Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma
Abstract
:Simple Summary
Abstract
1. Introduction
2. Mechanisms of Resistance to Antiangiogenic Therapies in GBM
2.1. Redundant Angiogenic Pathways
2.2. Increased Invasion and Metastasis
2.3. Hypoxia-Induced Resistance
2.4. Vascular Mimicry
2.5. Immune Modulation
3. Current Treatment Strategies to Overcome Antiangiogenic Resistance in GBM
3.1. Combination Therapies
3.2. Personalized Medicine
3.3. Novel Therapeutic Targets
3.4. Immunotherapy
3.5. Nanoparticle-Mediated Treatment Options
4. Limitations and Future Perspectives of Antiangiogenic Resistance in GBM
5. Conclusions
Author Contributions
Funding
Conflicts of Interest
References
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Drug Name | Molecular Signaling | Target Cells | Doses and Effects | Current Application in GBM | References |
---|---|---|---|---|---|
Bevacizumab + irinotecan | VEGF inhibition, topoisomerase I inhibition | Endothelial cells, tumor cells | Bevacizumab: 10 mg/kg; irinotecan: 125 mg/m2 | Used in recurrent GBM; aims to inhibit angiogenesis and tumor growth | [91] |
Temozolomide + bevacizumab | DNA alkylation, VEGF inhibition | Tumor cells, endothelial cells | Temozolomide: 150–200 mg/m2; bevacizumab: 10 mg/kg | Used in newly diagnosed and recurrent GBM; targets DNA and angiogenesis | [92] |
Bevacizumab + lomustine | VEGF inhibition, DNA alkylation | Endothelial cells, tumor cells | Bevacizumab: 10 mg/kg; lomustine: 110 mg/m2 | Used in recurrent GBM; aims to combine antiangiogenic and cytotoxic effects | [35] |
Nivolumab + bevacizumab | PD-1 inhibition, VEGF inhibition | Immune cells, endothelial cells | Nivolumab: 3 mg/kg; bevacizumab: 10 mg/kg | Used in clinical trials for recurrent GBM; aims to enhance immune response | [36] |
Bevacizumab + carboplatin | VEGF inhibition, DNA crosslinking | Endothelial cells, tumor cells | Bevacizumab: 10 mg/kg; carboplatin: AUC 5-6 | Investigated in recurrent GBM; aims to enhance DNA damage and inhibit angiogenesis | [93] |
Pembrolizumab + bevacizumab | PD-1 inhibition, VEGF inhibition | Immune cells, endothelial cells | Pembrolizumab: 200 mg; bevacizumab: 10 mg/kg | Used in clinical trials for recurrent GBM; aims to boost immune system and inhibit angiogenesis | [36] |
Bevacizumab + erlotinib | VEGF inhibition, EGFR inhibition | Endothelial cells, tumor cells | Bevacizumab: 10 mg/kg; erlotinib: 150 mg daily | Investigated in recurrent GBM; targets both angiogenesis and EGFR signaling | [94] |
Bevacizumab + temsirolimus | VEGF inhibition, mTOR inhibition | Endothelial cells, tumor cells | Bevacizumab: 10 mg/kg; temsirolimus: 25 mg weekly | Used in clinical trials for recurrent GBM; aims to inhibit angiogenesis and mTOR pathway | [14] |
Cediranib + lomustine | VEGFR inhibition, DNA alkylation | Endothelial cells, tumor cells | Cediranib: 30 mg daily; lomustine: 110 mg/m2 | Investigated in recurrent GBM; aims to inhibit angiogenesis and enhance cytotoxicity | [66] |
Bevacizumab + ipilimumab | VEGF inhibition, CTLA-4 inhibition | Endothelial cells, immune cells | Bevacizumab: 10 mg/kg; ipilimumab: 3 mg/kg | Used in clinical trials for recurrent GBM; aims to enhance immune response and inhibit angiogenesis | [95] |
Drug Name | Molecular Action | Target Cells | Doses | Current Application in GBM | References |
---|---|---|---|---|---|
Bevacizumab (Avastin) | VEGF inhibitor, blocks angiogenesis | Endothelial cells | 10 mg/kg IV every 2 weeks | Approved for recurrent GBM, reduces edema | [108] |
Temozolomide (TMZ) | Alkylating agent, induces DNA damage | Tumor cells | 150–200 mg/m2/day for 5 days every 28 days | Standard chemotherapy for newly diagnosed GBM | [109] |
Everolimus (Afinitor) | mTOR inhibitor, inhibits cell growth and proliferation | Tumor cells | 10 mg orally once daily | Under investigation, potential to target mTOR pathway | [110] |
Larotrectinib (Vitrakvi) | TRK fusion inhibitor, blocks TRK signaling | Tumor cells with NTRK fusions | 100 mg/m2 twice daily | Experimental, targeting NTRK fusion-positive GBM | [111] |
Enzastaurin (LY317615) | PKC-β inhibitor, induces apoptosis | Tumor cells | 500 mg orally once daily | Under investigation, potential anti-tumor activity | [112] |
Marizomib (NPI-0052) | Proteasome inhibitor, induces apoptosis | Tumor cells | 0.7 mg/m2 IV once weekly | Clinical trials, targeting proteasome in GBM | [113] |
Abemaciclib (Verzenio) | CDK4/6 inhibitor, inhibits cell cycle progression | Tumor cells | 150 mg orally twice daily | Experimental, targeting CDK4/6 pathway in GBM | [114] |
Olaparib (Lynparza) | PARP inhibitor, impairs DNA repair | Tumor cells | 300 mg orally twice daily | Investigational, for tumors with DNA repair deficiencies | [115] |
Nivolumab (Opdivo) | PD-1 inhibitor, boosts immune response | Tumor cells, immune cells | 3 mg/kg IV every 2 weeks | Under investigation, potential in immunotherapy | [116] |
Toca 511 and Toca FC | Gene therapy, converts prodrug to active chemotherapy | Tumor cells | Toca 511: intratumoral injection; Toca FC: 220 mg/m2 orally every 6 weeks | Experimental, gene therapy approach in GBM | [117] |
Compound Name | Molecular Mechanism | Target Cells | Current Application in GBM | References |
---|---|---|---|---|
Bevacizumab | VEGF inhibitor | Endothelial cells | Approved for recurrent GBM; reduces tumor blood supply | [127] |
Temozolomide | DNA methylation/damage | Tumor cells | Standard chemotherapy for GBM; induces cell death | [128] |
Cediranib | VEGFR tyrosine kinase inhibitor | Endothelial and tumor cells | Experimental; inhibits angiogenesis | [129] |
Sorafenib | Multi-kinase inhibitor (VEGFR, PDGFR, Raf kinases) | Tumor and endothelial cells | Experimental; inhibits cell proliferation and angiogenesis | [130] |
Sunitinib | Multi-kinase inhibitor (VEGFR, PDGFR) | Endothelial cells | Experimental; inhibits angiogenesis | [131] |
Erlotinib | EGFR tyrosine kinase inhibitor | Tumor cells | Experimental; inhibits tumor cell growth | [132] |
Dasatinib | Src family kinase inhibitor | Tumor cells | Experimental; inhibits cell migration and invasion | [133] |
Pazopanib | Multi-kinase inhibitor (VEGFR, PDGFR) | Tumor and endothelial cells | Experimental; inhibits angiogenesis and tumor growth | [134] |
Regorafenib | Multi-kinase inhibitor (VEGFR, PDGFR, FGFR) | Tumor and endothelial cells | Experimental; inhibits angiogenesis and tumor cell growth | [135] |
Axitinib | VEGFR tyrosine kinase inhibitor | Endothelial cells | Experimental; inhibits angiogenesis | [136] |
Drug Name | Molecular Action | Target Cells | Doses | Application in GBM | References |
---|---|---|---|---|---|
Nivolumab (Opdivo) | PD-1 inhibitor | T cells | 240 mg every 2 weeks | Investigational; ongoing clinical trials | [151] |
Pembrolizumab (Keytruda) | PD-1 inhibitor | T cells | 200 mg every 3 weeks | Investigational; ongoing clinical trials | [152] |
Ipilimumab (Yervoy) | CTLA-4 inhibitor | T cells | 3 mg/kg every 3 weeks for 4 doses | Investigational; combination trials with PD-1 inhibitors | [153] |
Avelumab (Bavencio) | PD-L1 inhibitor | Tumor cells, T cells | 10 mg/kg every 2 weeks | Investigational; ongoing clinical trials | [154] |
Durvalumab (Imfinzi) | PD-L1 inhibitor | Tumor cells, T cells | 10 mg/kg every 2 weeks | Investigational; ongoing clinical trials | [155] |
Bevacizumab (Avastin) | VEGF inhibitor | Endothelial cells | 10 mg/kg every 2 weeks | Approved for recurrent GBM | [156] |
Rindopepimut | EGFRvIII-targeted peptide vaccine | Tumor cells | Variable; typically administered intradermally | Phase II/III clinical trials | [157] |
DCVax-L | Dendritic cell-based vaccine | Dendritic cells | Personalized; dose varies | Phase III clinical trials | [158] |
ONC201 | Imipridone; induces TRAIL and DRD2 pathway activation | Tumor cells | 625 mg once a week | Phase II clinical trials | [159] |
CDX-110 (Rindopepimut) | EGFRvIII-targeted peptide vaccine | Tumor cells | Variable; typically administered intradermally | Phase II/III clinical trials | [160] |
Treatment Name | Nanoparticle Type | Mechanism of Action | Target/Focus | References |
---|---|---|---|---|
Bevacizumab-loaded nanoparticles | Lipid-based | Inhibits VEGF, reducing blood vessel formation | VEGF pathway | [168] |
Iron oxide nanoparticles | Magnetic | Targets tumor cells via magnetic fields, improving delivery | Hyperthermia, drug delivery | [169] |
Curcumin-loaded nanoparticles | Polymeric | Anti-inflammatory and antiangiogenic effects | NF-κB pathway | [170] |
Doxorubicin-loaded nanoparticles | Liposome-based | Improves drug accumulation in tumor, reducing angiogenesis | DNA intercalation, inhibiting topoisomerase | [171] |
Temozolomide-loaded nanoparticles | Polymeric | Enhances drug delivery and overcomes drug resistance | DNA alkylation, increasing tumor cell death | [172] |
Paclitaxel-loaded nanoparticles | Micelle-based | Enhances antiproliferative effects, targeting microtubules | Microtubule stabilization | [173] |
siRNA-loaded nanoparticles | Gold nanoparticles | Silences genes involved in angiogenesis and resistance | Gene expression inhibition | [174] |
HER2-targeted nanoparticles | Polymer-based | Targets HER2 receptor, enhancing specificity and reducing resistance | HER2 receptor | [175] |
Dual drug-loaded nanoparticles | Hybrid (e.g., polymer/lipid) | Combines different mechanisms to enhance therapeutic effects | Multiple targets | [176] |
Ceramide-loaded nanoparticles | Lipid-based | Induces apoptosis in resistant cancer cells | Sphingolipid metabolism | [177] |
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Rahman, M.A.; Ali, M.M. Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma. Cancers 2024, 16, 2975. https://doi.org/10.3390/cancers16172975
Rahman MA, Ali MM. Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma. Cancers. 2024; 16(17):2975. https://doi.org/10.3390/cancers16172975
Chicago/Turabian StyleRahman, Md Ataur, and Meser M. Ali. 2024. "Recent Treatment Strategies and Molecular Pathways in Resistance Mechanisms of Antiangiogenic Therapies in Glioblastoma" Cancers 16, no. 17: 2975. https://doi.org/10.3390/cancers16172975