Department of Neurosurgery, Fondazione Policlinico Universitario A. Gemelli IRCCS, 00168 Rome, Italy.
Department of Neurosurgery, F. Spaziani Hospital, 03100 Frosinone, Italy.
Int J Mol Sci. 2024 Aug 9;25(16):8700. doi: 10.3390/ijms25168700.
Glioblastoma (GBM) is a primary CNS tumor that is highly lethal in adults and has limited treatment options. Despite advancements in understanding the GBM biology, the standard treatment for GBM has remained unchanged for more than a decade. Only 6.8% of patients survive beyond five years. Telomerase, particularly the hTERT promoter mutations present in up to 80% of GBM cases, represents a promising therapeutic target due to its role in sustaining telomere length and cancer cell proliferation. This review examines the biology of telomerase in GBM and explores potential telomerase-targeted therapies. We conducted a systematic review following the PRISMA-P guidelines in the MEDLINE/PubMed and Scopus databases, from January 1995 to April 2024. We searched for suitable articles by utilizing the terms "GBM", "high-grade gliomas", "hTERT" and "telomerase". We incorporated studies addressing telomerase-targeted therapies into GBM studies, excluding non-English articles, reviews, and meta-analyses. We evaluated a total of 777 records and 46 full texts, including 36 studies in the final review. Several compounds aimed at inhibiting hTERT transcription demonstrated promising preclinical outcomes; however, they were unsuccessful in clinical trials owing to intricate regulatory pathways and inadequate pharmacokinetics. Direct hTERT inhibitors encountered numerous obstacles, including a prolonged latency for telomere shortening and the activation of the alternative lengthening of telomeres (ALT). The G-quadruplex DNA stabilizers appeared to be potential indirect inhibitors, but further clinical studies are required. Imetelstat, the only telomerase inhibitor that has undergone clinical trials, has demonstrated efficacy in various cancers, but its efficacy in GBM has been limited. Telomerase-targeted therapies in GBM is challenging due to complex hTERT regulation and inadequate inhibitor pharmacokinetics. Our study demonstrates that, despite promising preclinical results, no Telomerase inhibitors have been approved for GBM, and clinical trials have been largely unsuccessful. Future strategies may include Telomerase-based vaccines and multi-target inhibitors, which may provide more effective treatments when combined with a better understanding of telomere dynamics and tumor biology. These treatments have the potential to be integrated with existing ones and to improve the outcomes for patients with GBM.
胶质母细胞瘤(GBM)是一种原发于中枢神经系统的肿瘤,在成年人中具有高度致命性,且治疗选择有限。尽管对 GBM 生物学的认识有所进步,但 GBM 的标准治疗方法十年来一直没有改变。只有 6.8%的患者能存活超过五年。端粒酶,特别是在高达 80%的 GBM 病例中存在的 hTERT 启动子突变,由于其在维持端粒长度和癌细胞增殖方面的作用,代表了一个有前途的治疗靶点。本综述探讨了端粒酶在 GBM 中的生物学特性,并探讨了潜在的端粒酶靶向治疗方法。我们按照 PRISMA-P 指南,在 MEDLINE/PubMed 和 Scopus 数据库中进行了系统综述,检索时间从 1995 年 1 月至 2024 年 4 月。我们使用“GBM”、“高级别胶质瘤”、“hTERT”和“端粒酶”等术语搜索了合适的文章。我们将针对 GBM 研究中靶向端粒酶治疗的研究纳入了研究,排除了非英语文章、综述和荟萃分析。我们总共评估了 777 条记录和 46 篇全文,其中 36 项研究纳入最终综述。几种旨在抑制 hTERT 转录的化合物在临床前研究中显示出了有前景的结果;然而,由于复杂的调控途径和不理想的药代动力学,它们在临床试验中并未成功。直接的 hTERT 抑制剂也遇到了许多障碍,包括端粒缩短潜伏期延长和端粒的非经典延长(ALT)的激活。G-四链体 DNA 稳定剂似乎是潜在的间接抑制剂,但还需要进一步的临床研究。唯一经过临床试验的端粒酶抑制剂伊美替康在各种癌症中表现出疗效,但在 GBM 中的疗效有限。由于复杂的 hTERT 调控和不理想的抑制剂药代动力学,GBM 的端粒酶靶向治疗具有挑战性。我们的研究表明,尽管有很有前景的临床前结果,但没有一种端粒酶抑制剂被批准用于 GBM,临床试验也大多失败。未来的策略可能包括基于端粒酶的疫苗和多靶点抑制剂,当与更好地了解端粒动力学和肿瘤生物学相结合时,这些抑制剂可能提供更有效的治疗方法。这些治疗方法有可能与现有的治疗方法相结合,改善 GBM 患者的治疗效果。