Jump to content

Oncolytic virus

From Wikipedia, the free encyclopedia
(Redirected from Oncolytic)

An oncolytic virus is a virus that preferentially infects and kills cancer cells. As the infected cancer cells are destroyed by oncolysis, they release new infectious virus particles or virions to help destroy the remaining tumour.[1][2] Oncolytic viruses are thought not only to cause direct destruction of the tumour cells, but also to stimulate host anti-tumour immune system responses.[3][4] Oncolytic viruses also have the ability to affect the tumor micro-environment in multiple ways.[5][6]

The potential of viruses as anti-cancer agents was first realised in the early twentieth century, although coordinated research efforts did not begin until the 1960s.[7] A number of viruses including adenovirus, reovirus, measles, herpes simplex, Newcastle disease virus, and vaccinia have been clinically tested as oncolytic agents.[8] Most current oncolytic viruses are engineered for tumour selectivity, although there are naturally occurring examples such as reovirus and the senecavirus,[9] resulting in clinical trials.[10]

The first oncolytic virus to be approved by a national regulatory agency was genetically unmodified ECHO-7 strain enterovirus RIGVIR, which was approved in Latvia in 2004 for the treatment of skin melanoma;[11] the approval was withdrawn in 2019. An oncolytic adenovirus, a genetically modified adenovirus named H101, was approved in China in 2005 for the treatment of head and neck cancer.[12] In 2015, talimogene laherparepvec (OncoVex, T-VEC), an oncolytic herpes virus which is a modified herpes simplex virus, became the first oncolytic virus to be approved for use in the United States and the European Union, for the treatment of advanced inoperable melanoma.[13]

On 16 December 2022, the Food and Drug Administration approved nadofaragene firadenovec-vncg (Adstiladrin, Ferring Pharmaceuticals) for adult patients with high-risk Bacillus Calmette-Guérin (BCG) unresponsive non-muscle invasive bladder cancer (NMIBC) with carcinoma in situ (CIS) with or without papillary tumors. [14]

History

[edit]

A connection between cancer regression and viruses has long been theorised, and case reports of regression noted in cervical cancer, Burkitt lymphoma, and Hodgkin lymphoma, after immunisation or infection with an unrelated virus appeared at the beginning of the 20th century.[15] Efforts to treat cancer through immunisation or virotherapy (deliberate infection with a virus), began in the mid-20th century.[15][16] As the technology to create a custom virus did not exist, all early efforts focused on finding natural oncolytic viruses. During the 1960s, promising research involved using poliovirus,[17] adenovirus,[15] Coxsackie virus,[18] ECHO enterovirus RIGVIR,[19] and others.[16] The early complications were occasional cases of uncontrolled infection (resulting in significant morbidity and mortality); an immune response would also frequently develop. While not directly harmful to the patient,[15] the response destroyed the virus thus preventing it from destroying the cancer.[17] Early efforts also found that only certain cancers could be treated through virotherapy.[18] Even when a response was seen, these responses were neither complete nor durable.[15] The field of virotherapy was nearly abandoned for a time, as the technology required to modify viruses didn't exist whereas chemotherapy and radiotherapy technology enjoyed early success. However, now that these technologies have been thoroughly developed and cancer remains a major cause of mortality, there is still a need for novel cancer therapies, garnering this once-sidelined therapy renewed interest.[15][20] In one case report published in 2024, a scientist Beata Halassy treated her own stage 3 breast cancer using an Edmonston-Zagreb measles vaccine strain (MeV) and then a vesicular stomatitis virus Indiana strain (VSV), both prepared in her own laboratory, in combination with trastuzumab. While the treatment was successful and self-experimentation has a long history in science, the decision to publish the case report attracted controversy due to the unapproved nature of the viral agents and treatment protocol used.[21][22]

Herpes simplex virus

[edit]
Main article: Oncolytic herpes virus

Herpes simplex virus (HSV) was one of the first viruses to be adapted to attack cancer cells selectively, because it was well understood, easy to manipulate and relatively harmless in its natural state (merely causing cold sores) so likely to pose fewer risks. The herpes simplex virus type 1 (HSV-1) mutant 1716 lacks both copies of the ICP34.5 gene, and as a result is no longer able to replicate in terminally differentiated and non-dividing cells but will infect and cause lysis very efficiently in cancer cells, and this has proved to be an effective tumour-targeting strategy.[23][24] In a wide range of in vivo cancer models, the HSV1716 virus has induced tumour regression and increased survival times.[25][26][27]

In 1996, the first approval was given in Europe for a clinical trial using the oncolytic virus HSV1716. From 1997 to 2003, strain HSV1716 was injected into tumours of patients with glioblastoma multiforme, a highly malignant brain tumour, with no evidence of toxicity or side effects, and some long-term survivors.[28][29][30] Other safety trials have used HSV1716 to treat patients with melanoma and squamous-cell carcinoma of head and neck.[31][32] Since then other studies have shown that the outer coating of HSV1716 variants can be targeted to specific types of cancer cells,[33] and can be used to deliver a variety of additional genes into cancer cells, such as genes to split a harmless prodrug inside cancer cells to release toxic chemotherapy,[34] or genes which command infected cancer cells to concentrate protein tagged with radioactive iodine, so that individual cancer cells are killed by micro-dose radiation as well as by virus-induced cell lysis.[35]

Other oncolytic viruses based on HSV have also been developed and are in clinical trials.[36] One that has been approved by the FDA for advanced melanoma is Amgen's talimogene laherparepvec.[37]

Oncorine (H101)

[edit]

The first oncolytic virus to be approved by a regulatory agency was a genetically modified adenovirus named H101 by Shanghai Sunway Biotech. It gained regulatory approval in 2005 from China's State Food and Drug Administration (SFDA) for the treatment of head and neck cancer.[12][38] Sunway's H101 and the very similar Onyx-15 (dl1520) have been engineered to remove a viral defense mechanism that interacts with a normal human gene p53, which is very frequently dysregulated in cancer cells.[38] Despite the promises of early in vivo lab work, these viruses do not specifically infect cancer cells, but they still kill cancer cells preferentially.[38] While overall survival rates are not known, short-term response rates are approximately doubled for H101 plus chemotherapy when compared to chemotherapy alone.[38] It appears to work best when injected directly into a tumour, and when any resulting fever is not suppressed.[38] Systemic therapy (such as through infusion through an intravenous line) is desirable for treating metastatic disease.[39] It is now marketed under the brand name Oncorine.[40]

Mechanisms of action

[edit]

Immunotherapy

[edit]

With advances in cancer immunotherapy such as immune checkpoint inhibitors, increased attention has been given to using oncolytic viruses to increase antitumor immunity.[41] There are two main considerations of the interaction between oncolytic viruses and the immune system.[citation needed]

Immunity as an obstacle

[edit]

A major obstacle to the success of oncolytic viruses is the patient immune system which naturally attempts to deactivate any virus. This can be a particular problem for intravenous injection, where the virus must first survive interactions with the blood complement and neutralising antibodies.[42] It has been shown that immunosuppression by chemotherapy and inhibition of the complement system can enhance oncolytic virus therapy.[43][44][45]

Pre-existing immunity can be partly avoided by using viruses that are not common human pathogens. However, this does not avoid subsequent antibody generation. Yet, some studies have shown that pre-immunity to oncolytic viruses doesn't cause a significant reduction in efficacy.[46]

Alternatively, the viral vector can be coated with a polymer such as polyethylene glycol, shielding it from antibodies, but this also prevents viral coat proteins adhering to host cells.[47]

Another way to help oncolytic viruses reach cancer growths after intravenous injection, is to hide them inside macrophages (a type of white blood cell). Macrophages automatically migrate to areas of tissue destruction, especially where oxygen levels are low, characteristic of cancer growths, and have been used successfully to deliver oncolytic viruses to prostate cancer in animals.[48]

Immunity as an ally

[edit]

Although it poses a hurdle by inactivating viruses, the patient's immune system can also act as an ally against tumors; infection attracts the attention of the immune system to the tumour and may help to generate useful and long-lasting antitumor immunity.[49][50] One important mechanism is the release of substances by tumor lysis, such as tumor-associated antigens and danger associated-molecular patterns (DAMPs), which can elicit an antitumor immune response.[51] This essentially produces a personalised cancer vaccine.

Many cases of spontaneous remission of cancer have been recorded. Though the cause is not fully understood, they are thought likely to be a result of a sudden immune response or infection.[52] Efforts to induce this phenomenon have used cancer vaccines (derived from cancer cells or selected cancer antigens), or direct treatment with immune-stimulating factors on skin cancers.[53] Some oncolytic viruses are very immunogenic and may by infection of the tumour, elicit an anti-tumor immune response, especially viruses delivering cytokines or other immune stimulating factors.[54][55]

Viruses selectively infect tumor cells because of their defective anti-viral response.[41] Imlygic, an attenuated herpes simplex virus, has been genetically engineered to replicate preferentially within tumor cells and to generate antigens that elicit an immune response.[41]

Oncolytic behaviour of wild-type viruses

[edit]

Vaccinia virus

[edit]

Vaccinia virus (VACV) is arguably the most successful live biotherapeutic agent because of its critical role in the eradication of smallpox, one of the most deadly diseases in human history. Long before the smallpox eradication campaign was launched, VACV was exploited as a therapeutic agent for the treatment of cancer. In 1922, Levaditi and Nicolau reported that VACV was able to inhibit the growth of various tumors in mice and rats. This was the first demonstration of viral oncolysis in the laboratory. This virus was subsequently shown to selectively infect and destroy tumor cells with great potency, while sparing normal cells, both in cell cultures and in animal models. Since vaccinia virus has long been recognized as an ideal backbone for vaccines due to its potent antigen presentation capability, this combines well with its natural oncolytic activities as an oncolytic virus for cancer immunotherapy.[56]

Vesicular stomatitis virus

[edit]

Vesicular stomatitis virus (VSV) is a rhabdovirus, consisting of 5 genes encoded by a negative sense, single-stranded RNA genome. In nature, VSV infects insects as well as livestock, where it causes a relatively localized and non-fatal illness. The low pathogenicity of this virus is due in large part to its sensitivity to interferons, a class of proteins that are released into the tissues and bloodstream during infection. These molecules activate genetic anti-viral defence programs that protect cells from infection and prevent spread of the virus. However, in 2000, Stojdl, Lichty et al.[57] demonstrated that defects in these pathways render cancer cells unresponsive to the protective effects of interferons and therefore highly sensitive to infection with VSV. Since VSV undergoes a rapid cytolytic replication cycle, infection leads to death of the malignant cell and roughly a 1000-fold amplification of virus within 24h. VSV is therefore highly suitable for therapeutic application, and several groups have gone on to show that systemically administered VSV can be delivered to a tumour site, where it replicates and induces disease regression, often leading to durable cures.[58][59][60][61] Attenuation of the virus by engineering a deletion of Met-51 of the matrix protein ablates virtually all infection of normal tissues, while replication in tumour cells is unaffected.[58]

Recent research has shown that this virus has the potential to cure brain tumours, thanks to its oncolytic properties.[62]

Poliovirus

[edit]
Main article: PVSRIPO

Poliovirus is a natural invasive neurotropic virus, making it the obvious choice for selective replication in tumours derived from neuronal cells. Poliovirus has a plus-strand RNA genome, the translation of which depends on a tissue-specific internal ribosome entry site (IRES) within the 5' untranslated region of the viral genome, which is active in cells of neuronal origin and allows translation of the viral genome without a 5' cap. Gromeier et al. (2000)[63] replaced the normal poliovirus IRES with a rhinovirus IRES, altering tissue specificity. The resulting PV1(RIPO) virus was able to selectively destroy malignant glioma cells, while leaving normal neuronal cells untouched.[64]

Reovirus

[edit]

Reoviruses generally infect mammalian respiratory and bowel systems (the name deriving from an acronym, respiratory enteric orphan virus). Most people have been exposed to reovirus by adulthood; however, the infection does not typically produce symptoms. The reovirus' oncolytic potential was established after they were discovered to reproduce well in various cancer cell lines, lysing these cells.[65]

Reolysin is a formulation of reovirus intended to treat various cancers currently undergoing clinical trials.[66]

Senecavirus

[edit]

Senecavirus, also known as Seneca Valley Virus, is a naturally occurring wild-type oncolytic picornavirus discovered in 2001 as a tissue culture contaminate at Genetic Therapy, Inc. The initial isolate, SVV-001, is being developed as an anti-cancer therapeutic by Neotropix, Inc. under the name NTX-010 for cancers with neuroendocrine features including small cell lung cancer and a variety of pediatric solid tumours.[citation needed]

RIGVIR

[edit]

RIGVIR is a drug that was approved by the State Agency of Medicines of the Republic of Latvia in 2004.[67] It was also approved in Georgia[68] and Armenia.[69] It is wild type ECHO-7, a member of echovirus group.[70] The potential use of echovirus as an oncolytic virus to treat cancer was discovered by Latvian scientist Aina Muceniece in the 1960s and 1970s.[70] The data used to register the drug in Latvia is not sufficient to obtain approval to use it in the US, Europe, or Japan.[70][71] As of 2017 there was no good evidence that RIGVIR is an effective cancer treatment.[72][73] On 19 March 2019, the manufacturer of ECHO-7, SIA LATIMA, announced the drug's removal from sale in Latvia, quoting financial and strategic reasons and insufficient profitability.[74] However, several days later an investigative TV show revealed that State Agency of Medicines had run laboratory tests on the vials, and found that the amount of ECHO-7 virus is of a much smaller amount than claimed by the manufacturer. According to agency's lab director, "It's like buying what you think is lemon juice, but finding that what you have is lemon-flavored water". In March 2019, the distribution of ECHO-7 in Latvia has been stopped.[75] Based on the request of some patients, medical institutions and physicians were allowed to continue use despite the suspension of the registration certificate.[76]

Semliki Forest virus

[edit]

Semliki Forest virus (SFV) is a virus that naturally infects cells of the central nervous system and causes encephalitis. A genetically engineered form has been pre-clinically tested as an oncolytic virus against the severe brain tumour type glioblastoma. The SFV was genetically modified with microRNA target sequences so that it only replicated in brain tumour cells and not in normal brain cells. The modified virus reduced tumour growth and prolonged survival of mice with brain tumours.[77] The modified virus was also found to efficiently kill human glioblastoma tumour cell lines.[77]

Other

[edit]

The maraba virus, first identified in Brazilian sandflies, is being tested clinically.[78]

Coxsackievirus A21 is being developed by Viralytics under trade name Cavatak.[79] Coxsackievirus A21 belongs to Enterovirus C species.[80]

Influenza A is one of the earliest viruses anecdotally reported to induce cancer regression.[81] This has prompted preclinical development of genetically engineered oncolytic influenza A viruses.[82] Murine Respirovirus, which is frequently called Sendai virus in scientific literature, has shown some oncolytic properties that are described in the section Murine respirovirus as an oncolytic agent.[citation needed]

Engineering oncolytic viruses

[edit]

Directed evolution

[edit]

An innovative approach of drug development termed "directed evolution" involves the creation of new viral variants or serotypes specifically directed against tumour cells via rounds of directed selection using large populations of randomly generated recombinant precursor viruses. The increased biodiversity produced by the initial homologous recombination step provides a large random pool of viral candidates which can then be passed through a series of selection steps designed to lead towards a pre-specified outcome (e.g. higher tumor specific activity) without requiring any previous knowledge of the resultant viral mechanisms that are responsible for that outcome. The pool of resultant oncolytic viruses can then be further screened in pre-clinical models to select an oncolytic virus with the desired therapeutic characteristics.[83]

Directed evolution was applied on human adenovirus, one of many viruses that are being developed as oncolytic agents, to create a highly selective and yet potent oncolytic vaccine. As a result of this process, ColoAd1 (a novel chimeric member of the group B adenoviruses) was generated. This hybrid of adenovirus serotypes Ad11p and Ad3 shows much higher potency and tumour selectivity than the control viruses (including Ad5, Ad11p and Ad3) and was confirmed to generate approximately two logs more viral progeny on freshly isolated human colon tumour tissue than on matching normal tissue.[83]

Attenuation

[edit]

Attenuation involves deleting viral genes, or gene regions, to eliminate viral functions that are expendable in tumour cells, but not in normal cells, thus making the virus safer and more tumour-specific. Cancer cells and virus-infected cells have similar alterations in their cell signalling pathways, particularly those that govern progression through the cell cycle.[84] A viral gene whose function is to alter a pathway is dispensable in cells where the pathway is defective, but not in cells where the pathway is active.[citation needed]

The enzymes thymidine kinase and ribonucleotide reductase in cells are responsible for DNA synthesis and are only expressed in cells which are actively replicating.[85] These enzymes also exist in the genomes of certain viruses (E.g. HSV, vaccinia) and allow viral replication in quiescent(non-replicating) cells,[86] so if they are inactivated by mutation the virus will only be able to replicate in proliferating cells, such as cancer cells.

Tumour targeting

[edit]

There are two main approaches for generating tumour selectivity: transductional and non-transductional targeting.[87]

  • Transductional targeting involves modifying the viral coat proteins to target tumour cells while reducing entry to non-tumour cells. This approach to tumour selectivity has mainly focused on adenoviruses and HSV-1, although it is entirely viable with other viruses.[87]
  • Non-transductional targeting involves altering the genome of the virus so it can only replicate in cancer cells, most frequently as part of the attenuation of the virus.[87]
    • Transcription targeting can also be used, where critical parts of the viral genome are placed under the control of a tumour-specific promoter. A suitable promoter should be active in the tumour but inactive in the majority of normal tissue, particularly the liver, which is the organ that is most exposed to blood born viruses. Many such promoters have been identified and studied for the treatment of a range of cancers.[87]
    • Similarly, viral replication can be finely tuned with the use of microRNAs (miRNA) artificial target sites or miRNA response elements (MREs). Differential expression of miRNAs between healthy tissues and tumors permit to engineer oncolytic viruses detargeted from certain tissues of interest while allowing its replication in the tumor cells.[citation needed]

Double targeting with both transductional and non-transductional targeting methods is more effective than any one form of targeting alone.[88]

Further information: Oncolytic adenovirus

Reporter genes

[edit]
Viral luciferase expression in a mouse tumour

Both in the laboratory and in the clinic it is useful to have a simple means of identifying cells infected by the experimental virus. This can be done by equipping the virus with "reporter genes" not normally present in viral genomes, which encode easily identifiable protein markers. One example of such proteins is GFP (green fluorescent protein) which, when present in infected cells, will cause a fluorescent green light to be emitted when stimulated by blue light.[89][90] An advantage of this method is that it can be used on live cells and in patients with superficial infected lesions, it enables rapid non-invasive confirmation of viral infection.[91] Another example of a visual marker useful in living cells is luciferase, an enzyme from the firefly which in the presence of luciferin, emits light detectable by specialized cameras.[89]

Vaccinia virus infected cells expressing beta-glucuronidase (blue colour)

The E. coli enzymes beta-glucuronidase and beta-galactosidase can also be encoded by some viruses. These enzymes, in the presence of certain substrates, can produce intense colored compounds useful for visualizing infected cells and also for quantifying gene expression.[citation needed]

Modifications to improve oncolytic activity

[edit]

Oncolytic viruses can be used against cancers in ways that are additional to lysis of infected cells.

Suicide genes

[edit]

Viruses can be used as vectors for delivery of suicide genes, encoding enzymes that can metabolise a separately administered non-toxic pro-drug into a potent cytotoxin, which can diffuse to and kill neighbouring cells. One herpes simplex virus, encoding a thymidine kinase suicide gene, has progressed to phase III clinical trials. The herpes simplex virus thymidine kinase phosphorylates the pro-drug, ganciclovir, which is then incorporated into DNA, blocking DNA synthesis.[92] The tumour selectivity of oncolytic viruses ensures that the suicide genes are only expressed in cancer cells, however a "bystander effect" on surrounding tumour cells has been described with several suicide gene systems.[93]

Suppression of angiogenesis

[edit]

Angiogenesis (blood vessel formation) is an essential part of the formation of large tumour masses. Angiogenesis can be inhibited by the expression of several genes, which can be delivered to cancer cells in viral vectors, resulting in suppression of angiogenesis, and oxygen starvation in the tumour. The infection of cells with viruses containing the genes for angiostatin and endostatin synthesis inhibited tumour growth in mice. Enhanced antitumour activities have been demonstrated in a recombinant vaccinia virus encoding anti-angiogenic therapeutic antibody and with an HSV1716 variant expressing an inhibitor of angiogenesis.[94][95]

Radioiodine

[edit]
Adenoviral NIS gene expression in a mouse tumour (Located at the crosshairs) following intravenous delivery of virus (Left) compared to an uninfected control mouse (Right)

Addition of the sodium-iodide symporter (NIS) gene to the viral genome causes infected tumour cells to express NIS and accumulate iodine. When combined with radioiodine therapy it allows local radiotherapy of the tumour, as used to treat thyroid cancer. The radioiodine can also be used to visualise viral replication within the body by the use of a gamma camera.[89] This approach has been used successfully preclinically with adenovirus, measles virus and vaccinia virus.[96][97][98]

Approved therapeutic agents

[edit]

Oncolytic viruses in conjunction with existing cancer therapies

[edit]

It is in conjunction with conventional cancer therapies that oncolytic viruses have often showed the most promise, since combined therapies operate synergistically with no apparent negative effects.[105]

Clinical trials

[edit]

Onyx-015 (dl1520) underwent trials in conjunction with chemotherapy before it was abandoned in the early 2000s. The combined treatment gave a greater response than either treatment alone, but the results were not entirely conclusive.[106] Vaccinia virus GL-ONC1 was studied in a trial combined with chemo- and radiotherapy as Standard of Care for patients newly diagnosed with head & neck cancer.[107] Herpes simplex virus, adenovirus, reovirus and murine leukemia virus are also undergoing clinical trials as a part of combination therapies.[108]

Pre-clinical research

[edit]

Chen et al. (2001)[109] used CV706, a prostate-specific adenovirus, in conjunction with radiotherapy on prostate cancer in mice. The combined treatment resulted in a synergistic increase in cell death, as well as a significant increase in viral burst size (the number of virus particles released from each cell lysis). No alteration in viral specificity was observed.[citation needed]

SEPREHVIR (HSV-1716) has also shown synergy in pre-clinical research when used in combination with several cancer chemotherapies.[110][111]

The anti-angiogenesis drug bevacizumab (anti-VEGF antibody) has been shown to reduce the inflammatory response to oncolytic HSV and improve virotherapy in mice.[112] A modified oncolytic vaccinia virus encoding a single-chain anti-VEGF antibody (mimicking bevacizumab) was shown to have significantly enhanced antitumor activities than parental virus in animal models.[113]

In fiction

[edit]

In science fiction, the concept of an oncolytic virus was first introduced to the public in Jack Williamson's novel Dragon's Island, published in 1951, although Williamson's imaginary virus was based on a bacteriophage rather than a mammalian virus.[114] Dragon's Island is also known for being the source of the term "genetic engineering".[115]

The plot of the Hollywood film I Am Legend is based on the premise that a worldwide epidemic was caused by a viral cure for cancer.[116]

See also

[edit]

References

[edit]
  1. ^ Ferguson MS, Lemoine NR, Wang Y (2012). "Systemic delivery of oncolytic viruses: hopes and hurdles". Advances in Virology. 2012: 1–14. doi:10.1155/2012/805629. PMC 3287020. PMID 22400027.
  2. ^ Casjens S (2010). "Oncolytic virus". In Mahy BW, Van Regenmortel MH (eds.). Desk Encyclopedia of General Virology. Boston: Academic Press. p. 167. ISBN 978-0-12-375146-1.
  3. ^ Melcher A, Parato K, Rooney CM, Bell JC (June 2011). "Thunder and lightning: immunotherapy and oncolytic viruses collide". Molecular Therapy. 19 (6): 1008–16. doi:10.1038/mt.2011.65. PMC 3129809. PMID 21505424.
  4. ^ Lichty BD, Breitbach CJ, Stojdl DF, Bell JC (August 2014). "Going viral with cancer immunotherapy". Nature Reviews. Cancer. 14 (8): 559–67. doi:10.1038/nrc3770. PMID 24990523. S2CID 15182671.
  5. ^ De Silva, Naomi; Atkins, Harold; Kirn, David H.; Bell, John C.; Breitbach, Caroline J. (1 April 2010). "Double trouble for tumours: Exploiting the tumour microenvironment to enhance anticancer effect of oncolytic viruses". Cytokine & Growth Factor Reviews. Recent Advances in the Development of Oncolytic Viruses as Cancer Therapeutics. 21 (2): 135–141. doi:10.1016/j.cytogfr.2010.02.007. ISSN 1359-6101. PMID 20338801.
  6. ^ "Using Viruses to Treat Cancer | Science-Based Medicine". sciencebasedmedicine.org. 28 September 2022. Retrieved 4 November 2022.
  7. ^ Alemany R (March 2013). "Viruses in cancer treatment". Clinical & Translational Oncology. 15 (3): 182–8. doi:10.1007/s12094-012-0951-7. PMID 23143950. S2CID 6123610.
  8. ^ Donnelly OG, Errington-Mais F, Prestwich R, Harrington K, Pandha H, Vile R, Melcher AA (July 2012). "Recent clinical experience with oncolytic viruses". Current Pharmaceutical Biotechnology. 13 (9): 1834–41. doi:10.2174/138920112800958904. PMID 21740364.
  9. ^ Roberts MS, Lorence RM, Groene WS, Bamat MK (August 2006). "Naturally oncolytic viruses". Current Opinion in Molecular Therapeutics. 8 (4): 314–21. PMID 16955694.
  10. ^ Rudin CM, Poirier JT, Senzer NN, Stephenson J, Loesch D, Burroughs KD, Reddy PS, Hann CL, Hallenbeck PL (February 2011). "Phase I clinical study of Seneca Valley Virus (SVV-001), a replication-competent picornavirus, in advanced solid tumors with neuroendocrine features". Clinical Cancer Research. 17 (4): 888–95. doi:10.1158/1078-0432.CCR-10-1706. PMC 5317273. PMID 21304001.
  11. ^ "Rigvir šķīdums injekcijām". Medicinal product register of the Republic of Latvia. 29 April 2004. Retrieved 8 December 2016.
  12. ^ a b Frew SE, Sammut SM, Shore AF, Ramjist JK, Al-Bader S, Rezaie R, Daar AS, Singer PA (January 2008). "Chinese health biotech and the billion-patient market". Nature Biotechnology. 26 (1): 37–53. doi:10.1038/nbt0108-37. PMC 7096943. PMID 18183014.
  13. ^ Broderick J (29 April 2015). "FDA Panels Support Approval of T-VEC in Melanoma". OncLive. Retrieved 24 August 2015.
  14. ^ Research, Center for Drug Evaluation and (29 December 2022). "FDA approves first adenoviral vector-based gene therapy for high-risk Bacillus Calmette-Guérin unresponsive non-muscle invasive bladder cancer". FDA.
  15. ^ a b c d e f Kuruppu D, Tanabe KK (May 2005). "Viral oncolysis by herpes simplex virus and other viruses". Cancer Biology & Therapy. 4 (5): 524–31. doi:10.4161/cbt.4.5.1820. PMID 15917655.
  16. ^ a b Voroshilova MK (1989). "Potential use of nonpathogenic enteroviruses for control of human disease". Progress in Medical Virology. Fortschritte der Medizinischen Virusforschung. Progrès en Virologie Médicale. 36: 191–202. PMID 2555836.
  17. ^ a b Pond AR, Manuelidis EE (August 1964). "Oncolytic Effect of Poliomyelitis Virus on Human Epidermoid Carcinoma (Hela Tumor) Heterologously Transplanted to Guinea Pigs". The American Journal of Pathology. 45 (2): 233–49. PMC 1907181. PMID 14202523.
  18. ^ a b Kunin CM (December 1964). "Cellular Susceptibility to Enteroviruses". Bacteriological Reviews. 28 (4): 382–90. doi:10.1128/MMBR.28.4.382-390.1964. PMC 441234. PMID 14244713.
  19. ^ Chumakov PM, Morozova VV, Babkin IV, Baĭkov IK, Netesov SV, Tikunova NV (2012). "[Oncolytic enteroviruses]". Molekuliarnaia Biologiia (in Russian). 46 (5): 712–25. doi:10.1134/s0026893312050032. PMID 23156670. S2CID 3716727.
  20. ^ Kelly E, Russell SJ (April 2007). "History of oncolytic viruses: genesis to genetic engineering". Molecular Therapy. 15 (4): 651–9. doi:10.1038/sj.mt.6300108. PMID 17299401.
  21. ^ Forcic D, et al. An Unconventional Case Study of Neoadjuvant Oncolytic Virotherapy for Recurrent Breast Cancer. Vaccines 2024; 12(9): 958. doi:10.3390/vaccines12090958
  22. ^ Corbyn Z. This scientist treated her own cancer with viruses she grew in the lab. Nature News 2024 doi:10.1038/d41586-024-03647-0
  23. ^ MacLean AR, ul-Fareed M, Robertson L, Harland J, Brown SM (March 1991). "Herpes simplex virus type 1 deletion variants 1714 and 1716 pinpoint neurovirulence-related sequences in Glasgow strain 17+ between immediate early gene 1 and the 'a' sequence". The Journal of General Virology. 72 ( Pt 3) (3): 631–9. doi:10.1099/0022-1317-72-3-631. PMID 1848598.
  24. ^ Brown SM, Harland J, MacLean AR, Podlech J, Clements JB (September 1994). "Cell type and cell state determine differential in vitro growth of non-neurovirulent ICP34.5-negative herpes simplex virus types 1 and 2". The Journal of General Virology. 75 ( Pt 9) (9): 2367–77. doi:10.1099/0022-1317-75-9-2367. PMID 8077935.
  25. ^ Kesari S, Randazzo BP, Valyi-Nagy T, Huang QS, Brown SM, MacLean AR, Lee VM, Trojanowski JQ, Fraser NW (November 1995). "Therapy of experimental human brain tumors using a neuroattenuated herpes simplex virus mutant". Laboratory Investigation; A Journal of Technical Methods and Pathology. 73 (5): 636–48. PMID 7474937.
  26. ^ McKie EA, MacLean AR, Lewis AD, Cruickshank G, Rampling R, Barnett SC, Kennedy PG, Brown SM (September 1996). "Selective in vitro replication of herpes simplex virus type 1 (HSV-1) ICP34.5 null mutants in primary human CNS tumours--evaluation of a potentially effective clinical therapy". British Journal of Cancer. 74 (5): 745–52. doi:10.1038/bjc.1996.431. PMC 2074706. PMID 8795577.
  27. ^ Randazzo BP, Bhat MG, Kesari S, Fraser NW, Brown SM (June 1997). "Treatment of experimental subcutaneous human melanoma with a replication-restricted herpes simplex virus mutant". The Journal of Investigative Dermatology. 108 (6): 933–7. doi:10.1111/1523-1747.ep12295238. PMID 9182825.
  28. ^ Rampling R, Cruickshank G, Papanastassiou V, Nicoll J, Hadley D, Brennan D, Petty R, MacLean A, Harland J, McKie E, Mabbs R, Brown M (May 2000). "Toxicity evaluation of replication-competent herpes simplex virus (ICP 34.5 null mutant 1716) in patients with recurrent malignant glioma". Gene Therapy. 7 (10): 859–66. doi:10.1038/sj.gt.3301184. PMID 10845724.
  29. ^ Papanastassiou V, Rampling R, Fraser M, Petty R, Hadley D, Nicoll J, Harland J, Mabbs R, Brown M (March 2002). "The potential for efficacy of the modified (ICP 34.5(-)) herpes simplex virus HSV1716 following intratumoural injection into human malignant glioma: a proof of principle study". Gene Therapy. 9 (6): 398–406. doi:10.1038/sj.gt.3301664. PMID 11960316.
  30. ^ Harrow S, Papanastassiou V, Harland J, Mabbs R, Petty R, Fraser M, Hadley D, Patterson J, Brown SM, Rampling R (November 2004). "HSV1716 injection into the brain adjacent to tumour following surgical resection of high-grade glioma: safety data and long-term survival". Gene Therapy. 11 (22): 1648–58. doi:10.1038/sj.gt.3302289. PMID 15334111.
  31. ^ MacKie RM, Stewart B, Brown SM (February 2001). "Intralesional injection of herpes simplex virus 1716 in metastatic melanoma". Lancet. 357 (9255): 525–6. doi:10.1016/S0140-6736(00)04048-4. PMID 11229673. S2CID 34442464.
  32. ^ Mace AT, Ganly I, Soutar DS, Brown SM (August 2008). "Potential for efficacy of the oncolytic Herpes simplex virus 1716 in patients with oral squamous cell carcinoma". Head & Neck. 30 (8): 1045–51. doi:10.1002/hed.20840. PMID 18615711. S2CID 43914133.
  33. ^ Conner J, Braidwood L, Brown SM (December 2008). "A strategy for systemic delivery of the oncolytic herpes virus HSV1716: redirected tropism by antibody-binding sites incorporated on the virion surface as a glycoprotein D fusion protein". Gene Therapy. 15 (24): 1579–92. doi:10.1038/gt.2008.121. PMID 18701918.
  34. ^ Braidwood L, Dunn PD, Hardy S, Evans TR, Brown SM (June 2009). "Antitumor activity of a selectively replication competent herpes simplex virus (HSV) with enzyme prodrug therapy". Anticancer Research. 29 (6): 2159–66. PMID 19528476.
  35. ^ Sorensen A, Mairs RJ, Braidwood L, Joyce C, Conner J, Pimlott S, Brown M, Boyd M (April 2012). "In vivo evaluation of a cancer therapy strategy combining HSV1716-mediated oncolysis with gene transfer and targeted radiotherapy". Journal of Nuclear Medicine. 53 (4): 647–54. doi:10.2967/jnumed.111.090886. PMID 22414636.
  36. ^ Turnbull S, West EJ, Scott KJ, Appleton E, Melcher A, Ralph C (December 2015). "Evidence for Oncolytic Virotherapy: Where Have We Got to and Where Are We Going?". Viruses. 7 (12): 6291–312. doi:10.3390/v7122938. PMC 4690862. PMID 26633468.
  37. ^ Conry RM, Westbrook B, McKee S, Norwood TG (February 2018). "Talimogene laherparepvec: First in class oncolytic virotherapy". Human Vaccines & Immunotherapeutics. 14 (4): 839–846. doi:10.1080/21645515.2017.1412896. PMC 5893211. PMID 29420123.
  38. ^ a b c d e Garber K (March 2006). "China approves world's first oncolytic virus therapy for cancer treatment". Journal of the National Cancer Institute. 98 (5): 298–300. doi:10.1093/jnci/djj111. PMID 16507823.
  39. ^ Ayllón Barbellido S, Campo Trapero J, Cano Sánchez J, Perea García MA, Escudero Castaño N, Bascones Martínez A (January 2008). "Gene therapy in the management of oral cancer: review of the literature" (PDF). Medicina Oral, Patologia Oral y Cirugia Bucal. 13 (1): E15–21. PMID 18167474.
  40. ^ Guo J, Xin H (November 2006). "Chinese gene therapy. Splicing out the West?". Science. 314 (5803): 1232–5. doi:10.1126/science.314.5803.1232. PMID 17124300. S2CID 142897522.
  41. ^ a b c Marin-Acevedo JA, Soyano AE, Dholaria B, Knutson KL, Lou Y (January 2018). "Cancer immunotherapy beyond immune checkpoint inhibitors". Journal of Hematology & Oncology. 11 (1): 8. doi:10.1186/s13045-017-0552-6. PMC 5767051. PMID 29329556.
  42. ^ Schmidt C (May 2013). "Awaiting a moment of truth for oncolytic viruses". Journal of the National Cancer Institute. 105 (10): 675–6. doi:10.1093/jnci/djt111. PMID 23650626.
  43. ^ Kottke T, Thompson J, Diaz RM, Pulido J, Willmon C, Coffey M, Selby P, Melcher A, Harrington K, Vile RG (January 2009). "Improved systemic delivery of oncolytic reovirus to established tumors using preconditioning with cyclophosphamide-mediated Treg modulation and interleukin-2". Clinical Cancer Research. 15 (2): 561–9. doi:10.1158/1078-0432.CCR-08-1688. PMC 3046733. PMID 19147761.
  44. ^ Lolkema MP, Arkenau HT, Harrington K, Roxburgh P, Morrison R, Roulstone V, Twigger K, Coffey M, Mettinger K, Gill G, Evans TR, de Bono JS (February 2011). "A phase I study of the combination of intravenous reovirus type 3 Dearing and gemcitabine in patients with advanced cancer". Clinical Cancer Research. 17 (3): 581–8. doi:10.1158/1078-0432.CCR-10-2159. PMID 21106728.
  45. ^ Magge D, Guo ZS, O'Malley ME, Francis L, Ravindranathan R, Bartlett DL (June 2013). "Inhibitors of C5 complement enhance vaccinia virus oncolysis". Cancer Gene Therapy. 20 (6): 342–50. doi:10.1038/cgt.2013.26. PMC 4060830. PMID 23661042.
  46. ^ Heo J, Reid T, Ruo L, Breitbach CJ, Rose S, Bloomston M, Cho M, Lim HY, Chung HC, Kim CW, Burke J, Lencioni R, Hickman T, Moon A, Lee YS, Kim MK, Daneshmand M, Dubois K, Longpre L, Ngo M, Rooney C, Bell JC, Rhee BG, Patt R, Hwang TH, Kirn DH (March 2013). "Randomized dose-finding clinical trial of oncolytic immunotherapeutic vaccinia JX-594 in liver cancer". Nature Medicine. 19 (3): 329–36. doi:10.1038/nm.3089. PMC 4268543. PMID 23396206.
  47. ^ Wonganan P, Croyle MA (February 2010). "PEGylated Adenoviruses: From Mice to Monkeys". Viruses. 2 (2): 468–502. doi:10.3390/v2020468. PMC 3185605. PMID 21994645.
  48. ^ Muthana, Munitta; Rodrigues, Samuel; Chen, Yung-Yi; Welford, Abigail; Hughes, Russell; Tazzyman, Simon; Essand, Magnus; Morrow, Fiona; Lewis, Claire E. (15 January 2013). "Macrophage delivery of an oncolytic virus abolishes tumor regrowth and metastasis after chemotherapy or irradiation". Cancer Research. 73 (2): 490–495. doi:10.1158/0008-5472.CAN-12-3056. ISSN 1538-7445. PMID 23172310.
  49. ^ Tong AW, Senzer N, Cerullo V, Templeton NS, Hemminki A, Nemunaitis J (July 2012). "Oncolytic viruses for induction of anti-tumor immunity". Current Pharmaceutical Biotechnology. 13 (9): 1750–60. doi:10.2174/138920112800958913. PMID 21740355.
  50. ^ Naik JD, Twelves CJ, Selby PJ, Vile RG, Chester JD (July 2011). "Immune recruitment and therapeutic synergy: keys to optimizing oncolytic viral therapy?". Clinical Cancer Research. 17 (13): 4214–24. doi:10.1158/1078-0432.CCR-10-2848. PMC 3131422. PMID 21576084.
  51. ^ Keller, Brian A.; Bell, John C. (1 September 2016). "Oncolytic viruses—immunotherapeutics on the rise". Journal of Molecular Medicine. 94 (9): 979–991. doi:10.1007/s00109-016-1453-9. ISSN 1432-1440. PMID 27492706. S2CID 253638074.
  52. ^ O'Regan B, Hirshberg C (1993). Spontaneous Remission: An Annotated Bibliography. Sausalito, California: Institute of Noetic Sciences. ISBN 978-0-943951-17-1. Archived from the original on 21 March 2015. Retrieved 31 March 2013.[page needed]
  53. ^ Lattime E (2013). Gene Therapy of Cancer: Translational Approaches from Preclinical Studies to Clinical Implementation. Academic Press. ISBN 978-0-12-394295-1.[page needed]
  54. ^ Mastrangelo MJ, Lattime EC (December 2002). "Virotherapy clinical trials for regional disease: in situ immune modulation using recombinant poxvirus vectors". Cancer Gene Therapy. 9 (12): 1013–21. doi:10.1038/sj.cgt.7700538. PMID 12522440.
  55. ^ Lundstrom K (2018). "New frontiers in oncolytic viruses: optimizing and selecting for virus strains with improved efficacy". Biologics: Targets and Therapy. 12: 43–60. doi:10.2147/BTT.S140114. PMC 5810530. PMID 29445265.
  56. ^ "Oncolytic Viruses in cancer therapy". Retrieved 11 April 2023.
  57. ^ Stojdl DF, Lichty B, Knowles S, Marius R, Atkins H, Sonenberg N, Bell JC (July 2000). "Exploiting tumor-specific defects in the interferon pathway with a previously unknown oncolytic virus". Nature Medicine. 6 (7): 821–5. doi:10.1038/77558. PMID 10888934. S2CID 8492631.
  58. ^ a b Stojdl DF, Lichty BD, tenOever BR, Paterson JM, Power AT, Knowles S, Marius R, Reynard J, Poliquin L, Atkins H, Brown EG, Durbin RK, Durbin JE, Hiscott J, Bell JC (October 2003). "VSV strains with defects in their ability to shutdown innate immunity are potent systemic anti-cancer agents". Cancer Cell. 4 (4): 263–75. doi:10.1016/S1535-6108(03)00241-1. PMID 14585354.
  59. ^ Ahmed M, Cramer SD, Lyles DS (December 2004). "Sensitivity of prostate tumors to wild type and M protein mutant vesicular stomatitis viruses". Virology. 330 (1): 34–49. doi:10.1016/j.virol.2004.08.039. PMID 15527832.
  60. ^ Ebert O, Harbaran S, Shinozaki K, Woo SL (April 2005). "Systemic therapy of experimental breast cancer metastases by mutant vesicular stomatitis virus in immune-competent mice". Cancer Gene Therapy. 12 (4): 350–8. doi:10.1038/sj.cgt.7700794. PMID 15565179.
  61. ^ Porosnicu M, Mian A, Barber GN (December 2003). "The oncolytic effect of recombinant vesicular stomatitis virus is enhanced by expression of the fusion cytosine deaminase/uracil phosphoribosyltransferase suicide gene". Cancer Research. 63 (23): 8366–76. PMID 14678998.
  62. ^ Bridle BW, Stephenson KB, Boudreau JE, Koshy S, Kazdhan N, Pullenayegum E, Brunellière J, Bramson JL, Lichty BD, Wan Y (August 2010). "Potentiating cancer immunotherapy using an oncolytic virus". Molecular Therapy. 18 (8): 1430–9. doi:10.1038/mt.2010.98. PMC 2927075. PMID 20551919.
  63. ^ Gromeier M, Lachmann S, Rosenfeld MR, Gutin PH, Wimmer E (June 2000). "Intergeneric poliovirus recombinants for the treatment of malignant glioma". Proceedings of the National Academy of Sciences of the United States of America. 97 (12): 6803–8. Bibcode:2000PNAS...97.6803G. doi:10.1073/pnas.97.12.6803. JSTOR 122718. PMC 18745. PMID 10841575.
  64. ^ Goetz C, Gromeier M (2010). "Preparing an oncolytic poliovirus recombinant for clinical application against glioblastoma multiforme". Cytokine & Growth Factor Reviews. 21 (2–3): 197–203. doi:10.1016/j.cytogfr.2010.02.005. PMC 2881183. PMID 20299272.
  65. ^ Lal R, Harris D, Postel-Vinay S, de Bono J (October 2009). "Reovirus: Rationale and clinical trial update". Current Opinion in Molecular Therapeutics. 11 (5): 532–9. PMID 19806501.
  66. ^ Thirukkumaran C, Morris DG (2009). "Oncolytic Viral Therapy Using Reovirus". Gene Therapy of Cancer. Methods in Molecular Biology. Vol. 542. pp. 607–34. doi:10.1007/978-1-59745-561-9_31. ISBN 978-1-934115-85-5. PMID 19565924.
  67. ^ "Latvijas Zāļu reģistrs". www.zva.gov.lv. Retrieved 17 December 2017.
  68. ^ "Georgia Today". Archived from the original on 28 March 2019. Retrieved 23 September 2015.
  69. ^ "Latvian Rigvir anti-cancer medicine registered in Armenia". The Baltic Course. 11 May 2016. Retrieved 3 January 2018.
  70. ^ a b c Babiker, HM; Riaz, IB; Husnain, M; Borad, MJ (2017). "Oncolytic virotherapy including Rigvir and standard therapies in malignant melanoma". Oncolytic Virotherapy. 6: 11–18. doi:10.2147/OV.S100072. PMC 5308590. PMID 28224120.
  71. ^ "Feasibility study for registration of medicine RIGVIR with the European Medicine Agency". European Commission. 8 January 2016. Archived from the original on 2 November 2016. Retrieved 2 November 2016. However, further use and commercialisation in the EU is prevented as EU regulations require cancer medicines to be registered centrally through the European Medicine Agency (EMA). National registrations are not considered.
  72. ^ Gorski D (18 September 2017). "Rigvir: Another unproven and dubious cancer therapy to be avoided". Science-Based Medicine.
  73. ^ Gorski, David (25 September 2017). "Ty Bollinger's "The Truth About Cancer" and the unethical marketing of the unproven cancer virotherapy Rigvir". Science-Based Medicine.
  74. ^ "Rigvir medication distribution in Latvia halted temporarily". 19 March 2019.
  75. ^ "Rigvir cancer treatment at center of fresh controversy". eng.lsm.lv.
  76. ^ "Apturēta Rigvir reģistrācija; informācija esošajiem pacientiem | Zāļu valsts aģentūra".
  77. ^ a b Ramachandran M, Yu D, Dyczynski M, Baskaran S, Zhang L, Lulla A, Lulla V, Saul S, Nelander S, Dimberg A, Merits A, Leja-Jarblad J, Essand M (March 2017). "Safe and Effective Treatment of Experimental Neuroblastoma and Glioblastoma Using Systemically Delivered Triple MicroRNA-Detargeted Oncolytic Semliki Forest Virus". Clinical Cancer Research. 23 (6): 1519–1530. doi:10.1158/1078-0432.CCR-16-0925. PMID 27637889.
  78. ^ Clinical trial number NCT02285816 for "MG1 Maraba/MAGE-A3, With and Without Adenovirus Vaccine, With Transgenic MAGE-A3 Insertion in Patients With Incurable MAGE-A3-Expressing Solid Tumours (I214)" at ClinicalTrials.gov
  79. ^ Annels, Nicola E; Mansfield, David; Arif, Mehreen; Ballesteros-Merino, Carmen; Simpson, Guy R; Denyer, Mick; Sandhu, Sarbjinder S; Melcher, Alan; Harrington, Kevin J; Davies, BronwYn; Au, Gough; Grose, Mark; Bagwan, Izhar N; Fox, Bernard A.; Vile, Richard G; Mostafid, Hugh; Shafren, Darren; Pandha, Hardev (2019). "Viral targeting of non-muscle invasive bladder cancer and priming of anti-tumour immunity following intravesical Coxsackievirus A21" (PDF). Clinical Cancer Research. 25 (19): 5818–5831. doi:10.1158/1078-0432.CCR-18-4022. ISSN 1078-0432. PMID 31273010.
  80. ^ Van Leer-Buter, Coretta C.; Poelman, Randy; Borger, Renze; Niesters, Hubert G. M.; Tang, Y.-W. (2016). "Newly Identified Enterovirus C Genotypes, Identified in the Netherlands through Routine Sequencing of All Enteroviruses Detected in Clinical Materials from 2008 to 2015". Journal of Clinical Microbiology. 54 (9): 2306–2314. doi:10.1128/JCM.00207-16. ISSN 0095-1137. PMC 5005491. PMID 27358467.
  81. ^ Dock, George. "The influence of complicating diseases upon leukaemia". The American Journal of the Medical Sciences (1827-1924); Philadelphia. 127 (4).
  82. ^ Kabiljo, Julijan; Laengle, Johannes; Bergmann, Michael (2020). "From threat to cure: understanding of virus-induced cell death leads to highly immunogenic oncolytic influenza viruses". Cell Death Discovery. 6: 48. doi:10.1038/s41420-020-0284-1. ISSN 2058-7716. PMC 7288254. PMID 32542113.
  83. ^ a b Kuhn I, Harden P, Bauzon M, Chartier C, Nye J, Thorne S, Reid T, Ni S, Lieber A, Fisher K, Seymour L, Rubanyi GM, Harkins RN, Hermiston TW (June 2008). "Directed evolution generates a novel oncolytic virus for the treatment of colon cancer". PLOS ONE. 3 (6): e2409. Bibcode:2008PLoSO...3.2409K. doi:10.1371/journal.pone.0002409. PMC 2423470. PMID 18560559.
  84. ^ Chow AY. "Cell Cycle Control by Oncogenes and Tumor Suppressors: Driving the Transformation of Normal Cells into Cancerous Cells". Nature Education. 3 (9): 7. Retrieved 5 April 2013.
  85. ^ "Thymidine kinase". Medical Dictionary. Merriam-Webster. Retrieved 5 April 2013.
  86. ^ Gentry GA (1992). "Viral thymidine kinases and their relatives". Pharmacology & Therapeutics. 54 (3): 319–55. doi:10.1016/0163-7258(92)90006-L. PMID 1334563.
  87. ^ a b c d Singh PK, Doley J, Kumar GR, Sahoo AP, Tiwari AK (October 2012). "Oncolytic viruses & their specific targeting to tumour cells". The Indian Journal of Medical Research. 136 (4): 571–84. PMC 3516024. PMID 23168697.
  88. ^ Davydova J, Le LP, Gavrikova T, Wang M, Krasnykh V, Yamamoto M (June 2004). "Infectivity-enhanced cyclooxygenase-2-based conditionally replicative adenoviruses for esophageal adenocarcinoma treatment". Cancer Research. 64 (12): 4319–27. doi:10.1158/0008-5472.CAN-04-0064. PMID 15205347.
  89. ^ a b c Haddad D, Chen CH, Carlin S, Silberhumer G, Chen NG, Zhang Q, Longo V, Carpenter SG, Mittra A, Carson J, Au J, Gonen M, Zanzonico PB, Szalay AA, Fong Y (2012). Gelovani JG (ed.). "Imaging characteristics, tissue distribution, and spread of a novel oncolytic vaccinia virus carrying the human sodium iodide symporter". PLOS ONE. 7 (8): e41647. Bibcode:2012PLoSO...741647H. doi:10.1371/journal.pone.0041647. PMC 3422353. PMID 22912675.
  90. ^ Poirier JT, Reddy PS, Idamakanti N, Li SS, Stump KL, Burroughs KD, Hallenbeck PL, Rudin CM (December 2012). "Characterization of a full-length infectious cDNA clone and a GFP reporter derivative of the oncolytic picornavirus SVV-001". The Journal of General Virology. 93 (Pt 12): 2606–13. doi:10.1099/vir.0.046011-0. PMID 22971818.
  91. ^ Yu YA, Shabahang S, Timiryasova TM, Zhang Q, Beltz R, Gentschev I, Goebel W, Szalay AA (March 2004). "Visualization of tumors and metastases in live animals with bacteria and vaccinia virus encoding light-emitting proteins". Nature Biotechnology. 22 (3): 313–20. doi:10.1038/nbt937. PMID 14990953. S2CID 1063835.
  92. ^ Freeman SM, Whartenby KA, Freeman JL, Abboud CN, Marrogi AJ (February 1996). "In situ use of suicide genes for cancer therapy". Seminars in Oncology. 23 (1): 31–45. PMID 8607030.
  93. ^ Duarte S, Carle G, Faneca H, de Lima MC, Pierrefite-Carle V (November 2012). "Suicide gene therapy in cancer: where do we stand now?". Cancer Letters. 324 (2): 160–70. doi:10.1016/j.canlet.2012.05.023. hdl:10316/24816. PMID 22634584.
  94. ^ Frentzen A, Yu YA, Chen N, Zhang Q, Weibel S, Raab V, Szalay AA (August 2009). "Anti-VEGF single-chain antibody GLAF-1 encoded by oncolytic vaccinia virus significantly enhances antitumor therapy". Proceedings of the National Academy of Sciences of the United States of America. 106 (31): 12915–20. Bibcode:2009PNAS..10612915F. doi:10.1073/pnas.0900660106. JSTOR 40484625. PMC 2722284. PMID 19617539.
  95. ^ Conner J, Braidwood L (July 2012). "Expression of inhibitor of growth 4 by HSV1716 improves oncolytic potency and enhances efficacy". Cancer Gene Therapy. 19 (7): 499–507. doi:10.1038/cgt.2012.24. PMID 22595793.
  96. ^ Grünwald GK, Klutz K, Willhauck MJ, Schwenk N, Senekowitsch-Schmidtke R, Schwaiger M, Zach C, Göke B, Holm PS, Spitzweg C (June 2013). "Sodium iodide symporter (NIS)-mediated radiovirotherapy of hepatocellular cancer using a conditionally replicating adenovirus". Gene Therapy. 20 (6): 625–33. doi:10.1038/gt.2012.79. PMID 23038026.
  97. ^ Penheiter AR, Wegman TR, Classic KL, Dingli D, Bender CE, Russell SJ, Carlson SK (August 2010). "Sodium iodide symporter (NIS)-mediated radiovirotherapy for pancreatic cancer". AJR. American Journal of Roentgenology. 195 (2): 341–9. doi:10.2214/AJR.09.3672. PMC 3117397. PMID 20651188.
  98. ^ Li H, Peng KW, Dingli D, Kratzke RA, Russell SJ (August 2010). "Oncolytic measles viruses encoding interferon beta and the thyroidal sodium iodide symporter gene for mesothelioma virotherapy". Cancer Gene Therapy. 17 (8): 550–8. doi:10.1038/cgt.2010.10. PMC 2907639. PMID 20379224.
  99. ^ Clinical trial number NCT00769704 for "Efficacy and Safety Study of OncoVEXGM-CSF Compared to GM-CSF in Melanoma" at ClinicalTrials.gov
  100. ^ "FDA approves Amgen's Injected Immunotherapy for Melanoma". Reuters. 27 October 2015.
  101. ^ Sheridan C (June 2015). "First oncolytic virus edges towards approval in surprise vote". Nature Biotechnology. 33 (6): 569–70. doi:10.1038/nbt0615-569. PMID 26057953. S2CID 205268968.
  102. ^ "Amgen, Form 8-K, Current Report, Filing Date Jan 26, 2012" (PDF). secdatabase.com. Retrieved 8 January 2013.
  103. ^ Clinical trial number NCT01161498 for "Study of Safety and Efficacy of OncoVEXGM-CSF With Cisplatin for Treatment of Locally Advanced Head and Neck Cancer" at ClinicalTrials.gov
  104. ^ "Delytact scores a first with Japanese approval for malignant glioma". www.thepharmaletter.com. Retrieved 21 December 2022.
  105. ^ Ottolino-Perry K, Diallo JS, Lichty BD, Bell JC, McCart JA (February 2010). "Intelligent design: combination therapy with oncolytic viruses". Molecular Therapy. 18 (2): 251–63. doi:10.1038/mt.2009.283. PMC 2839289. PMID 20029399.
  106. ^ Khuri FR, Nemunaitis J, Ganly I, Arseneau J, Tannock IF, Romel L, Gore M, Ironside J, MacDougall RH, Heise C, Randlev B, Gillenwater AM, Bruso P, Kaye SB, Hong WK, Kirn DH (August 2000). "a controlled trial of intratumoral ONYX-015, a selectively-replicating adenovirus, in combination with cisplatin and 5-fluorouracil in patients with recurrent head and neck cancer". Nature Medicine. 6 (8): 879–85. doi:10.1038/78638. PMID 10932224. S2CID 3199209.
  107. ^ Mell LK, Brumund KT, Daniels GA, Advani SJ, Zakeri K, Wright ME, Onyeama SJ, Weisman RA, Sanghvi PR, Martin PJ, Szalay AA (October 2017). "Phase I Trial of Intravenous Oncolytic Vaccinia Virus (GL-ONC1) with Cisplatin and Radiotherapy in Patients with Locoregionally Advanced Head and Neck Carcinoma" (PDF). Clinical Cancer Research. 23 (19): 5696–5702. doi:10.1158/1078-0432.CCR-16-3232. PMID 28679776. S2CID 30604400.
  108. ^ Suryawanshi YR, Zhang T, Essani K (March 2017). "Oncolytic viruses: emerging options for the treatment of breast cancer". Medical Oncology. 34 (3): 43. doi:10.1007/s12032-017-0899-0. PMID 28185165. S2CID 44562857.
  109. ^ Chen Y, DeWeese T, Dilley J, Zhang Y, Li Y, Ramesh N, Lee J, Pennathur-Das R, Radzyminski J, Wypych J, Brignetti D, Scott S, Stephens J, Karpf DB, Henderson DR, Yu DC (July 2001). "CV706, a prostate cancer-specific adenovirus variant, in combination with radiotherapy produces synergistic antitumor efficacy without increasing toxicity". Cancer Research. 61 (14): 5453–60. PMID 11454691.
  110. ^ Mace AT, Harrow SJ, Ganly I, Brown SM (August 2007). "Cytotoxic effects of the oncolytic herpes simplex virus HSV1716 alone and in combination with cisplatin in head and neck squamous cell carcinoma". Acta Oto-Laryngologica. 127 (8): 880–7. doi:10.1080/00016480601075381. PMID 17763002. S2CID 44252457.
  111. ^ Toyoizumi T, Mick R, Abbas AE, Kang EH, Kaiser LR, Molnar-Kimber KL (December 1999). "Combined therapy with chemotherapeutic agents and herpes simplex virus type 1 ICP34.5 mutant (HSV-1716) in human non-small cell lung cancer". Human Gene Therapy. 10 (18): 3013–29. doi:10.1089/10430349950016410. PMID 10609661. S2CID 20072243.
  112. ^ Currier MA, Eshun FK, Sholl A, Chernoguz A, Crawford K, Divanovic S, Boon L, Goins WF, Frischer JS, Collins MH, Leddon JL, Baird WH, Haseley A, Streby KA, Wang PY, Hendrickson BW, Brekken RA, Kaur B, Hildeman D, Cripe TP (May 2013). "VEGF blockade enables oncolytic cancer virotherapy in part by modulating intratumoral myeloid cells". Molecular Therapy. 21 (5): 1014–23. doi:10.1038/mt.2013.39. PMC 3666636. PMID 23481323.
  113. ^ Frentzen A, Yu YA, Chen N, Zhang Q, Weibel S, Raab V, Szalay AA (August 2009). "Anti-VEGF single-chain antibody GLAF-1 encoded by oncolytic vaccinia virus significantly enhances antitumor therapy". Proceedings of the National Academy of Sciences of the United States of America. 106 (31): 12915–20. Bibcode:2009PNAS..10612915F. doi:10.1073/pnas.0900660106. PMC 2722284. PMID 19617539.
  114. ^ Williamson J (2002). Dragon's Island and other stories. Waterville, Me.: Five Star. ISBN 978-0-7862-4314-3.[page needed]
  115. ^ Stableford BM (2004). Historical dictionary of science fiction literature. Scarecrow Press. p. 133. ISBN 978-0-8108-4938-9.
  116. ^ Dalhousie University (9 May 2008). "A Real-life 'I Am Legend?' Researcher Champions Development Of 'Reovirus' As Potential Treatment For Cancer". Science Daily.

Further reading

[edit]
Scholia has a profile for oncolytic virus (Q1560099).
Retrieved from "https://wiki.riteme.site/w/index.php?title=Oncolytic_virus&oldid=1257883153"