Targeting Melanoma with Cancer-Killing Viruses

Zhang, Tiantian; Suryawanshi, Yogesh R.; Woyczesczyk, Helene M.; Essani, Karim

doi:10.2174/1874357901711010028

Cited by 8 publications

(5 citation statements)

References 166 publications

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“…Results showed that in melanoma cells that carried V600D or V600E BRAF mutations there had been an increased apoptosis [ 42 ]. Also, the combination of reovirus and radiation has shown to increase the tumor growth delay of the melanoma xenografts in the treated animals, and significantly improve the overall survival rate compared to the treatment with either of the individual therapies [ 118 ]. Importantly, Ras mutation is one of the driver mutations for melanoma and is associated with radio-resistance [ 58 ].…”

Section: Combinatorial Approaches With Ovs In Melanoma Treatmentsmentioning

confidence: 99%

From Conventional Therapies to Immunotherapy: Melanoma Treatment in Review

Kuryk

Bertinato

Staniszewska

et al. 2020

Cancers

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In this review, we discuss the use of oncolytic viruses and checkpoint inhibitors in cancer immunotherapy in melanoma, with a particular focus on combinatory therapies. Oncolytic viruses are promising and novel anti-cancer agents, currently under investigation in many clinical trials both as monotherapy and in combination with other therapeutics. They have shown the ability to exhibit synergistic anticancer activity with checkpoint inhibitors, chemotherapy, radiotherapy. A coupling between oncolytic viruses and checkpoint inhibitors is a well-accepted strategy for future cancer therapies. However, eradicating advanced cancers and tailoring the immune response for complete tumor clearance is an ongoing problem. Despite current advances in cancer research, monotherapy has shown limited efficacy against solid tumors. Therefore, current improvements in virus targeting, genetic modification, enhanced immunogenicity, improved oncolytic properties and combination strategies have a potential to widen the applications of immuno-oncology (IO) in cancer treatment. Here, we summarize the strategy of combinatory therapy with an oncolytic vector to combat melanoma and highlight the need to optimize current practices and improve clinical outcomes.

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Section: Combinatorial Approaches With Ovs In Melanoma Treatmentsmentioning

confidence: 99%

From Conventional Therapies to Immunotherapy: Melanoma Treatment in Review

Kuryk

Bertinato

Staniszewska

et al. 2020

Cancers

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“…Furthermore, a novel oHSV Ld0-GFP (which was derived from the oncolytic ICP0-null HSV) targeting hepatocellular carcinoma (HCC) has recently been reported [12]. In 2016, the oHSV T-VEC has been approved for the treatment of melanoma [13,14].…”

Section: Ivyspringmentioning

confidence: 99%

Transcriptional Regulation of Latency-Associated Transcripts (LATs) of Herpes Simplex Viruses

Zhang

Xin

Zhang³

et al. 2020

J. Cancer

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Herpes simplex viruses (HSVs) cause cold sores and genital herpes and can establish lifelong latent infection in neurons. An engineered oncolytic HSV (oHSV) has recently been approved to treat tumors in clinics. HSV latency-associated transcripts (LATs) are associated with the latent infection, but LAT transcriptional regulation was seldom reported. For a better treatment of HSV infection and tumors, here we sequenced the LAT encoding DNA and LAT transcription regulatory region of our recently isolated new strain HSV-1-LXMW and did comparative analysis of the sequences together with those of other four HSV-1 and two HSV-2 strains. Phylogenetic analysis of LATs revealed that HSV-1-LXMW is evolutionarily close to HSV-1-17 from MRC University, Glasgow, UK. For the first time, Using a weight matrix-based program Match and multi-sequences alignment of the 6 HSV strains, we identified HSV LAT transcription regulatory sequences that bind to 9 transcription factors: AP-1, C-REL, Comp1, E2F, Hairy, HFH-3, Kr, TCF11/MAFG, v-Myb. Interestingly, these transcription regulatory sequences and factors are either conserved or unique among LATs of HSV-1 and HSV-2, suggesting they are potentially functional. Furthermore, literature analysis found that the transcription factors v-myb and AP-1 family member JunD are functional in regulating HSV gene transcription, including LAT transcription. For the first time, we discovered seven novel transcription factors and their corresponding transcription regulatory sequences of HSV LATs. Based on our findings and other reports, we proposed potential mechanisms of the initiation and maintenance of HSV latent infection. Our findings may have significant implication in our understanding of HSV latency and engineering of better oncolytic HSVs.

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“…Oncolytic virotherapy uses replication-competent viruses that can selectively replicate and kill cancer cells [ 11 , 12 , 13 , 14 , 15 , 16 ]. Oncolytic viruses (OVs) lead to cancer cell death through different mechanisms including apoptosis, pyroptosis, and necroptosis.…”

Section: Introductionmentioning

confidence: 99%

Oncolytic Viruses for Malignant Glioma: On the Verge of Success?

Suryawanshi

Schulze

2021

Viruses

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Glioblastoma is one of the most difficult tumor types to treat with conventional therapy options like tumor debulking and chemo- and radiotherapy. Immunotherapeutic agents like oncolytic viruses, immune checkpoint inhibitors, and chimeric antigen receptor T cells have revolutionized cancer therapy, but their success in glioblastoma remains limited and further optimization of immunotherapies is needed. Several oncolytic viruses have demonstrated the ability to infect tumors and trigger anti-tumor immune responses in malignant glioma patients. Leading the pack, oncolytic herpesvirus, first in its class, awaits an approval for treating malignant glioma from MHLW, the federal authority of Japan. Nevertheless, some major hurdles like the blood–brain barrier, the immunosuppressive tumor microenvironment, and tumor heterogeneity can engender suboptimal efficacy in malignant glioma. In this review, we discuss the current status of malignant glioma therapies with a focus on oncolytic viruses in clinical trials. Furthermore, we discuss the obstacles faced by oncolytic viruses in malignant glioma patients and strategies that are being used to overcome these limitations to (1) optimize delivery of oncolytic viruses beyond the blood–brain barrier; (2) trigger inflammatory immune responses in and around tumors; and (3) use multimodal therapies in combination to tackle tumor heterogeneity, with an end goal of optimizing the therapeutic outcome of oncolytic virotherapy.

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Targeting Melanoma with Cancer-Killing Viruses

Cited by 8 publications

References 166 publications

From Conventional Therapies to Immunotherapy: Melanoma Treatment in Review

From Conventional Therapies to Immunotherapy: Melanoma Treatment in Review

Transcriptional Regulation of Latency-Associated Transcripts (LATs) of Herpes Simplex Viruses

Oncolytic Viruses for Malignant Glioma: On the Verge of Success?

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