic agent allowing noninvasive imaging and radioiodine therapy

et al. 2012

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Anaplastic thyroid cancer is an extremely aggressive disease resistant to radioiodine treatment because of loss of sodium iodide symporter (NIS) expression. To enhance prognosis of this fatal cancer, we validated the preclinical efficacy of measles virus (MV)-NIS, the vaccine strain of the oncolytic MV (MV-Edm), modified to include the NIS gene. Western blotting analysis confirmed that a panel of eight anaplastic thyroid cancer (ATC)-derived cell lines do not express NIS protein, but do express CD46, the MV receptor. In vitro cell death assays and in vivo xenograft studies demonstrate the oncolytic efficacy of MV-NIS in BHT-101 and KTC-3, ATC-derived cell lines. Radioactive iodine uptake along with single-photon emission computed tomography (SPECT)-computed tomography imaging of KTC-3 xenografts after 99 Tc m administration confirmed NIS expression in vitro and in vivo, respectively, after virus treatment. Adjuvant administration of RAI, to MV-NIS-treated KTC-3 tumors showed a trend for increased tumor cell killing. As current treatment for ATC is only palliative, and MV-NIS is currently Food and Drug Administration approved for human clinical trials in myeloma, our data indicate that targeting ATC with MV-NIS could prove to be a novel therapeutic strategy for effective treatment of iodine-resistant ATC and will expedite its testing in clinical trials for this aggressive disease.

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“…A MV expressing the sodium iodide symporter (MV-NIS) has been constructed, which allows for in vivo monitoring of 99m Tc or 123 I uptake or in combination with 131 I for radiotherapy. 96 Oncolytic MV (MV-NIS) has been shown to infect, replicate, and kill human GSCs and prolong survival of GSC tumor bearing mice. 97 …”

Section: Measles Virusmentioning

confidence: 99%

“…MV-CEA MV Edmonston-B vaccine strain, CEA + Nude, i.c. GSC [97] MV-NIS MV Edmonston-B vaccine strain, NIS + Nude, s.c. U251 [96] Nude, i.c. primary GBM VSV ΔM51 VSV ΔM51…”

Section: Abbreviationsmentioning

confidence: 99%

Current Status of Gene Therapy for Brain Tumors∗

Ning

Rabkin

2015

Translating Gene Therapy to the Clinic

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Glioblastoma (GBM) is the most common and deadliest primary brain tumor in adults, with current treatments having limited impact on disease progression. Therefore the development of alternative treatment options is greatly needed. Gene therapy is a treatment strategy that relies on the delivery of genetic material, usually transgenes or viruses, into cells for therapeutic purposes, and has been applied to GBM with increasing promise. We have included selectively replicationcompetent oncolytic viruses within this strategy, although the virus acts directly as a complex biologic anti-tumor agent rather than as a classic gene delivery vehicle. GBM is a good candidate for gene therapy because tumors remain locally within the brain and only rarely metastasize to other tissues; the majority of cells in the brain are post-mitotic, which allows for specific targeting of dividing tumor cells; and tumors can often be accessed neurosurgically for administration of therapy. Delivery vehicles used for brain tumors include nonreplicating viral vectors, normal adult stem/progenitor cells, and oncolytic viruses. The therapeutic transgenes or viruses are typically cytotoxic or express prodrug activating suicide genes to kill glioma cells, immunostimulatory to induce or amplify anti-tumor immune responses, and/or modify the tumor microenvironment such as blocking angiogenesis. This review describes current preclinical and clinical gene therapy strategies for the treatment of glioma.Treating malignant gliomas, of which glioblastoma (GBM) is the most common and least curable, remains a daunting challenge even after substantial efforts to develop alternative therapies. The current standard of care is maximal surgical resection followed by radiation and temozolomide chemotherapy; however, the median survival still remains less than 15 months. 1,2 This poor survival is due to the aggressive and invasive nature of the tumor cells, resistance to treatment, and the challenges of delivering therapeutics into the brain. 3 GBM is thought to be derived from a small population of glioblastoma stem cells (GSCs), so-called because of their stem cell-like properties of self-renewal and multilineage differentiation while being highly tumorigenic. [4][5][6] GSCs have become an important model for studying GBM because their xenografts mimic the heterogeneous histopathology of the patient's tumor from which they were derived 7,8 and they remain genotypically similar to the patient's tumor, in contrast to serum-cultured cell lines. 9 These cells have provided insights into the origin of tumor-initiating cells and new targets for therapy. Other GBM animal models include established glioma cell lines (human and rodent) implanted intracranially into immunodeficient or immunocompetent animals, and genetically engineered mice that spontaneously develop brain tumors or are induced with viral vectors. 10 GENE DELIVERY VEHICLES FOR GLIOBLASTOMAMost gene therapies for GBM use biologic vectors such as viruses or cells. Replicationdefective or non-repli...

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Effective Radiovirotherapy for Malignant Gliomas by Using Oncolytic Measles Virus Strains Encoding the Sodium Iodide Symporter (MV-NIS)

Cited by 49 publications

References 30 publications

Human sodium iodide transporter gene-mediated imaging and therapy of mouse glioma, comparison between 188Re and 131I

Human sodium iodide transporter gene-mediated imaging and therapy of mouse glioma, comparison between 188Re and 131I

Preclinical efficacy of the oncolytic measles virus expressing the sodium iodide symporter in iodine non-avid anaplastic thyroid cancer: a novel therapeutic agent allowing noninvasive imaging and radioiodine therapy

Current Status of Gene Therapy for Brain Tumors∗

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