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DOI 10.34014/2227-1848-2021-4-32-44

NEW POTENTIAL TREATMENT FOR BRAIN GLIOMA

A.A. Gorbunov, T.M. Shipitsyna, E.B. Pilipenko-Koshel'

V.I. Vernadsky Crimean Federal University, Simferopol, Russia

 

According to the latest statistics, brain gliomas are the most common cause of death from CNS tumors. Brain gliomas are also ranked as the second (after stroke) cause of brain surgery The mortality rate from gliomas is high and sometimes reaches 80 %. It is because the tumor grows from undifferentiated cells, which causes its peracute development and malignant transformation. Symptoms of glioma occur at stages 3 and 4, when all treatment is symptomatic, and operations are palliative. In this regard, it is necessary to develop and introduce methods for non-surgical glioma treatment. These methods include the use of antisense oligonucleotides, optogenetics, and oncolytic viruses.

The aim of antisense oligonucleotides is to replace a section in a glioma cell genome with a foreign one, which disrupts cell division and leads to apoptosis and necrosis of the entire tumor. Optogenetics excludes the introduction of substances into the body. It provides a certain light signal to glioma cells, which also suppresses the growth of an undifferentiated tumor. Oncolytic viruses are genetically modified viruses that identify tumor cells, penetrate into them and start a cascade of apoptotic reactions Despite all success, such methods are still studied at the laboratory level, their implementation in practical medicine is slow and cautious. However, insufficient knowledge retards the widespread use of potentially promising and effective drugs. Scientists around the world are developing methods to treat brain gliomas at different stages of their development. This article reflects modern achievements of scientists and neurosurgeons, describing new methods for brain glioma treatment.

Key words: brain glioma, optogenetics, antisense oligonucleotides, oncolytic viruses, p53 gene.

Conflict of interest. The authors declare no conflict of interest.

 

References

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  34. Naumann U., Bähr O., Wolburg H., Altenberend S., Wick W., Liston P. Adenoviral expression of XIAP antisense RNA induces apoptosis in glioma cells and suppresses the growth of xenografts in nude mice. Gene Ther. 2017; 14: 147–161.

  35. Deisseroth K. Optogenetics. Nat. Methods. 2017; 8: 26–29.

  36. Nagel G., Ollig D., Fuhrmann M., Kateriya S., Musti A.M., Bamberg E., Hegemann P. Channelrhodopsin-1: a light-gated proton channel in green algae. Science. 2020; 296: 2395–2398.

  37. Naso M.F., Tomkowicz B., Perry W.L., Strohl W.R. Adeno-associated virus (AAV) as a vector for gene therapy. Bio. Drugs. 2017; 31: 317–334.

  38. Bentley J.N., Chestek C., Stacey W.C., Patil P.G. Optogenetics in epilepsy. Neurosurg. Focus. 2013; 34: E4.

  39. Bruno Camporeze, Bruno Alcântara Manica. Optogenetics: the new molecular approach to control functions of neural cells in epilepsy, depression and tumors of the central nervous system. Am. J. Cancer. Res. 2018; 8 (10): 1900–1918.

  40. Marcus H.J., Carpenter K.L.H., Price S.J., Hutchinson P.J. In vivo assessment of high-grade glioma biochemistry using microdialysis: a study of energy-related molecules, growth factors and cytokines. J. Neuro-Oncol. 2016; 97: 11–23.

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  45. Gunaydin L.A., Yizhar O., Berndt A., Sohal V.S., Deisseroth K., Hegemann P. Ultrafast optogenetic control. Nat. Neurosci. 2016; 13: 387–392.

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Received October 11, 2021; accepted November 14, 2021.

 

Information about the authors

Gorbunov Aleksandr Andreevich, 5th-year Student, Medical Academy named after S.I. Georgievsky, V.I. Vernadsky Crimean Federal University. 295051, Russia, Simferopol, Lenin Ave., 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0002-2886-6178

Shipitsyna Tat'yana Mikhaylovna, 6th-year Student, Medical Academy named after S.I. Georgievsky, V.I. Vernadsky Crimean Federal University. 295051, Russia, Simferopol, Lenin Ave., 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0003-1480-466X

Pilipenko-Koshel' Ekaterina Borisovna, Teaching Assistant, Chair of Nervous Diseases and Neurosurgery, Medical Academy named after S.I. Georgievsky, V.I. Vernadsky Crimean Federal University. 295051, Russia, Simferopol, Lenin Ave., 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0002-6027-4682

 

For citation

Gorbunov A.A., Shipitsyna T.M., Pilipenko-Koshel' E.B. Novye potentsial'nye metody lecheniya gliom golovnogo mozga [New potential treatment for brain glioma]. Ul'yanovskiy mediko-biologicheskiy zhurnal. 2021; 4: 32–44. DOI: 10.34014/2227-1848-2021-4-32-44 (in Russian).

 

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УДК 616.8-006+616.8-085.2/.3

DOI 10.34014/2227-1848-2021-4-32-44

 

НОВЫЕ ПОТЕНЦИАЛЬНЫЕ МЕТОДЫ ЛЕЧЕНИЯ ГЛИОМ ГОЛОВНОГО МОЗГА

А.А. Горбунов, Т.М. Шипицына, Е.Б. Пилипенко-Кошель

ФГАОУ ВО «Крымский федеральный университет им. В.И. Вернадского», г. Симферополь, Россия

 

Согласно последним данным статистики, глиомы мозга являются наиболее частой причиной смертей от онкологии центральной нервной системы, а также занимают второе место по частоте как причина хирургических вмешательств на головной мозг, уступая инсультам. Смертность от глиом высока и порой достигает 80 %. Причина этого заключается в том, что опухоль растет из недифференцированных клеток, что обусловливает её молниеносный рост и быстрое озлокачествление. Симптомы глиомы возникают на 3–4 стадии развития, когда все лечение направлено на ликвидацию симптомов, а операции носят паллиативный характер. В связи с этим необходима разработка и внедрение методов по нехирургическому лечению глиом. Такими методами являются использование антисмысловых олигонуклеотидов, оптогенетика, применение онколитических вирусов.

Суть использования антисмысловых олигонуклеотидов заключается в замене участка генома клетки глиомы на инородный, попавший извне, что нарушает деление клеток и приводит к апоптозу и некрозу всей опухоли. Оптогенетика исключает введение веществ в организм и заключается в подаче определенного светового сигнала на глиозные клетки, что также тормозит рост недифференцированной опухоли. Онколитические вирусы – это генномодифицированные вирусы, которые определяют опухолевые клетки, проникают в них и запускают каскад апоптотических реакций.

Несмотря на все успехи, данные методы продолжают изучаться на уровне лабораторий, их внедрение в практическую медицину происходит медленно и со страхом. Однако недостаточная изученность тормозит широкое применение потенциально перспективных и эффективных лекарств. Учеными мира разрабатываются методы, позволяющие лечить глиомы мозга на разных стадиях их развития. Данная статья отображает современные достижения ученых и нейрохирургов в поисках возможности применения такого рода методов.

Ключевые слова: глиома мозга, оптогенетика, антисмысловые олигонуклеотиды, онколитические вирусы, ген р53.

 

Литература

  1. Gibson E.M., Purger D., Mount C.W. Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. Science. 2014; 344 (6183): 1252304.

  2. Monje M., Mitra S.S., Freret M.E. Hedgehog-responsive candidate cell of origin for diffuse intrinsic pontine glioma. Proc. Natl. Acad. Sci. USA. 2019; 108 (11): 4453–4458.

  3. Venkatesh H.S., Johung T.B., Caretti V. Neuronal activity promotes glioma growth through neuroligin-3 secretion. Cell. 2015; 161 (4): 803–816.

  4. Liu C., Sage J.C., Miller M.R. Mosaic analysis with double markers reveals tumor cell of origin in glioma. Cell. 2017; 146 (2): 209–221.

  5. Arenkiel B.R., Peca J., Davison I.G. In vivo light-induced activation of neural circuitry in transgenic mice expressing channelrhodopsin-2. Neuron. 2017; 54 (2): 205–218.

  6. Mariella G. Filbin, Rosalind A. Segal. How neuronal activity regulates glioma cell proliferation. Neuro-Oncology. 2015; 17 (12). DOI: 10.1093/neuonc/nov188.

  7. Fujiwara T., Grimm E.A., Mukhopadhyay T., Zhang W.W., Owen-Schaub L.B., Roth J.A. Induction of chemosensitivity in human lung cancer cells in vivo by adenovirus-mediated transfer of the wild-type p53 gene. Cancer Res. 2018; 54: 2287–2291.

  8. Bullock A.N., Fersht A.R. Rescuing the function of mutant p53. Nat. Rev. Cancer. 2018; 1: 68–76.

  9. Kamal Datta, Preeti Shah. Sensitizing glioma cells to cisplatin by abrogating the p53 response with antisense oligonucleotides. Cancer Gene Therapy. 2016; 11: 525–531. DOI: 10.1038/sj.cgt.7700724.

  10. Venkatesh H.S. Neuronal Activity Promotes Glioma Growth through Neuroligin-3 Secretion. Cell. 2015; 161 (4).

  11. Andreansky S., He B., van Cott J., McGhee J., Markert J.M., Gillespie G.Y. Treatment of intracranial gliomas in immunocompetent mice using herpes simplex viruses that express murine interleukins. Gen. Ther. 2017; 5: 121–130.

  12. Wang Y., Yang J., Zheng H. Expression of mutant p53 proteins implicates a lineage relationship between neural stem cells and malignant astrocytic glioma in a murine model. Cancer Cell. 2019; 15 (6): 514–526.

  13. Gerardo Caruso, Maria Caffo. Antisense Oligonucleotides in the Treatment of Cerebral Gliomas. Review of Concerning Patents. Recent Patents on CNS Drug Discovery. 2017; 9: 2–12.

  14. Pirollo K.F., Raita A., Sleerb L.S., Chang E.H. Antisense therapeutics: from theory to clinical practice. Pharmacol. Ther. 2018; 99: 55–77.

  15. Tamm I. Antisense therapy in malignant disease: status quo and quo vadis? Clin. Sci. 2016; 110: 427–442.

  16. Venkatesh H.S. Neuronal activity promotes glioma growth on mouse with ChR2. Cell. 2015; 161 (4): 803–816.

  17. Dean N.M., Bennett F.C. Antisense oligonucleotide-based therapeutics for cancer. Oncogene. 2019; 22: 9087–9096.

  18. Caruso G., Caffo M., Alafaci C., Raudino G., Salpietro F.M., Tomasello F. Antisense oligonucleotides as an innovative therapeutic strategy in the treatment of high-grade gliomas. Recent Pat. CNS Drug Discov. 2019; 5: 53–69.

  19. Amantana A., Iversen P.L. Phamacokinetics and biodistribution of phosphorodiamidate morpholino antisense oligomers. Curr. Opin-Pharmacol. 2015; 5: 550–555.

  20. Landen C.N. Jr., Chavez-Reyes A., Bucana C., Schmandt R., Deavers M.T., Lopez-Berestein G. Therapeutic EphA2 gene targeting in vivo using neutral liposomal small interfering RNA delivery. Cancer Res. 2015; 65: 6910–6918.

  21. Akinc A., Zumbuehl A., Goldberg M., Leshchiner E.S., Busini V., Hossain N. A combinatorial library of lipid-like materials for delivery of RNAi therapeutics. Nat. Biotechnol. 2018; 26: 561–569.

  22. Ito T.K., Ishii G., Chiba H., Ochiai A. The VEGF angiogenic switch of fibroblasts is regulated by MMP-7 from cancer cells. Oncogene. 2017; 26: 7194–7203.

  23. Kang C., Yuan X., Li F., Pu P., Yu S., Shen C. Evaluation of folate-PAMAM for the delivery of antisense oligonucleotides to rat C6 glioma cells in vitro and in vivo. J. Biomed. Mater. Res. 2017; 93: 585–594.

  24. Lin Z.X., Yang L.J., Huang Q., Lin J.H., Ren J., Chen Z.B. Inhibition of tumor-induced edema by antisense VEGF is mediated by suppressive vesiculo-vacuolar organelles (VVO) formation. Cancer Sci. 2018; 99: 2540–2546.

  25. Yang L., Lin Z., Huang Q., Lin J., Chen Z., Zhou L. Effect of vascular endothelial growth factor on remodeling of C6 glioma tissue in vivo. J. Neurooncol. 2018; 103: 33–41.

  26. Tian X.X., Zhang Y.G., Du J., Zheng J. Effect of antisense epidermal growth factor receptor cDNA transfection on telomerase activity of glioblastomas cells. Beijing Da Xue Xue Bao. 2015; 37: 314–319.

  27. Deidda G., Allegra M., Cerri C., Naskar S., Bony G., Zunino G. Early depolarizing GABA controls critical-period plasticity in the rat visual cortex. Nat. Neurosc. 2017: 564. DOI: https://doi.org/ 10.1038/nn.3890.

  28. Chu S., Yuan X., Li Z., Jiang P., Zhang J. C-Met antisense oligodeoxynucleotide inhibits growth of glioma cells. Surg. Neurol. 2016; 65: 533–538.

  29. Halatsch M.E., Schmidt U., Behnke-Mursch J., Unterberg A., Rainer Wirtz C. Epidermal growth factor receptor inhibition for the treatment of glioblastoma multiforme and other malignant brain tumors. Cancer Treat. Rev. 2016; 32: 74–89.

  30. Morrison R.S. Suppression of basic fibroblast growth factor expression by antisense oligodeoxynucleotides inhibits the growth of transformed human astrocytes. J. Biol. Chem. 2017; 266: 728–734.

  31. Kamps D., Dehmelt L. De-blurring signal network dynamics. Chem. Biol. 2017; 4: 1–12.

  32. Nagel G., Ollig D., Fuhrmann M., Kateriya S., Musti A.M., Bamberg E., Hegemann P. Channelrhodopsin-1: a light-gated proton channel in green algae. Science. 2020; 296: 2395–2398.

  33. Feldbauer K., Zimmermann D., Pintschovius V., Spitz J., Bamann C., Bamberg E. Channelrhodopsin-2 is a leaky proton pump. PNAS. 2019; 106: 12317–12322.

  34. Naumann U., Bähr O., Wolburg H., Altenberend S., Wick W., Liston P. Adenoviral expression of XIAP antisense RNA induces apoptosis in glioma cells and suppresses the growth of xenografts in nude mice. Gene Ther. 2017; 14: 147–161.

  35. Deisseroth K. Optogenetics. Nat. Methods. 2017; 8: 26–29.

  36. Nagel G., Ollig D., Fuhrmann M., Kateriya S., Musti A.M., Bamberg E., Hegemann P. Channelrhodopsin-1: a light-gated proton channel in green algae. Science. 2020; 296: 2395–2398.

  37. Naso M.F., Tomkowicz B., Perry W.L., Strohl W.R. Adeno-associated virus (AAV) as a vector for gene therapy. Bio. Drugs. 2017; 31: 317–334.

  38. Bentley J.N., Chestek C., Stacey W.C., Patil P.G. Optogenetics in epilepsy. Neurosurg. Focus. 2013; 34: E4.

  39. Bruno Camporeze, Bruno Alcântara Manica. Optogenetics: the new molecular approach to control functions of neural cells in epilepsy, depression and tumors of the central nervous system. Am. J. Cancer. Res. 2018; 8 (10): 1900–1918.

  40. Marcus H.J., Carpenter K.L.H., Price S.J., Hutchinson P.J. In vivo assessment of high-grade glioma biochemistry using microdialysis: a study of energy-related molecules, growth factors and cytokines. J. Neuro-Oncol. 2016; 97: 11–23.

  41. Rzeski W., Turski L., Ikonomidou C. Glutamate antagonists limit tumor growth. PNAS. 2019; 98: 6372–6377.

  42. Spalletti C., Alia C., Lai S., Panarese A., Conti S., Micera S. Combining robotic training and inactivation of the healthy hemisphere restores pre-stroke motor patterns in mice. Elife. 2018; 6: 1–31. DOI: https://doi.org/10.7554/eLife.28662.

  43. Matsuno A., Nagashima T., Katayama H., Tamura A. In vitro and in vivo delivery of antisense oligodeoxynucleotides using lipofection: application of antisense technique to growth suppression of experimental glioma. In: Phillips M.I., ed. Antisense techniques: methods in enzymology. Vol. 313. Orlando: Academic Press; 2018: 359–372.

  44. Akira Matsuno. Tadashi Nagashima Specific gene suppression using antisense strategy for growth suppression of glioma. Med. Electron. Microsc. 2017; 37: 158–161.

  45. Gunaydin L.A., Yizhar O., Berndt A., Sohal V.S., Deisseroth K., Hegemann P. Ultrafast optogenetic control. Nat. Neurosci. 2016; 13: 387–392.

  46. Coen D.M., Kosz-Vnenchak M., Jacobson J.G., Leib D.A., Bogard C.L., Schaffer P.A. Thymidine kinase-negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate. Proc. Natl. Acad. Sci. USA. 2018; 86: 4736–4740.

  47. Jiang H., Clise-Dwyer K., Ruisaard K.E., Fan X., Tian W., Gumin J. Delta-24-RGD oncolytic adenovirus elicits anti-glioma immunity in an immunocompetent mouse model. PLoS ONE. 2014; 9: e97407.

  48. Yamaguchi F., Morrison R.S., Takahashi H., Teramoto A. Anti-telomerase therapy suppressed glioma proliferation. Oncol. Rep. 2019; 6: 773–776.

  49. Dias N., Stein C.A. Antisense oligonucleotides: Basic concept and mechanisms. Mol. Cancer Ther. 2019; 1: 347–355.

  50. Ko D., Hawkins L., Yu D.C. Development of transcriptionally regulated oncolytic adenoviruses. Oncogene. 2015; 24: 7763–7774.

  51. Caffo M., Caruso G., Barresi V., Pino M.A., Venza M., Alataci C. Immunohistochemical study of CD68 and CR3/43 in astrocytic gliomas. J. Analyt. Oncol. 2019; 1: 42–49.

Поступила в редакцию 11.10.2021; принята 14.11.2021.

 

Авторский коллектив

Горбунов Александр Андреевич – студент 5 курса Медицинской академии им. С.И. Георгиевского, ФГАОУ ВО «Крымский федеральный университет им. В.И. Вернадского». 295051, Россия, г. Симферополь, бул. Ленина, 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0002-2886-6178

Шипицына Татьяна Михайловна – студентка 6 курса Медицинской академии им. С.И. Георгиевского, ФГАОУ ВО «Крымский федеральный университет им. В.И. Вернадского». 295051, Россия, г. Симферополь, бул. Ленина, 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0003-1480-466Х

Пилипенко-Кошель Екатерина Борисовна – ассистент кафедры нервных болезней и нейрохирургии Медицинской академии им. С.И. Георгиевского, ФГАОУ ВО «Крымский федеральный университет им. В.И. Вернадского». 295051, Россия, г. Симферополь, бул. Ленина, 5/7; e-mail: Этот адрес электронной почты защищён от спам-ботов. У вас должен быть включен JavaScript для просмотра., ORCID ID: https://orcid.org/0000-0002-6027-4682

 

Образец цитирования

Горбунов А.А., Шипицына Т.М., Пилипенко-Кошель Е.Б. Новые потенциальные методы лечения глиом головного мозга. Ульяновский медико-биологический журнал. 2021; 4: 32–44. DOI: 10.34014/2227-1848-2021-4-32-44.