CoChat
Sign Up
Cited by 271

The DOI matches its Crossref record; 54 of the 54 references it cites were found in a registry or an index.

Glioblastoma Therapy: Past, Present and Future

Obrador, Elena, Moreno-Murciano, Paz, Oriol-Caballo, María, López-Blanch, Rafael, Pineda, Begoña, Gutiérrez-Arroyo, Julia, Loras, Alba, Gonzalez-Bonet, Luis, Martinez-Cadenas, Conrado, Estrela, José, Marqués-Torrejón, María·2024·International Journal of Molecular Sciences
DOI 10.3390/ijms25052529PMC PMC10931797
Open this paper in CoChat — free account

Abstract

Glioblastoma (GB) stands out as the most prevalent and lethal form of brain cancer. Although great efforts have been made by clinicians and researchers, no significant improvement in survival has been achieved since the Stupp protocol became the standard of care (SOC) in 2005. Despite multimodality treatments, recurrence is almost universal with survival rates under 2 years after diagnosis. Here, we discuss the recent progress in our understanding of GB pathophysiology, in particular, the importance of glioma stem cells (GSCs), the tumor microenvironment conditions, and epigenetic mechanisms involved in GB growth, aggressiveness and recurrence. The discussion on therapeutic strategies first covers the SOC treatment and targeted therapies that have been shown to interfere with different signaling pathways (pRB/CDK4/RB1/P16ink4, TP53/MDM2/P14arf, PI3k/Akt-PTEN, RAS/RAF/MEK, PARP) involved in GB tumorigenesis, pathophysiology, and treatment resistance acquisition. Below, we analyze several immunotherapeutic approaches (i.e., checkpoint inhibitors, vaccines, CAR-modified NK or T cells, oncolytic virotherapy) that have been used in an attempt to enhance the immune response against GB, and thereby avoid recidivism or increase survival of GB patients. Finally, we present treatment attempts made using nanotherapies (nanometric structures having active anti-GB agents such as antibodies, chemotherapeutic/anti-angiogenic drugs or sensitizers, radionuclides, and molecules that target GB cellular receptors or open the blood–brain barrier) and non-ionizing energies (laser interstitial thermal therapy, high/low intensity focused ultrasounds, photodynamic/sonodynamic therapies and electroporation). The aim of this review is to discuss the advances and limitations of the current therapies and to present novel approaches that are under development or following clinical trials.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3390/ijms25052529

Cites

54 of 54 references verified0 citation errors · 0 not checkable

Statistics

Figures

Figure 1 WHO diagnostic criteria for glioblastoma.
Figure 1 WHO diagnostic criteria for glioblastoma.CC BY · PubMed Central
Figure 2 Origin of glioblastoma. During normal embryonic development and in the adult brain, neural stem cells (NSCs) generate glial and neuronal cells. Glioma stem cells (GSCs) arise from NSCs, astrocytes, oligodendrocytes, or glial precursor cells through the activation of oncogenic pathways (inactivation of TP53, NF1 or PTEN). GSCs are described as slow-dividing or quiescent cells, with multilineage differentiation capacity that allows them to differentiate into GB cells and cells with astrocytic, neuronal, and endothelial features and even trans-differentiation abilities. In GB tumors, there exists a dynamic equilibrium between quiescent and proliferative GSCs, and between GSC populations and their lineage-committed counterparts (differentiated non-GSC) that can also dedifferentiate into stem-lineage GSCs. Created with BioRender.com, accessed on 24 January 2024.
Figure 2 Origin of glioblastoma. During normal embryonic development and in the adult brain, neural stem cells (NSCs) generate glial and neuronal cells. Glioma stem cells (GSCs) arise from NSCs, astrocytes, oligodendrocytes, or glial precursor cells through the activation of oncogenic pathways (inactivation of TP53, NF1 or PTEN). GSCs are described as slow-dividing or quiescent cells, with multilineage differentiation capacity that allows them to differentiate into GB cells and cells with astrocytic, neuronal, and endothelial features and even trans-differentiation abilities. In GB tumors, there exists a dynamic equilibrium between quiescent and proliferative GSCs, and between GSC populations and their lineage-committed counterparts (differentiated non-GSC) that can also dedifferentiate into stem-lineage GSCs. Created with BioRender.com, accessed on 24 January 2024.CC BY · PubMed Central
Figure 3 PTEN/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK axis, and list of related chemotherapeutics clinically assayed against glioblastoma. Created with BioRender.com.
Figure 3 PTEN/PI3K/Akt/mTOR and RAS/RAF/MEK/ERK axis, and list of related chemotherapeutics clinically assayed against glioblastoma. Created with BioRender.com.CC BY · PubMed Central
Figure 4 Viruses modified to infect only GB cells or to specifically induce cancer cell elimination can be delivered either directly into brain tumors or intravenously. Created with BioRender.com. Accessed on 15 January 2024.
Figure 4 Viruses modified to infect only GB cells or to specifically induce cancer cell elimination can be delivered either directly into brain tumors or intravenously. Created with BioRender.com. Accessed on 15 January 2024.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 54 references

Research works printed but not linked: 1055

  1. Berger, 2022, World Health Organization 2021 Classification of Central Nervous System Tumors and Implications for Therapy for Adult-Type Gliomas: A Review, JAMA Oncol., 8, 1493, 10.1001/jamaoncol.2022.2844 · DOI
  2. Kurokawa, 2022, Major Changes in 2021 World Health Organization Classification of Central Nervous System Tumors, RadioGraphics, 42, 1474, 10.1148/rg.210236 · DOI
  3. Torp, 2022, The WHO 2021 Classification of Central Nervous System Tumours: A Practical Update on What Neurosurgeons Need to Know—A Minireview, Acta Neurochir, 164, 2453, 10.1007/s00701-022-05301-y · DOI · Paper page
  4. Thomas, 2023, 2021 Updates to the World Health Organization Classification of Adult-Type and Pediatric-Type Diffuse Gliomas: A Clinical Practice Review, Chin. Clin. Oncol., 12, 7, 10.21037/cco-22-120 · DOI
  5. Singer, 2021, The Impact of the Molecular Classification of Glioblastoma on the Interpretation of Therapeutic Clinical Trial Results, Chin. Clin. Oncol., 10, 38, 10.21037/cco-21-33 · DOI
  6. Vehlow, 2013, Invasion as Target for Therapy of Glioblastoma Multiforme, Biochim. Biophys. Acta (BBA) Rev. Cancer, 1836, 236, 10.1016/j.bbcan.2013.07.001 · DOI
  7. Davis, 2016, Glioblastoma: Overview of Disease and Treatment, Clin. J. Oncol. Nurs., 20, S2-8, 10.1188/16.CJON.S1.2-8 · DOI
  8. Cantrell, 2019, Progress Toward Long-Term Survivors of Glioblastoma, Mayo Clin. Proc., 94, 1278, 10.1016/j.mayocp.2018.11.031 · DOI
  9. Thakkar, 2014, Epidemiologic and Molecular Prognostic Review of Glioblastoma, Cancer Epidemiol. Biomark. Prev., 23, 1985, 10.1158/1055-9965.EPI-14-0275 · DOI
  10. Aldoghachi, 2022, Recent Advances in the Therapeutic Strategies of Glioblastoma Multiforme, Neuroscience, 491, 240, 10.1016/j.neuroscience.2022.03.030 · DOI
  11. Stupp, 2017, Effect of Tumor-Treating Fields Plus Maintenance Temozolomide vs Maintenance Temozolomide Alone on Survival in Patients With Glioblastoma: A Randomized Clinical Trial, JAMA, 318, 2306, 10.1001/jama.2017.18718 · DOI · Paper page
  12. 2021, Extent of Resection and Survival in Patients with Glioblastoma Multiforme: Systematic Review and Meta-Analysis, Medicine, 100, e26432, 10.1097/MD.0000000000026432 · DOI
  13. Ostrom, 2022, CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2015–2019, Neuro Oncol., 24, v1, 10.1093/neuonc/noac202 · DOI
  14. Perrin, 2019, Glioblastoma Heterogeneity and the Tumour Microenvironment: Implications for Preclinical Research and Development of New Treatments, Biochem. Soc. Trans., 47, 625, 10.1042/BST20180444 · DOI
  15. 2018, Sequencing the next Generation of Glioblastomas, Crit. Rev. Clin. Lab. Sci., 55, 264, 10.1080/10408363.2018.1462759 · DOI
  16. Kim, 2015, Whole-Genome and Multisector Exome Sequencing of Primary and Post-Treatment Glioblastoma Reveals Patterns of Tumor Evolution, Genome Res., 25, 316, 10.1101/gr.180612.114 · DOI · Paper page
  17. Wang, 2017, Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment, Cancer Cell, 32, 42, 10.1016/j.ccell.2017.06.003 · DOI
  18. Becker, A.P., Sells, B.E., Haque, S.J., and Chakravarti, A. (2021). Tumor Heterogeneity in Glioblastomas: From Light Microscopy to Molecular Pathology. Cancers, 13. · DOI
  19. Wu, 2021, Glioblastoma Multiforme (GBM): An Overview of Current Therapies and Mechanisms of Resistance, Pharmacol. Res., 171, 105780, 10.1016/j.phrs.2021.105780 · DOI
  20. Ahmed, 2023, Unveiling the Enigma of the Blood–Brain Barrier in Glioblastoma: Current Advances from Preclinical and Clinical Studies, Curr. Opin. Oncol., 35, 522, 10.1097/CCO.0000000000000990 · DOI
  21. Stiles, 2008, Glioma Stem Cells: A Midterm Exam, Neuron, 58, 832, 10.1016/j.neuron.2008.05.031 · DOI
  22. Safa, 2015, Glioblastoma Stem Cells (GSCs) Epigenetic Plasticity and Interconversion between Differentiated Non-GSCs and GSCs, Genes Dis., 2, 152, 10.1016/j.gendis.2015.02.001 · DOI
  23. Xie, 2022, Quiescent Human Glioblastoma Cancer Stem Cells Drive Tumor Initiation, Expansion, and Recurrence Following Chemotherapy, Dev. Cell, 57, 32, 10.1016/j.devcel.2021.12.007 · DOI
  24. Hu, 2023, The Evolution of Tumor Microenvironment in Gliomas and Its Implication for Target Therapy, Int. J. Biol. Sci., 19, 4311, 10.7150/ijbs.83531 · DOI
  25. Franceschi, 2022, Glioblastoma Microenvironment: From an Inviolable Defense to a Therapeutic Chance, Front. Oncol., 12, 852950, 10.3389/fonc.2022.852950 · DOI
  26. Schaff, 2023, Glioblastoma and Other Primary Brain Malignancies in Adults: A Review, JAMA, 329, 574, 10.1001/jama.2023.0023 · DOI
  27. Furnari, 2007, Malignant Astrocytic Glioma: Genetics, Biology, and Paths to Treatment, Genes Dev., 21, 2683, 10.1101/gad.1596707 · DOI · Paper page
  28. Atkins, 2015, Repair Mechanisms Help Glioblastoma Resist Treatment, J. Clin. Neurosci., 22, 14, 10.1016/j.jocn.2014.09.003 · DOI
  29. Yalamarty, S.S.K., Filipczak, N., Li, X., Subhan, M.A., Parveen, F., Ataide, J.A., Rajmalani, B.A., and Torchilin, V.P. (2023). Mechanisms of Resistance and Current Treatment Options for Glioblastoma Multiforme (GBM). Cancers, 15. · DOI
  30. Eckerdt, F., and Platanias, L.C. (2023). Emerging Role of Glioma Stem Cells in Mechanisms of Therapy Resistance. Cancers, 15. · DOI
  31. Bao, 2006, Glioma Stem Cells Promote Radioresistance by Preferential Activation of the DNA Damage Response, Nature, 444, 756, 10.1038/nature05236 · DOI
  32. Steponaitis, G., and Tamasauskas, A. (2021). Mesenchymal and Proneural Subtypes of Glioblastoma Disclose Branching Based on GSC Associated Signature. Int. J. Mol. Sci., 22. · DOI
  33. Fayzullin, 2019, Phenotypic and Expressional Heterogeneity in the Invasive Glioma Cells, Transl. Oncol., 12, 122, 10.1016/j.tranon.2018.09.014 · DOI
  34. Seliger, C., Meyer, A.-L., Leidgens, V., Rauer, L., Moeckel, S., Jachnik, B., Proske, J., Dettmer, K., Rothhammer-Hampl, T., and Kaulen, L.D. (2022). Metabolic Heterogeneity of Brain Tumor Cells of Proneural and Mesenchymal Origin. Int. J. Mol. Sci., 23. · DOI
  35. Khettab, 2023, On the Origin and Development of Glioblastoma: Multifaceted Role of Perivascular Mesenchymal Stromal Cells, Acta Neuropathol. Commun., 11, 104, 10.1186/s40478-023-01605-x · DOI
  36. Teo, 2019, Relevance of a TCGA-Derived Glioblastoma Subtype Gene-Classifier among Patient Populations, Sci. Rep., 9, 7442, 10.1038/s41598-019-43173-y · DOI
  37. Uribe, D., Niechi, I., Rackov, G., Erices, J.I., San Martín, R., and Quezada, C. (2022). Adapt to Persist: Glioblastoma Microenvironment and Epigenetic Regulation on Cell Plasticity. Biology, 11. · DOI
  38. Lee, 2018, Comparison of Glioblastoma (GBM) Molecular Classification Methods, Semin. Cancer Biol., 53, 201, 10.1016/j.semcancer.2018.07.006 · DOI
  39. Wang, 2020, Cell Lineage-Based Stratification for Glioblastoma, Cancer Cell, 38, 366, 10.1016/j.ccell.2020.06.003 · DOI
  40. Ofek, 2021, Proteogenomics of Glioblastoma Associates Molecular Patterns with Survival, Cell Rep., 34, 108787, 10.1016/j.celrep.2021.108787 · DOI
  41. Steponaitis, G., Kucinskas, V., Golubickaite, I., Skauminas, K., and Saudargiene, A. (2022). Glioblastoma Molecular Classification Tool Based on mRNA Analysis: From Wet-Lab to Subtype. Int. J. Mol. Sci., 23. · DOI
  42. Grech, 2020, Rising Incidence of Glioblastoma Multiforme in a Well-Defined Population, Cureus, 12, e8195
  43. Tan, 2020, Management of Glioblastoma: State of the Art and Future Directions, CA A Cancer J. Clin., 70, 299, 10.3322/caac.21613 · DOI
  44. Carrano, A., Juarez, J.J., Incontri, D., Ibarra, A., and Cazares, H.G. (2021). Sex-Specific Differences in Glioblastoma. Cells, 10. · DOI
  45. Verma, M. (2009). Cancer Epidemiology: Modifiable Factors, Humana Press. Methods in Molecular Biology. · DOI
  46. Lopes, 2022, Ionizing Radiation Exposure during Adulthood and Risk of Developing Central Nervous System Tumors: Systematic Review and Meta-Analysis, Sci. Rep., 12, 16209, 10.1038/s41598-022-20462-7 · DOI
  47. Dadey, 2023, Risk of Developing Glioblastoma Following Non-CNS Primary Cancer: A SEER Analysis between 2000 and 2018, J. Neurooncol., 164, 655, 10.1007/s11060-023-04460-x · DOI
  48. Ostrom, Q.T., Patil, N., Cioffi, G., Waite, K., Kruchko, C., and Barnholtz-Sloan, J.S. (2020). Corrigendum to: CBTRUS Statistical Report: Primary Brain and Other Central Nervous System Tumors Diagnosed in the United States in 2013-2017. Neuro Oncol., noaa269. · DOI
  49. Wick, 2016, Evaluation of Pseudoprogression Rates and Tumor Progression Patterns in a Phase III Trial of Bevacizumab plus Radiotherapy/Temozolomide for Newly Diagnosed Glioblastoma, Neuro Oncol., 18, 1434, 10.1093/neuonc/now091 · DOI
  50. Okada, 2015, Immunotherapy Response Assessment in Neuro-Oncology (iRANO): A Report of the RANO Working Group, Lancet Oncol., 16, e534, 10.1016/S1470-2045(15)00088-1 · DOI
  51. Leao, 2020, Response Assessment in Neuro-Oncology Criteria for Gliomas: Practical Approach Using Conventional and Advanced Techniques, AJNR Am. J. Neuroradiol., 41, 10, 10.3174/ajnr.A6358 · DOI
  52. Hooper, G.W., Ansari, S., Johnson, J.M., and Ginat, D.T. (2023). Advances in the Radiological Evaluation of and Theranostics for Glioblastoma. Cancers, 15. · DOI
  53. Soni, N., Ora, M., Jena, A., Rana, P., Mangla, R., Ellika, S., Almast, J., Puri, S., and Meyers, S.P. (2023). Amino Acid Tracer PET MRI in Glioma Management: What a Neuroradiologist Needs to Know. Am. J. Neuroradiol. · DOI
  54. Reeves, 2022, 18F-FMISO PET Imaging Identifies Hypoxia and Immunosuppressive Tumor Microenvironments and Guides Targeted Evofosfamide Therapy in Tumors Refractory to PD-1 and CTLA-4 Inhibition, Clin. Cancer Res., 28, 327, 10.1158/1078-0432.CCR-21-2394 · DOI
  55. Ma, 2009, Adult Neural Stem Cells in the Mammalian Central Nervous System, Cell Res., 19, 672, 10.1038/cr.2009.56 · DOI
  56. Lee, 2018, Human Glioblastoma Arises from Subventricular Zone Cells with Low-Level Driver Mutations, Nature, 560, 243, 10.1038/s41586-018-0389-3 · DOI · Paper page
  57. Altmann, C., Keller, S., and Schmidt, M.H.H. (2019). The Role of SVZ Stem Cells in Glioblastoma. Cancers, 11. · DOI
  58. Kwan, 2019, Tracing the Origin of Glioblastoma: Subventricular Zone Neural Stem Cells, Neurosurgery, 84, E15, 10.1093/neuros/nyy512 · DOI
  59. Hira, 2021, Immunohistochemical Detection of Neural Stem Cells and Glioblastoma Stem Cells in the Subventricular Zone of Glioblastoma Patients, J. Histochem. Cytochem., 69, 349, 10.1369/0022155421994679 · DOI
  60. Beiriger, 2022, The Subventricular Zone in Glioblastoma: Genesis, Maintenance, and Modeling, Front. Oncol., 12, 790976, 10.3389/fonc.2022.790976 · DOI
  61. Loras, A., Gonzalez-Bonet, L.G., Gutierrez-Arroyo, J.L., Martinez-Cadenas, C., and Marques-Torrejon, M.A. (2023). Neural Stem Cells as Potential Glioblastoma Cells of Origin. Life, 13. · DOI
  62. Matarredona, 2019, Neural Stem Cells of the Subventricular Zone as the Origin of Human Glioblastoma Stem Cells. Therapeutic Implications, Front. Oncol., 9, 779, 10.3389/fonc.2019.00779 · DOI
  63. Yamaki, 2020, Relationships between Recurrence Patterns and Subventricular Zone Involvement or CD133 Expression in Glioblastoma, J. Neurooncol., 146, 489, 10.1007/s11060-019-03381-y · DOI
  64. Brockman, 2021, Histological Studies of the Ventricular-Subventricular Zone as Neural Stem Cell and Glioma Stem Cell Niche, J. Histochem. Cytochem., 69, 819, 10.1369/00221554211032003 · DOI
  65. Mistry, 2017, Influence of Glioblastoma Contact with the Lateral Ventricle on Survival: A Meta-Analysis, J. Neurooncol., 131, 125, 10.1007/s11060-016-2278-7 · DOI
  66. Huang, 2021, A Retrospective Analysis of the Risk Factors Affecting Recurrence Time in Patients with Recurrent Glioblastoma, Ann. Palliat. Med., 10, 5391, 10.21037/apm-21-823 · DOI
  67. Li, 2023, Targeting the Neural Stem Cells in Subventricular Zone for the Treatment of Glioblastoma: An Update from Preclinical Evidence to Clinical Interventions, Stem Cell Res. Ther., 14, 125, 10.1186/s13287-023-03325-4 · DOI
  68. Bushong, 2012, Dedifferentiation of Neurons and Astrocytes by Oncogenes Can Induce Gliomas in Mice, Science, 338, 1080, 10.1126/science.1226929 · DOI
  69. Shahar, 2017, Percentage of Mesenchymal Stem Cells in High-Grade Glioma Tumor Samples Correlates with Patient Survival, Neuro Oncol., 19, 660
  70. Uhrbom, 2002, Ink4a-Arf Loss Cooperates with KRas Activation in Astrocytes and Neural Progenitors to Generate Glioblastomas of Various Morphologies Depending on Activated Akt1, Cancer Res., 62, 5551
  71. Li, 2016, Rapid Reprogramming of Primary Human Astrocytes into Potent Tumor-Initiating Cells with Defined Genetic Factors, Cancer Res., 76, 5143, 10.1158/0008-5472.CAN-16-0171 · DOI
  72. Bradshaw, 2016, Cancer Stem Cell Hierarchy in Glioblastoma Multiforme, Front. Surg., 3, 21
  73. Lan, 2017, Fate Mapping of Human Glioblastoma Reveals an Invariant Stem Cell Hierarchy, Nature, 549, 227, 10.1038/nature23666 · DOI
  74. Schneider, 2016, A Paired Comparison between Glioblastoma “Stem Cells” and Differentiated Cells, Int. J. Cancer, 138, 1709, 10.1002/ijc.29908 · DOI
  75. Liau, 2017, Adaptive Chromatin Remodeling Drives Glioblastoma Stem Cell Plasticity and Drug Tolerance, Cell Stem Cell, 20, 233, 10.1016/j.stem.2016.11.003 · DOI · Paper page
  76. Gimple, 2019, Glioblastoma Stem Cells: Lessons from the Tumor Hierarchy in a Lethal Cancer, Genes Dev., 33, 591, 10.1101/gad.324301.119 · DOI · Paper page
  77. Glumac, 2018, The Role of CD133 in Cancer: A Concise Review, Clin. Transl. Med., 7, 18, 10.1186/s40169-018-0198-1 · DOI
  78. Si, 2020, High Expression of CD44 Predicts a Poor Prognosis in Glioblastomas, Cancer Manag. Res., 12, 769, 10.2147/CMAR.S233423 · DOI
  79. Rosenberg, 2018, ATP Binding Cassette (ABC) Transporters: Expression and Clinical Value in Glioblastoma, J. Neurooncol., 138, 479, 10.1007/s11060-018-2819-3 · DOI
  80. Vieira de Castro, J., Gonçalves, C.S., Hormigo, A., and Costa, B.M. (2020). Exploiting the Complexities of Glioblastoma Stem Cells: Insights for Cancer Initiation and Therapeutic Targeting. Int. J. Mol. Sci., 21. · DOI
  81. Zhang, 2021, Role and Mechanism of Neural Stem Cells of the Subventricular Zone in Glioblastoma, World J. Stem Cells, 13, 877, 10.4252/wjsc.v13.i7.877 · DOI
  82. Soda, 2011, Transdifferentiation of Glioblastoma Cells into Vascular Endothelial Cells, Proc. Natl. Acad. Sci. USA, 108, 4274, 10.1073/pnas.1016030108 · DOI
  83. Garner, J.M., Ellison, D.W., Finkelstein, D., Ganguly, D., Du, Z., Sims, M., Yang, C.H., Interiano, R.B., Davidoff, A.M., and Pfeffer, L.M. (2015). Molecular Heterogeneity in a Patient-Derived Glioblastoma Xenoline Is Regulated by Different Cancer Stem Cell Populations. PLoS ONE, 10. · DOI
  84. Matarredona, 2018, Interactions Between Neural Progenitor Cells and Microglia in the Subventricular Zone: Physiological Implications in the Neurogenic Niche and After Implantation in the Injured Brain, Front. Cell Neurosci., 12, 268, 10.3389/fncel.2018.00268 · DOI
  85. Kuo, 2021, Astrocyte and Oligodendrocyte Responses From the Subventricular Zone After Injury, Front. Cell Neurosci., 15, 797553, 10.3389/fncel.2021.797553 · DOI
  86. Pallini, 2010, Tumour Vascularization via Endothelial Differentiation of Glioblastoma Stem-like Cells, Nature, 468, 824, 10.1038/nature09557 · DOI
  87. Cheng, 2013, Glioblastoma Stem Cells Generate Vascular Pericytes to Support Vessel Function and Tumor Growth, Cell, 153, 139, 10.1016/j.cell.2013.02.021 · DOI · Paper page
  88. Molina, 2010, Invasive Glioblastoma Cells Acquire Stemness and Increased Akt Activation, Neoplasia, 12, 453, 10.1593/neo.10126 · DOI
  89. Masliantsev, 2018, Impact of STAT3 Phosphorylation in Glioblastoma Stem Cells Radiosensitization and Patient Outcome, Oncotarget, 9, 3968, 10.18632/oncotarget.23374 · DOI
  90. Beier, 2012, Efficacy of Clinically Relevant Temozolomide Dosing Schemes in Glioblastoma Cancer Stem Cell Lines, J. Neurooncol., 109, 45, 10.1007/s11060-012-0878-4 · DOI
  91. McCord, M., Bartom, E., Burdett, K., Baran, A., Eckerdt, F.D., Balyasnikova, I.V., McCortney, K., Sears, T., Cheng, S.-Y., and Sarkaria, J.N. (2022). Modeling Therapy-Driven Evolution of Glioblastoma with Patient-Derived Xenografts. Cancers, 14. · DOI
  92. Pavlova, 2022, Reparative Properties of Human Glioblastoma Cells after Single Exposure to a Wide Range of X-Ray Doses, Front. Oncol., 12, 912741, 10.3389/fonc.2022.912741 · DOI
  93. Vilar, J.B., Christmann, M., and Tomicic, M.T. (2022). Alterations in Molecular Profiles Affecting Glioblastoma Resistance to Radiochemotherapy: Where Does the Good Go?. Cancers, 14. · DOI
  94. Ahmed, 2015, Selective Inhibition of Parallel DNA Damage Response Pathways Optimizes Radiosensitization of Glioblastoma Stem-like Cells, Cancer Res., 75, 4416, 10.1158/0008-5472.CAN-14-3790 · DOI
  95. Tachon, G., Cortes, U., Guichet, P.-O., Rivet, P., Balbous, A., Masliantsev, K., Berger, A., Boissonnade, O., Wager, M., and Karayan-Tapon, L. (2018). Cell Cycle Changes after Glioblastoma Stem Cell Irradiation: The Major Role of RAD51. Int. J. Mol. Sci., 19. · DOI
  96. Lau, 2015, STAT3 Blockade Inhibits Radiation-Induced Malignant Progression in Glioma, Cancer Res., 75, 4302, 10.1158/0008-5472.CAN-14-3331 · DOI
  97. Sherry, 2009, STAT3 Is Required for Proliferation and Maintenance of Multipotency in Glioblastoma Stem Cells, Stem Cells, 27, 2383, 10.1002/stem.185 · DOI · Paper page
  98. Ganguly, 2018, The Critical Role That STAT3 Plays in Glioma-Initiating Cells: STAT3 Addiction in Glioma, Oncotarget, 9, 22095, 10.18632/oncotarget.25188 · DOI
  99. Wang, 2022, SS-4 Is a Highly Selective Small Molecule Inhibitor of STAT3 Tyrosine Phosphorylation That Potently Inhibits GBM Tumorigenesis in Vitro and in Vivo, Cancer Lett., 533, 215614, 10.1016/j.canlet.2022.215614 · DOI
  100. Groot, 2022, A First-in-Human Phase I Trial of the Oral p-STAT3 Inhibitor WP1066 in Patients with Recurrent Malignant Glioma, CNS Oncol., 11, CNS87, 10.2217/cns-2022-0005 · DOI
  101. Sharma, 2023, Tumor Microenvironment in Glioblastoma: Current and Emerging Concepts, Neurooncol. Adv., 5, vdad009
  102. Lemos, 2023, Immunotherapy in Glioblastoma Treatment: Current State and Future Prospects, World J. Clin. Oncol., 14, 138, 10.5306/wjco.v14.i4.138 · DOI
  103. Otvos, 2016, Cancer Stem Cell-Secreted Macrophage Migration Inhibitory Factor Stimulates Myeloid Derived Suppressor Cell Function and Facilitates Glioblastoma Immune Evasion, Stem Cells, 34, 2026, 10.1002/stem.2393 · DOI
  104. Broekman, 2018, Multidimensional Communication in the Microenvirons of Glioblastoma, Nat. Rev. Neurol., 14, 482, 10.1038/s41582-018-0025-8 · DOI
  105. Wei, 2019, Osteopontin Mediates Glioblastoma-Associated Macrophage Infiltration and Is a Potential Therapeutic Target, J. Clin. Investig., 129, 137, 10.1172/JCI121266 · DOI
  106. Himes, 2020, The Role of Extracellular Vesicles and PD-L1 in Glioblastoma-Mediated Immunosuppressive Monocyte Induction, Neuro Oncol., 22, 967, 10.1093/neuonc/noaa029 · DOI
  107. Garcia, J.H., Jain, S., and Aghi, M.K. (2021). Metabolic Drivers of Invasion in Glioblastoma. Front. Cell Dev. Biol., 9. · DOI
  108. Erices, J.I., Bizama, C., Niechi, I., Uribe, D., Rosales, A., Fabres, K., Navarro-Martínez, G., Torres, Á., San Martín, R., and Roa, J.C. (2023). Glioblastoma Microenvironment and Invasiveness: New Insights and Therapeutic Targets. Int. J. Mol. Sci., 24. · DOI
  109. Siebzehnrubl, 2018, Infiltrative and Drug-Resistant Slow-Cycling Cells Support Metabolic Heterogeneity in Glioblastoma, EMBO J., 37, e98772, 10.15252/embj.201798772 · DOI
  110. Verdugo, 2022, An Update on the Molecular Biology of Glioblastoma, with Clinical Implications and Progress in Its Treatment, Cancer Commun., 42, 1083, 10.1002/cac2.12361 · DOI
  111. Stanke, K.M., Wilson, C., and Kidambi, S. (2021). High Expression of Glycolytic Genes in Clinical Glioblastoma Patients Correlates With Lower Survival. Front. Mol. Biosci., 8. · DOI
  112. Flavahan, 2013, Brain Tumor Initiating Cells Adapt to Restricted Nutrition through Preferential Glucose Uptake, Nat. Neurosci., 16, 1373, 10.1038/nn.3510 · DOI
  113. Libby, 2021, A Role for GLUT3 in Glioblastoma Cell Invasion That Is Not Recapitulated by GLUT1, Cell Adh Migr., 15, 101, 10.1080/19336918.2021.1903684 · DOI
  114. Wolf, 2011, Hexokinase 2 Is a Key Mediator of Aerobic Glycolysis and Promotes Tumor Growth in Human Glioblastoma Multiforme, J. Exp. Med., 208, 313, 10.1084/jem.20101470 · DOI · Paper page
  115. Labak, 2016, Glucose Transport: Meeting the Metabolic Demands of Cancer, and Applications in Glioblastoma Treatment, Am. J. Cancer Res., 6, 1599
  116. Kou, Y., Geng, F., and Guo, D. (2022). Lipid Metabolism in Glioblastoma: From De Novo Synthesis to Storage. Biomedicines, 10. · DOI
  117. Obara-Michlewska, M., and Szeliga, M. (2020). Targeting Glutamine Addiction in Gliomas. Cancers, 12. · DOI
  118. Natarajan, S.K., and Venneti, S. (2019). Glutamine Metabolism in Brain Tumors. Cancers, 11. · DOI
  119. Barzegar Behrooz, A., Talaie, Z., Jusheghani, F., Łos, M.J., Klonisch, T., and Ghavami, S. (2022). Wnt and PI3K/Akt/mTOR Survival Pathways as Therapeutic Targets in Glioblastoma. Int. J. Mol. Sci., 23. · DOI
  120. Karatsai, 2020, Effects of Arginine and Its Deprivation on Human Glioblastoma Physiology and Signaling, Adv. Exp. Med. Biol., 1202, 243, 10.1007/978-3-030-30651-9_12 · DOI
  121. Kesarwani, 2018, Tryptophan Metabolism Contributes to Radiation-Induced Immune Checkpoint Reactivation in Glioblastoma, Clin. Cancer Res., 24, 3632, 10.1158/1078-0432.CCR-18-0041 · DOI
  122. Lyons, 2007, Autocrine Glutamate Signaling Promotes Glioma Cell Invasion, Cancer Res., 67, 9463, 10.1158/0008-5472.CAN-07-2034 · DOI
  123. Corsi, L., Mescola, A., and Alessandrini, A. (2019). Glutamate Receptors and Glioblastoma Multiforme: An Old “Route” for New Perspectives. Int. J. Mol. Sci., 20. · DOI
  124. Savaskan, 2015, Neurodegeneration in the Brain Tumor Microenvironment: Glutamate in the Limelight, Curr. Neuropharmacol., 13, 258, 10.2174/1570159X13666150122224158 · DOI
  125. Kumaria, 2023, Novel Therapeutic Strategies in Glioma Targeting Glutamatergic Neurotransmission, Brain Res., 1818, 148515, 10.1016/j.brainres.2023.148515 · DOI
  126. Maule, 2016, Annexin 2A Sustains Glioblastoma Cell Dissemination and Proliferation, Oncotarget, 7, 54632, 10.18632/oncotarget.10565 · DOI
  127. Yu, 2020, GBP2 Enhances Glioblastoma Invasion through Stat3/Fibronectin Pathway, Oncogene, 39, 5042, 10.1038/s41388-020-1348-7 · DOI
  128. Wu, 2022, High Expression of Fibronectin 1 Predicts a Poor Prognosis in Glioblastoma, Curr. Med. Sci., 42, 1055, 10.1007/s11596-022-2638-9 · DOI
  129. Bezrookove, 2020, PHIP Drives Glioblastoma Motility and Invasion by Regulating the Focal Adhesion Complex, Proc. Natl. Acad. Sci. USA, 117, 9064, 10.1073/pnas.1914505117 · DOI
  130. Cosset, 2017, Glut3 Addiction Is a Druggable Vulnerability for a Molecularly Defined Subpopulation of Glioblastoma, Cancer Cell, 32, 856, 10.1016/j.ccell.2017.10.016 · DOI
  131. Santoni, 2012, Functional Role of T-Type Calcium Channels in Tumour Growth and Progression: Prospective in Cancer Therapy, Br. J. Pharmacol., 166, 1244, 10.1111/j.1476-5381.2012.01908.x · DOI
  132. Portela, 2020, New Cellular Dimensions on Glioblastoma Progression, Neurosci. Insights, 15, 2633105520923076, 10.1177/2633105520923076 · DOI
  133. Kuga, 1990, Actions of Ca2+ Antagonists on Two Types of Ca2+ Channels in Rat Aorta Smooth Muscle Cells in Primary Culture, Circ. Res., 67, 469, 10.1161/01.RES.67.2.469 · DOI
  134. Pointer, 2017, Administration of Non-Torsadogenic Human Ether-à-Go-Go-Related Gene Inhibitors Is Associated with Better Survival for High hERG-Expressing Glioblastoma Patients, Clin. Cancer Res., 23, 73, 10.1158/1078-0432.CCR-15-3169 · DOI
  135. Chen, D., Song, M., Mohamad, O., and Yu, S.P. (2014). Inhibition of Na+/K+-ATPase Induces Hybrid Cell Death and Enhanced Sensitivity to Chemotherapy in Human Glioblastoma Cells. BMC Cancer, 14. · DOI
  136. Dong, 2019, Epigenetic Modulation of Metabolism in Glioblastoma, Semin. Cancer Biol., 57, 45, 10.1016/j.semcancer.2018.09.002 · DOI
  137. Uddin, 2022, Epigenetics of Glioblastoma Multiforme: From Molecular Mechanisms to Therapeutic Approaches, Semin. Cancer Biol., 83, 100, 10.1016/j.semcancer.2020.12.015 · DOI
  138. Zhao, 2020, Single Nucleotide Alterations in MicroRNAs and Human Cancer-A Not Fully Explored Field, Non-Coding RNA Res., 5, 27, 10.1016/j.ncrna.2020.02.003 · DOI
  139. Galardi, 2005, Extensive Modulation of a Set of microRNAs in Primary Glioblastoma, Biochem. Biophys. Res. Commun., 334, 1351, 10.1016/j.bbrc.2005.07.030 · DOI · Paper page
  140. Shea, 2016, MicroRNAs in Glioblastoma Multiforme Pathogenesis and Therapeutics, Cancer Med., 5, 1917, 10.1002/cam4.775 · DOI
  141. Chen, 2021, Role of microRNAs in Glioblastoma, Oncotarget, 12, 1707, 10.18632/oncotarget.28039 · DOI · Paper page
  142. Wu, 2011, MicroRNA-7 Regulates Glioblastoma Cell Invasion via Targeting Focal Adhesion Kinase Expression, Chin. Med. J., 124, 2616
  143. Liu, 2014, miR-7 Inhibits Glioblastoma Growth by Simultaneously Interfering with the PI3K/ATK and Raf/MEK/ERK Pathways, Int. J. Oncol., 44, 1571, 10.3892/ijo.2014.2322 · DOI
  144. Tamim, S., Vo, D.T., Uren, P.J., Qiao, M., Bindewald, E., Kasprzak, W.K., Shapiro, B.A., Nakaya, H.I., Burns, S.C., and Araujo, P.R. (2014). Genomic Analyses Reveal Broad Impact of miR-137 on Genes Associated with Malignant Transformation and Neuronal Differentiation in Glioblastoma Cells. PLoS ONE, 9. · DOI
  145. Zhang, 2017, Identification of miRNA-7 by Genome-Wide Analysis as a Critical Sensitizer for TRAIL-Induced Apoptosis in Glioblastoma Cells, Nucleic Acids Res., 45, 5930, 10.1093/nar/gkx317 · DOI
  146. Sun, 2011, MicroRNA-10b Induces Glioma Cell Invasion by Modulating MMP-14 and uPAR Expression via HOXD10, Brain Res., 1389, 9, 10.1016/j.brainres.2011.03.013 · DOI
  147. Gabriely, 2011, Human Glioma Growth Is Controlled by MicroRNA-10b, Cancer Res., 71, 3563, 10.1158/0008-5472.CAN-10-3568 · DOI · Paper page
  148. Teplyuk, 2015, MicroRNA-10b Inhibition Reduces E2F1-Mediated Transcription and miR-15/16 Activity in Glioblastoma, Oncotarget, 6, 3770, 10.18632/oncotarget.3009 · DOI
  149. Li, 2009, MicroRNA-34a Inhibits Glioblastoma Growth by Targeting Multiple Oncogenes, Cancer Res., 69, 7569, 10.1158/0008-5472.CAN-09-0529 · DOI · Paper page
  150. Luan, 2010, MicroRNA-34a: A Novel Tumor Suppressor in P53-Mutant Glioma Cell Line U251, Arch. Med. Res., 41, 67, 10.1016/j.arcmed.2010.02.007 · DOI
  151. Guessous, 2010, microRNA-34a Is Tumor Suppressive in Brain Tumors and Glioma Stem Cells, Cell Cycle, 9, 1031, 10.4161/cc.9.6.10987 · DOI
  152. Li, 2011, MicroRNA-34a Targets Notch1 and Inhibits Cell Proliferation in Glioblastoma Multiforme, Cancer Biol. Ther., 12, 477, 10.4161/cbt.12.6.16300 · DOI
  153. Vo, 2011, The Oncogenic RNA-Binding Protein Musashi1 Is Regulated by Tumor Suppressor miRNAs, RNA Biol., 8, 817, 10.4161/rna.8.5.16041 · DOI
  154. Silber, J., Jacobsen, A., Ozawa, T., Harinath, G., Pedraza, A., Sander, C., Holland, E.C., and Huse, J.T. (2012). miR-34a Repression in Proneural Malignant Gliomas Upregulates Expression of Its Target PDGFRA and Promotes Tumorigenesis. PLoS ONE, 7. · DOI
  155. Yin, 2013, miR-34a Functions as a Tumor Suppressor Modulating EGFR in Glioblastoma Multiforme, Oncogene, 32, 1155, 10.1038/onc.2012.132 · DOI
  156. Fan, Y.N., Meley, D., Pizer, B., and Sée, V. (2014). Mir-34a Mimics Are Potential Therapeutic Agents for P53-Mutated and Chemo-Resistant Brain Tumour Cells. PLoS ONE, 9. · DOI
  157. Rathod, 2014, Tumor Suppressive miRNA-34a Suppresses Cell Proliferation and Tumor Growth of Glioma Stem Cells by Targeting Akt and Wnt Signaling Pathways, FEBS Open Bio, 4, 485, 10.1016/j.fob.2014.05.002 · DOI
  158. Duan, 2016, MicroRNA-34a Inhibits Cell Proliferation and Induces Cell Apoptosis of Glioma Cells via Targeting of Bcl-2, Mol. Med. Rep., 14, 432, 10.3892/mmr.2016.5255 · DOI
  159. Lages, E., Guttin, A., El Atifi, M., Ramus, C., Ipas, H., Dupré, I., Rolland, D., Salon, C., Godfraind, C., and deFraipont, F. (2011). MicroRNA and Target Protein Patterns Reveal Physiopathological Features of Glioma Subtypes. PLoS ONE, 6. · DOI · Paper page
  160. Chan, 2005, MicroRNA-21 Is an Antiapoptotic Factor in Human Glioblastoma Cells, Cancer Res., 65, 6029, 10.1158/0008-5472.CAN-05-0137 · DOI · Paper page
  161. Corsten, 2007, MicroRNA-21 Knockdown Disrupts Glioma Growth In Vivo and Displays Synergistic Cytotoxicity with Neural Precursor Cell–Delivered S-TRAIL in Human Gliomas, Cancer Res., 67, 8994, 10.1158/0008-5472.CAN-07-1045 · DOI · Paper page
  162. Ren, Y., Zhou, X., Mei, M., Yuan, X.-B., Han, L., Wang, G.-X., Jia, Z.-F., Xu, P., Pu, P.-Y., and Kang, C.-S. (2010). MicroRNA-21 Inhibitor Sensitizes Human Glioblastoma Cells U251 (PTEN-Mutant) and LN229 (PTEN-Wild Type) to Taxol. BMC Cancer, 10. · DOI
  163. Godlewski, 2008, Targeting of the Bmi-1 Oncogene/Stem Cell Renewal Factor by MicroRNA-128 Inhibits Glioma Proliferation and Self-Renewal, Cancer Res., 68, 9125, 10.1158/0008-5472.CAN-08-2629 · DOI · Paper page
  164. Cui, 2010, Micro-RNA-128 (miRNA-128) down-Regulation in Glioblastoma Targets ARP5 (ANGPTL6), Bmi-1 and E2F-3a, Key Regulators of Brain Cell Proliferation, J. Neurooncol., 98, 297, 10.1007/s11060-009-0077-0 · DOI
  165. Rao, 2010, Genome-Wide Expression Profiling Identifies Deregulated miRNAs in Malignant Astrocytoma, Mod. Pathol., 23, 1404, 10.1038/modpathol.2010.135 · DOI
  166. Lavon, 2010, Gliomas Display a microRNA Expression Profile Reminiscent of Neural Precursor Cells, Neuro-Oncology, 12, 422, 10.1093/neuonc/nop061 · DOI
  167. Fang, 2011, MicroRNA miR-93 Promotes Tumor Growth and Angiogenesis by Targeting Integrin-Β8, Oncogene, 30, 806, 10.1038/onc.2010.465 · DOI
  168. Hua, 2012, A Catalogue of Glioblastoma and Brain MicroRNAs Identified by Deep Sequencing, OMICS A J. Integr. Biol., 16, 690, 10.1089/omi.2012.0069 · DOI
  169. Papagiannakopoulos, 2012, Pro-Neural miR-128 Is a Glioma Tumor Suppressor That Targets Mitogenic Kinases, Oncogene, 31, 1884, 10.1038/onc.2011.380 · DOI · Paper page
  170. Piwecka, 2015, Comprehensive Analysis of microRNA Expression Profile in Malignant Glioma Tissues, Mol. Oncol., 9, 1324, 10.1016/j.molonc.2015.03.007 · DOI · Paper page
  171. Shan, 2016, miR128-1 Inhibits the Growth of Glioblastoma Multiforme and Glioma Stem-like Cells via Targeting BMI1 and E2F3, Oncotarget, 7, 78813, 10.18632/oncotarget.12385 · DOI · Paper page
  172. Shi, Z., Wang, J., Yan, Z., You, Y., Li, C., Qian, X., Yin, Y., Zhao, P., Wang, Y., and Wang, X. (2012). MiR-128 Inhibits Tumor Growth and Angiogenesis by Targeting p70S6K1. PLoS ONE, 7. · DOI
  173. Chen, 2016, MicroRNA-93 Promotes the Malignant Phenotypes of Human Glioma Cells and Induces Their Chemoresistance to Temozolomide, Biol. Open, 5, 669, 10.1242/bio.015552 · DOI
  174. Bhaskaran, 2019, The Functional Synergism of microRNA Clustering Provides Therapeutically Relevant Epigenetic Interference in Glioblastoma, Nat. Commun., 10, 442, 10.1038/s41467-019-08390-z · DOI · Paper page
  175. Huang, 2019, MIR93 (microRNA-93 ) Regulates Tumorigenicity and Therapy Response of Glioblastoma by Targeting Autophagy, Autophagy, 15, 1100, 10.1080/15548627.2019.1569947 · DOI
  176. Huang, 2009, Targeted Therapy for Malignant Glioma Patients: Lessons Learned and the Road Ahead, Neurotherapeutics, 6, 500, 10.1016/j.nurt.2009.04.008 · DOI
  177. Zhang, 2023, Underlying Mechanisms and Clinical Potential of circRNAs in Glioblastoma, Oncol. Res., 31, 449, 10.32604/or.2023.029062 · DOI
  178. Guo, X., and Piao, H. (2021). Research Progress of circRNAs in Glioblastoma. Front. Cell Dev. Biol., 9. · DOI
  179. Peng, 2018, New Insights into Long Noncoding RNAs and Their Roles in Glioma, Mol. Cancer, 17, 61, 10.1186/s12943-018-0812-2 · DOI
  180. Zottel, A., Šamec, N., Videtič Paska, A., and Jovčevska, I. (2020). Coding of Glioblastoma Progression and Therapy Resistance through Long Noncoding RNAs. Cancers, 12. · DOI
  181. Dai, 2022, Systematic Characterization and Biological Functions of Non-coding RNAs in Glioblastoma, Cell Prolif., 56, e13375, 10.1111/cpr.13375 · DOI
  182. Yadav, 2022, Metastasis Associated Long Noncoding RNAs in Glioblastoma: Biomarkers and Therapeutic Targets, J. Cell. Physiol., 237, 401, 10.1002/jcp.30577 · DOI
  183. Shen, 2018, Serum HOTAIR and GAS5 Levels as Predictors of Survival in Patients with Glioblastoma, Mol. Carcinog., 57, 137, 10.1002/mc.22739 · DOI
  184. Xi, 2018, Long Non-Coding RNAs in Glioma Progression, Cancer Lett., 419, 203, 10.1016/j.canlet.2018.01.041 · DOI
  185. Yu, 2021, Identification of Immune-Related lncRNA Prognostic Signature and Molecular Subtypes for Glioblastoma, Front. Immunol., 12, 706936, 10.3389/fimmu.2021.706936 · DOI
  186. Eraky, 2022, Serum Long Non-Coding RNAs as Potential Noninvasive Biomarkers for Glioblastoma Diagnosis, Prognosis, and Chemoresistance, JIN, 21, 111, 10.31083/j.jin2104111 · DOI
  187. Chen, 2017, LncRNA-TP53TG1 Participated in the Stress Response Under Glucose Deprivation in Glioma, J. Cell. Biochem., 118, 4897, 10.1002/jcb.26175 · DOI
  188. Wang, 2017, LEF1-AS1, a Long-Noncoding RNA, Promotes Malignancy in Glioblastoma, OncoTargets Ther., 10, 4251, 10.2147/OTT.S130365 · DOI
  189. Hegi, 2008, Correlation of O 6-Methylguanine Methyltransferase (MGMT) Promoter Methylation With Clinical Outcomes in Glioblastoma and Clinical Strategies to Modulate MGMT Activity, JCO, 26, 4189, 10.1200/JCO.2007.11.5964 · DOI
  190. Mansouri, 2019, Hypoxia Can Induce Migration of Glioblastoma Cells Through a Methylation-Dependent Control of ODZ1 Gene Expression, Front. Oncol., 9, 1036, 10.3389/fonc.2019.01036 · DOI
  191. Wu, Q., Berglund, A.E., and Etame, A.B. (2021). The Impact of Epigenetic Modifications on Adaptive Resistance Evolution in Glioblastoma. Int. J. Mol. Sci., 22. · DOI
  192. Scoumanne, 2009, PRMT5 Is Required for Cell-Cycle Progression and P53 Tumor Suppressor Function, Nucleic Acids Res., 37, 4965, 10.1093/nar/gkp516 · DOI
  193. Russell, 2017, PRMT5-PTEN Molecular Pathway Regulates Senescence and Self-Renewal of Primary Glioblastoma Neurosphere Cells, Oncogene, 36, 263, 10.1038/onc.2016.199 · DOI
  194. Welker, 2018, PRMT5 as a Druggable Target for Glioblastoma Therapy, Neuro-Oncology, 20, 753, 10.1093/neuonc/nox206 · DOI
  195. Yang, 2021, Histone Deacetylase 6 Acts Upstream of DNA Damage Response Activation to Support the Survival of Glioblastoma Cells, Cell Death Dis., 12, 884, 10.1038/s41419-021-04182-w · DOI
  196. Pastorino, O., Gentile, M.T., Mancini, A., Del Gaudio, N., Di Costanzo, A., Bajetto, A., Franco, P., Altucci, L., Florio, T., and Stoppelli, M.P. (2019). Histone Deacetylase Inhibitors Impair Vasculogenic Mimicry from Glioblastoma Cells. Cancers, 11. · DOI
  197. Yang, 2018, HDAC6 Inhibition Induces Glioma Stem Cells Differentiation and Enhances Cellular Radiation Sensitivity through the SHH/Gli1 Signaling Pathway, Cancer Lett., 415, 164, 10.1016/j.canlet.2017.12.005 · DOI
  198. Zhang, 2018, Inhibition of Glioblastoma Cell Proliferation, Invasion, and Mechanism of Action of a Novel Hydroxamic Acid Hybrid Molecule, Cell Death Discov., 4, 41, 10.1038/s41420-018-0103-0 · DOI
  199. LEE, 2015, Mechanisms and Clinical Significance of Histone Deacetylase Inhibitors: Epigenetic Glioblastoma Therapy, Anticancer. Res., 35, 615
  200. Rahman, M.A., Engelsen, A.S.T., Sarowar, S., Bindesbøll, C., Birkeland, E., Goplen, D., Lotsberg, M.L., Knappskog, S., Simonsen, A., and Chekenya, M. (2022). Bortezomib Abrogates Temozolomide-Induced Autophagic Flux through an ATG5 Dependent Pathway. Front. Cell Dev. Biol., 10. · DOI

200 of 1055 shown

Cited by

Sorted by citations

Metadata

Authors
Obrador, E., Moreno-Murciano, P., Oriol-Caballo, M., López-Blanch, R., Pineda, B., Gutiérrez-Arroyo, J., Loras, A., Gonzalez-Bonet, L., Martinez-Cadenas, C., Estrela, J., & Marqués-Torrejón, M.
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2024-02-21
Volume
25
Issue
5
Pages
2529
ISSN
1422-0067
DOI
10.3390/ijms25052529
PMC
PMC10931797
Cited by
271
References
54
Language
en
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • MCIN/AEI/10.13039/501100011033/ (CPP2021-8817, SBT-001, 21-076, MAZ/2021/03 UP2021-021, RYC2022-038481-by MCIN/AEI/ 10.13039/501100011033)
  • Scientia BioTech S.L.-Spain (CPP2021-8817, SBT-001, 21-076, MAZ/2021/03 UP2021-021, RYC2022-038481-by MCIN/AEI/ 10.13039/501100011033)
  • European Union-Next generation EU (CPP2021-8817, SBT-001, 21-076, MAZ/2021/03 UP2021-021, RYC2022-038481-by MCIN/AEI/ 10.13039/501100011033)
  • ‘Maria Zambrano’ research contract (CPP2021-8817, SBT-001, 21-076, MAZ/2021/03 UP2021-021, RYC2022-038481-by MCIN/AEI/ 10.13039/501100011033)
  • Ramon y Cajal Research Fellow (CPP2021-8817, SBT-001, 21-076, MAZ/2021/03 UP2021-021, RYC2022-038481-by MCIN/AEI/ 10.13039/501100011033)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review