Academic literature on the topic 'Angiogenesis, high grade gliomas, VEGF'
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Journal articles on the topic "Angiogenesis, high grade gliomas, VEGF"
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Xue, Song, Man Hu, Jinming Yu, Bingjie Fan, and Ji Ma. "Correlation of PD-L1 with VEGF and KI-67 index in patients with primary glioma." Journal of Clinical Oncology 35, no. 7_suppl (March 1, 2017): 94. http://dx.doi.org/10.1200/jco.2017.35.7_suppl.94.
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94 Background: The treatment strategies for glioma, especially glioblastoma multiforme, are not effective. The programmed death ligand 1 (PD-L1) immune escape and increased angiogenesis may be two of the underlying sources of treatment resistance. However, the relationship between these pathways in human glioma is still unknown. Methods: Data for 64 patients with primary glioma recorded from June 2007 to December 2013 in Shan Dong Cancer Hospital were immunohistochemically evaluated for the expressions of PD-L1, VEGF, MMP-9 and KI-67 index. Image ProPlus software was used to quantify the mean optical density (MOD) of the immunohistochemical image. Results: PD-L1 expression was observed in 65.22% of low-grade glioma and 90.24% of high-grade glioma, respectively. The whole expression rate of PD-L1 in glioma was 81.25%. The expression of PD-L1 is significantly related to pathological grade ( p <0.001), VEGF ( p= 0.017) and KI-67 index ( p= 0.009). The mean of PD-L1 MOD in High-grade group was 0.1144±0.02754, higher than that in low-grade group, 0.005129±0.001441 ( p= 0.004). In addition, Expression of VEGF, MMP-9 and KI-67 was significantly different between low-grade and high-grade gliomas ( p= 0.008, 0.04, 0.004 for VEGF, MMP-9 and KI-67, respectively). When analyzed as a continuous variable, the expressions of PD-L1 was positively correlated with VEGF (r = 0.392, p= 0.001) and KI-67 (r = 0.388, p= 0.001). Conclusions: These data suggest, for the first time, that PD-L1 play an important role in glioma angiogenesis and proliferation potential, providing the possibility for considering additional combinations of targeted VEGF therapies and anti-PD-L1 immunotherapy for the treatment of human brain glioma.
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Badu, S. K. "The role of angiogenic factors eNOS / VEGF in the treatment of anaplastic glioma." Vestnik nevrologii, psihiatrii i nejrohirurgii (Bulletin of Neurology, Psychiatry and Neurosurgery), no. 11 (October 20, 2022): 883–92. http://dx.doi.org/10.33920/med-01-2211-07.
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Introduction: Anaplastic gliomas (AG) account for 6–15 % of all primary brain tumors. These include: anaplastic astrocytoma (AA), anaplastic oligodendroglioma (AO), anaplastic oligoastrocytoma (AOA), and rarer forms — anaplastic pleomorphic xanthoastrocytoma and anaplastic ganglioma. According to the data on these factors, endothelial nitric oxide synthase (eNOS) is promising in terms of the prognostic value of the course of the tumor process. It was reported that a number of vascular VEGF factors interact with eNOS, contributing to the formation of an intra-tumor vascular network, which can create conditions for uneven prolonged hypoxia, leading to the emergence of more stable tumor cells. Its role in the development of a higher anaplasia level has not been studied in isolation, which determines the relevance of this study. The prognostic role of changes in endothelial nitric oxide synthase (eNOS) in the continued growth and malignant transformation of anaplastic gliomas was studied. Results: Histological samples of brain tumors of 22 patients at the University Clinic in Nizhny Novgorod from 2017 to 2019 were examined and verified for the presence of high-grade III glioma, according to the data of the World Health Organization. The average age of the patients was 50.7 years. The material was obtained as a result of surgical removal of recurrent tumors after chemo and radiotherapy. Discussion: The microenvironment of anaplastic glioma plays an essential role in its pathogenesis. More importantly, angiogenesis, which causes the supply of glioma cells with oxygen, growth factors, nutrients, and hormones, is a significant process of tumor dissemination and growth. The degree of microvascular proliferation and angiogenesis was associated with poor survival rate, transition from a lower grade to a high grade, and relapse. In high-grade glioma, such as anaplastic glioma, neoangiogenesis is an important physiological process that provides adequate blood supply for the proliferation, survival, and invasion of glioma cells. Conclusion: The high mortality rate in gliomas underscores the urgent need for effective treatment. The glioma pathogenesis is complex and can be caused by various mechanisms, as evidenced by abnormal activation of tumor angiogenesis and mutation of isocitrate dehydrogenase. VEGF acts as a regulator of angiogenesis and is widely recognized as a critical factor in glioma development and progression. Our results suggest that VEGF and eNOS inhibition may be an effective way to control and/or block endothelial barrier damage and prevent tumor progression.
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Peles, Einat, Zvi Lidar, Amos J. Simon, Rachel Grossman, Dvora Nass, and Zvi Ram. "Angiogenic Factors in the Cerebrospinal Fluid of Patients with Astrocytic Brain Tumors." Neurosurgery 55, no. 3 (September 1, 2004): 562–68. http://dx.doi.org/10.1227/01.neu.0000134383.27713.9a.
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Abstract OBJECTIVE: Gliomas account for most primary brain tumors in adults, and survival correlates with the grade and vascularity of the tumor. The degree of tumor-related angiogenesis seems to be a significant predictor of tumor progression, recurrence, and metastatic spread in a variety of malignant diseases, including brain tumors. Our study's objective was to quantify the levels of two angiogenic factors, basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF), in the cerebrospinal fluid (CSF) and serum of patients with gliomas and to correlate these levels with tumor grade, vascularity, and overall survival. METHODS: Twenty-six patients with the diagnosis of cerebral glioma (19 high-grade, 7 low-grade) comprised the study group. Ten patients with communicating hydrocephalus served as controls. Levels of VEGF and bFGF in the CSF and serum were determined using enzyme-linked immunosorbent assay analysis. Tumor vascularity was graded qualitatively using immunohistochemical staining for CD34. Nonparametric statistical techniques were used for data analysis. RESULTS: Median levels of bFGF and VEGF in the CSF were significantly higher in patients with high-grade glioma as compared with patients with low-grade glioma or hydrocephalus (bFGF levels, 52, 26, and 24 ng/ml, respectively, P < 0.0001; VEGF levels, 17.6, 7.2, and 8.3 ng/ml, respectively, P < 0.005). A significant correlation was found comparing CSF levels of bFGF with levels of VEGF (P < 0.001). The levels of the angiogenic factors in the CSF correlated with the degree of tumor vascularity and were adversely associated with patient survival. Serum levels of the angiogenic factors showed no correlation to tumor grade, vascularity, or survival. CONCLUSION: Our data suggest that CSF levels of bFGF and VEGF may serve as an additional marker for tumor grading and vascularity and may help predict survival.
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Newton, Herbert B. "Bevacizumab: Review of Development, Pharmacology, and Application to Brain Tumors." Clinical Medicine. Therapeutics 1 (January 2009): CMT.S2042. http://dx.doi.org/10.4137/cmt.s2042.
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Bevacizumab is a humanised monoclonal antibody targeted to the vascular endothelial growth factor (VEGF). VEGF is the ligand for VEGF receptors (VEGFR), which are important for the development and maintenance of the angiogenic phenotype in high-grade solid tumors, including malignant gliomas. An overview of angiogenesis, VEGF, VEGFR, and the pharmacology of bevacizumab will be presented. Bevacizumab is active in pre-clinical testing against glioma tissue cultures and xenograft models. In the clinical setting, in combination with irinotecan and other chemotherapy agents, it has shown significant activity in patients with glioblastoma multiforme (GBM) and other brain tumors. Objective responses on neuro-imaging have been noted in 30%-60% of reported cases. Prolongation of progression-free survival and overall survival have also been suggested in many reports. Treatment of bevacizumab is associated with potential side effects, including thromboembolic disorders, fatigue, intracranial hemorrhage, proteinuria, hypertension, and bowel perforation.
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BITERGE-SUT, Burcu. "A comprehensive analysis of the angiogenesis-related genes in glioblastoma multiforme vs. brain lower grade glioma." Arquivos de Neuro-Psiquiatria 78, no. 1 (January 2020): 34–38. http://dx.doi.org/10.1590/0004-282x20190131.
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Abstract Brain tumors are one of the most common causes of cancer-related deaths around the world. Angiogenesis is critical in high-grade malignant gliomas, such as glioblastoma multiforme. Objective: The aim of this study is to comparatively analyze the angiogenesis-related genes, namely VEGFA, VEGFB, KDR, CXCL8, CXCR1 and CXCR2 in LGG vs. GBM to identify molecular distinctions using datasets available on The Cancer Genome Atlas (TCGA). Methods: DNA sequencing and mRNA expression data for 514 brain lower grade glioma (LGG) and 592 glioblastoma multiforme (GBM) patients were acquired from The Cancer Genome Atlas (TCGA), and the genetic alterations and expression levels of the selected genes were analyzed. Results: We identified six distinct KDR mutations in the LGG patients and 18 distinct KDR mutations in the GBM patients, including missense and nonsense mutations, frame shift deletion and altered splice region. Furthermore, VEGFA and CXCL8 were significantly overexpressed within GBM patients. Conclusions: VEGFA and CXCL8 are important factors for angiogenesis, which are suggested to have significant roles during tumorigenesis. Our results provide further evidence that VEGFA and CXCL8 could induce angiogenesis and promote LGG to progress into GBM. These findings could be useful in developing novel targeted therapeutics approaches in the future.
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Vasconcelos, Vivian Castro Antunes, Gustavo Jacob Lourenço, Angelo Borsarelli Carvalho Brito, Victor Leal Vasconcelos, Marcos Vinicius Calfat Maldaun, Helder Tedeschi, Suely Kaue Nagashi Marie, Sueli Mieko Oba Shinjo, and Carmen Silvia Passos Lima. "Associations of VEGFA and KDR single-nucleotide polymorphisms and increased risk and aggressiveness of high-grade gliomas." Tumor Biology 41, no. 9 (September 2019): 101042831987209. http://dx.doi.org/10.1177/1010428319872092.
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Angiogenesis, induced by the vascular endothelial growth factor A through its ligation to the vascular endothelial growth receptor 2, has been described as a crucial point in high-grade glioma development. The aim of this study was to evaluate the influence of VEGFA–2578C/A, −2489C/T, −1154G/A, −634G/C, and −460C/T, and KDR–604T/C, −271G/A, +1192G/A, and +1719A/T single-nucleotide polymorphisms on risk and clinicopathological aspects of high-grade glioma. This case–control study enrolled 205 high-grade glioma patients and 205 controls. Individuals with VEGFA–2578 CC or CA, VEGFA–1154 GG, VEGFA–634 GC or CC, and VEGFA–460 CT or TT genotypes were under 2.56, 1.53, 1.54, and 1.84 increased risks of high-grade glioma, compared to others, respectively. And 1.61, 2.66, 2.52, 2.53, and 2.02 increased risks of high-grade glioma were seen in individuals with VEGFA–2578 CC plus VEGFA–1154 GG, VEGFA–2578 CC or CA plus VEGFA–634 GC or CC, VEGFA–2578 CC or CA plus VEGFA–460 CT or TT, VEGFA–1154 GG or GA plus VEGFA–634 GC or CC, and VEGFA 634 GC or CC plus VEGFA–460 CT or TT combined genotypes, respectively, when compared to others. The “CAGT” haplotype of KDR single-nucleotide polymorphisms was more common in patients with grade IV than in those with grade III tumors, and individuals carrying this haplotype were at 1.76 increased risk of developing grade IV tumors than others. We present, for the first time, preliminary evidence that VEGFA–2578C/A and VEGFA–1154G/A single-nucleotide polymorphisms increases high-grade glioma risk, and “CAGT” haplotype of the KDR gene alters high-grade glioma aggressiveness and risk of grade IV tumors in Brazil.
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Степанов, И. А., В. А. Белобородов, and М. А. Шамеева. "Molecular and cellular mechanisms of glioblastoma resistance to vascular endothelial growth factor inhibitors." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 3() (September 16, 2020): 137–45. http://dx.doi.org/10.25557/0031-2991.2020.03.137-145.
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Представлен обзор современных источников литературы, посвященных изучению молекулярных и клеточных механизмов резистентности глиобластомы к антиангиогенным лекарственным средствам. Ангиогенез представляет собой важнейший патофизиологический механизм роста и прогрессирования глиобластомы за счет активного развития микрососудистой сети. Ускоренное развитие микрососудистой сети в глиобластоме происходит благодаря синтезу опухолевыми клетками большого количества фактора роста эндотелия сосудов (Vascular Endothelial Growth Factor, VEGF). Среди основных молекулярных и клеточных механизмов лекарственной устойчивости глиобластомы к анти-VEGF агентам принято относить VEGF-независимые пути ангиогенеза, активность клеток костного мозга и перицитов, а также сосудистую кооперацию, периваскулярную инвазию и феномен аутофагии. Изложены современные данные о рациональном и наиболее эффективном использовании анти-VEGF-лекарственных средств у пациентов с глиомами высокой степени злокачественности. Обозначены актуальные, остающиеся нерешенными вопросы, что обусловливает необходимость проведения дальнейших экспериментальных и клинических исследований, посвященных изучению механизмов лекарственной устойчивости глиобластомы к анти-VEGF-препаратам. This state-of-the-art review focuses on molecular and cellular factors associated with glioblastoma resistance to antiangiogenic drugs. Angiogenesis is an important pathophysiological mechanism for the growth and progression of glioblastoma facilitated by active development of microvasculature. The accelerated development of the microvascular network in glioblastoma occurs due to the synthesis of a large number of vascular endothelial growth factor (VEGF) by tumor cells Among the major molecular and cellular factors, glioblastoma drug resistance to anti-VEGF agents is commonly attributed to VEGF-independent pathways of angiogenesis, bone marrow cell and pericyte activity as well as to vascular co-option, perivascular invasion, and the phenomenon of autophagy. The authors provided current data on the rational and most effective use of anti-VEGF drugs for patients with high-grade gliomas. Relevant unsolved problems associated with drug resistance of glioblastoma to anti-VEGF drugs were highlighted.
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Kikuchi, Ryogo, Ryo Ueda, Katsuya Saito, Shunsuke Shibao, Hideaki Nagashima, Ryota Tamura, Yukina Morimoto, et al. "A Pilot Study of Vaccine Therapy with Multiple Glioma Oncoantigen/Glioma Angiogenesis-Associated Antigen Peptides for Patients with Recurrent/Progressive High-Grade Glioma." Journal of Clinical Medicine 8, no. 2 (February 20, 2019): 263. http://dx.doi.org/10.3390/jcm8020263.
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High-grade gliomas (HGGs) carry a dismal prognosis despite current treatments. We previously confirmed the safety and immunogenicity of a vaccine treatment targeting tumor angiogenesis with synthetic peptides, for vascular endothelial growth factor receptor (VEGFR) epitopes in recurrent HGG patients. In this study, we evaluated a novel vaccine therapy targeting not only tumor vasculature but also tumor cells, using multiple glioma oncoantigen (GOA)/glioma angiogenesis-associated antigen (GAAA) peptides in HLA-A2402+ recurrent/progressive HGG patients. The vaccine included peptide epitopes from four GOAs (LY6K, DEPDC1, KIF20A, and FOXM1) and two GAAAs (VEGFR1 and VEGFR2). Ten patients received subcutaneous vaccinations. The primary endpoint was the safety of the treatment. T-lymphocyte responses against GOA/GAAA epitopes and treatment response were evaluated secondarily. The treatment was well tolerated without any severe systemic adverse events. The vaccinations induced immunoreactivity to at least three vaccine-targeted GOA/GAAA in all six evaluable patients. The median overall survival time in all patients was 9.2 months. Five achieved progression-free status lasting at least six months. Two recurrent glioblastoma patients demonstrated stable disease. One patient with anaplastic oligoastrocytoma achieved complete response nine months after the vaccination. Taken together, this regimen was well tolerated and induced robust GOA/GAAA-specific T-lymphocyte responses in recurrent/progressive HGG patients.
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Gilbert, M. R., M. Wang, K. Aldape, A. Lassman, A. G. Sorensen, T. Mikkelson, M. Groves, M. Werner-Wasik, W. Regine, and M. Mehta. "RTOG 0625: A phase II study of bevacizumab with irinotecan in recurrent glioblastoma (GBM)." Journal of Clinical Oncology 27, no. 15_suppl (May 20, 2009): 2011. http://dx.doi.org/10.1200/jco.2009.27.15_suppl.2011.
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2011 Background: Angiogenesis is a hallmark of GBM, making the tumor vasculature an attractive therapeutic target. In gliomas, vascular endothelial growth factor (VEGF) promotes both angiogenesis and invasion of tumor cells. Bevacizumab is a humanized monoclonal antibody against VEGF-A that rapidly reduces the concentration of VEGF in the circulation. Irinotecan may enhance efficacy by synergistic tumor endothelial cell death or improved tumor delivery of the chemotherapy via “normalized” tumor vasculature. Prior studies of this combination demonstrated high radiographic response and 6-month progression free (6-mPFS) rates. This study was designed to determine the efficacy and safety of this regimen in the cooperative group setting. Methods: Eligibility included age ≥ 18, centrally confirmed GBM or gliosarcoma, progressive or recurrent disease. Enzyme-inducing anticonvulsants were not allowed. Treatment was intravenous bevacizumab 10 mg/kg and irinotecan 200 mg/m2 every 2 weeks. Accrual goal was 57 eligible patients. Primary endpoint was 6-mPFS rate where an estimate of ≥ 35% would define efficacy (15% improvement over historical data). Results: Full enrollment (57) was achieved, median age was 57, median KPS was 80; all had prior radiation and temozolomide treatment. The 6m-PFS rate was 37% (95% CI: 24–50%), with 21 of 57 patients progression-free at 6 months. Moderate toxicity was noted with 21(37%) grade 3, seven (12%) grade 4, and one (<2%) treatment-related death (intracranial hemorrhage). There were six episodes of venous thrombosis, 14 episodes of grade 3 or 4 hematologic toxicity, predominantly lymphopenia (7), and neutropenia (4), no opportunistic infections or febrile neutropenia were noted. Other toxicities included fatigue (9), diarrhea (2), and hypertension (2). Conclusions: These results, in the cooperative group context, corroborate the efficacy of the bevacizumab and irinotecan combination for recurrent GBM with the 6m-PFS surpassing the predetermined efficacy threshold. Previously described toxicities were confirmed with a moderately high rate of venous thrombosis, one intracranial hemorrhage, and moderate hypertension. Studies to determine the contribution of the cytotoxic agent to efficacy and the role of bevacizumab in newly diagnosed GBM are planned. [Table: see text]
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Friedland, D. M., S. A. Ali, A. Ahmad, M. Rahman, G. Bejjani, and M. Braffet. "Bevacizumab plus irinotecan therapy in relapsed, heavily pre-treated malignant glioma: A case series." Journal of Clinical Oncology 25, no. 18_suppl (June 20, 2007): 12500. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.12500.
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12500 Background: Endothelial proliferation has been recognized as a marker of high grade or aggressive glioma in several grading classifications and it has been demonstrated that the degree of microvascularity as assessed by the endothelial cell/capillary density correlates well with the biologic aggressiveness of these tumors. These features suggest that high grade gliomas are a suitable target for angiogenesis inhibiting therapies. Bevacizumab (B) is a humanized IgG1 monoclonal antibody to VEGF that has been shown to have activity in malignant gliomas when combined with irinotecan (CPT-11), a topoisomerase 1 inhibitor. Methods: We report a case series of 10 patients with recurrent, heavily pre-treated malignant glioma who were treated with the combination of B and CPT-11. Nine patients had WHO grade 4 tumors while one had a grade 3 lesion. All patients had failed standard therapy with primary resection followed by adjuvant chemotherapy and radiation. Most had also failed additional resection, chemotherapy and radiation after their initial relapse. The mean number of failed therapies in addition to adjuvant therapy prior to starting B and CPT-11 was 3 (range 1–6) and the median ECOG performance status was 2 (range 1–3). Nine patients were started on B at a dose of 5 mg/kg every 2 weeks and were given CPT-11 at a dose of 125 mg/m2 every week for 3 weeks with 1 week off. The tenth patient received B at a dose of 10 mg/kg but with CPT-11 at 125 mg/m2 every 2 weeks. Results: This regimen was well tolerated with no CNS hemorrhages or >grade 1 bleeding. One patient had treatment held for repair of an anal fissure but then had it restarted. One patient had a DVT while on therapy. The objective response rate was 80% (8 PR and 2 SD).The median progression- free interval on treatment is 25 weeks with 5 patients still having a response at the time of this report. In patients with progressive disease, the median time to progression is 25 weeks. The median overall survival has not been reached, and exceeds 6 months. There has been one death due to disease progression. Conclusion: The combination of B and CPT-11 is safe and has excellent activity even in this relapsed, heavily pre-treated population of patients with high grade malignant glioma, most of whom would not be candidates for clinical trials. No significant financial relationships to disclose.
Dissertations / Theses on the topic "Angiogenesis, high grade gliomas, VEGF"
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CUPPINI, LUCIA. "Antiangiogenic therapies for malignant gliomas: new markers for targeted treatment." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2012. http://hdl.handle.net/10281/28473.
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Bevacizumab has shown activity in different tumor types, including high grade gliomas (HGG). However, the use of bevacizumab and other antiangiogenic drugs in the clinical setting limited by the lack of markers to predict responses.
We report that the combined treatment with bevacizumab and irinotecan is effective in recurrent HGG patients, particularly in those with local disease, with mild toxicity. Median OS and PFS were 33 and 18 weeks, respectively. PFS at 6 and 12 months were 32% and 12%. OS at 6 months was 60%. Patients with distant intracerebral disease or leptomeningeal dissemination at baseline magnetic resonance had shorter PFS and OS.
We analyzed circulating endothelial cells (CECs) and their progenitors (CEPs), as previous studies supported their involvement in responses to bevacizumab. Higher levels of CD109+ CECs, CEPs and CD45dimCD34+CD133+ hematopoietic committed progenitors before treatment were associated with longer PFS. Moreover, long-term responders showed higher baseline CD109+ CECs and CD45dimCD34+VEGFR2+ hematopoietic progenitors.
These findings pave the way for larger studies further addressing the potential of CECs and CEPs as biomarkers to target patient populations that may benefit from bevacizumab and possibly other antiangiogenic drugs.
Book chapters on the topic "Angiogenesis, high grade gliomas, VEGF"
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Drappatz, Jan, Andrew D. Norden, and Patrick Y. Wen. "Aflibercept (VEGF-Trap) in High-Grade Gliomas." In Controversies in Neuro-Oncology (Avastin and Malignant Gliomas), 171–75. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/978160805132811001010171.
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R. Parashar, Tanvi, Febina Ravindran, and Bibha Choudhary. "DNA Damage Repair Genes and Noncoding RNA in High-Grade Gliomas and Its Clinical Relevance." In CNS Malignancies [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97074.
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Gliomas are the most common malignant tumors originating from the glial cells in the central nervous system. Grades III and IV, considered high-grade gliomas occur at a lower incidence (1.5%) but have higher mortality. Several genomic alterations like IDH mutation, MGMT mutation, 1p19q Codeletion, and p53 mutations have been attributed to its pathogenicity. Recently, several noncoding RNAs have also been identified to alter the expression of crucial genes. Current chemotherapeutic drugs include temozolomide targeting hypermethylated MGMT, a DNA repair protein; or bevacizumab, which targets VEGF. This book chapter delves deeper into the DNA damage repair pathway including its correlation with survival and the regulation of these genes by noncoding RNAs. Novel therapeutic drugs being developed are also highlighted.