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开发一种针对替莫唑胺耐药性脑胶质瘤的临床相关增敏剂。

Developing a clinically relevant radiosensitizer for temozolomide-resistant gliomas.

机构信息

Department of Neurological Surgery, Keck School of Medicine (KSOM), University of Southern California (USC), Los Angeles, California (CA), United States of America.

Haiphong University School of Pharmacy, Haiphong, Vietnam.

出版信息

PLoS One. 2020 Sep 3;15(9):e0238238. doi: 10.1371/journal.pone.0238238. eCollection 2020.

Abstract

The prognosis for patients with glioblastoma (GB) remains grim. Concurrent temozolomide (TMZ) radiation-the cornerstone of glioma control-extends the overall median survival of GB patients by only a few months over radiotherapy alone. While these survival gains could be partly attributed to radiosensitization, this benefit is greatly minimized in tumors expressing O6-methylguanine DNA methyltransferase (MGMT), which specifically reverses O6-methylguanine lesions. Theoretically, non-O6-methylguanine lesions (i.e., the N-methylpurine adducts), which represent up to 90% of TMZ-generated DNA adducts, could also contribute to radiosensitization. Unfortunately, at concentrations attainable in clinical practice, the alkylation capacity of TMZ cannot overwhelm the repair of N-methylpurine adducts to efficiently exploit these lesions. The current therapeutic application of TMZ therefore faces two main obstacles: (i) the stochastic presence of MGMT and (ii) a blunted radiosensitization potential at physiologic concentrations. To circumvent these limitations, we are developing a novel molecule called NEO212-a derivatization of TMZ generated by coupling TMZ to perillyl alcohol. Based on gas chromatography/mass spectrometry and high-performance liquid chromatography analyses, we determined that NEO212 had greater tumor cell uptake than TMZ. In mouse models, NEO212 was more efficient than TMZ at crossing the blood-brain barrier, preferentially accumulating in tumoral over normal brain tissue. Moreover, in vitro analyses with GB cell lines, including TMZ-resistant isogenic variants, revealed more potent cytotoxic and radiosensitizing activities for NEO212 at physiologic concentrations. Mechanistically, these advantages of NEO212 over TMZ could be attributed to its enhanced tumor uptake presumably leading to more extensive DNA alkylation at equivalent dosages which, ultimately, allows for N-methylpurine lesions to be better exploited for radiosensitization. This effect cannot be achieved with TMZ at clinically relevant concentrations and is independent of MGMT. Our findings establish NEO212 as a superior radiosensitizer and a potentially better alternative to TMZ for newly diagnosed GB patients, irrespective of their MGMT status.

摘要

胶质母细胞瘤(GB)患者的预后仍然严峻。替莫唑胺(TMZ)放疗联合治疗——神经胶质瘤控制的基石——仅将 GB 患者的总中位生存期延长了几个月,而单独放疗则无法延长。虽然这些生存获益部分归因于放射增敏作用,但在表达 O6-甲基鸟嘌呤 DNA 甲基转移酶(MGMT)的肿瘤中,这种益处大大降低,因为 MGMT 专门逆转 O6-甲基鸟嘌呤损伤。从理论上讲,非 O6-甲基鸟嘌呤损伤(即 N-甲基嘌呤加合物),占 TMZ 产生的 DNA 加合物的 90%左右,也可能有助于放射增敏。不幸的是,在临床实践中可达到的浓度下,TMZ 的烷化能力无法克服 N-甲基嘌呤加合物的修复,从而无法有效地利用这些损伤。因此,TMZ 的当前治疗应用面临两个主要障碍:(i)MGMT 的随机存在,以及(ii)在生理浓度下放射增敏潜力减弱。为了规避这些限制,我们正在开发一种名为 NEO212 的新型分子,它是通过将 TMZ 与胡椒醇偶联而生成的 TMZ 衍生物。基于气相色谱/质谱和高效液相色谱分析,我们确定 NEO212 比 TMZ 具有更高的肿瘤细胞摄取率。在小鼠模型中,NEO212 比 TMZ 更有效地穿过血脑屏障,优先在肿瘤组织中积累,而不是在正常脑组织中积累。此外,与包括 TMZ 耐药同基因变体在内的 GB 细胞系的体外分析表明,NEO212 在生理浓度下具有更强的细胞毒性和放射增敏作用。从机制上讲,NEO212 优于 TMZ 的这些优势可以归因于其增强的肿瘤摄取,这可能导致在等效剂量下更广泛的 DNA 烷化,最终允许更好地利用 N-甲基嘌呤损伤进行放射增敏。在临床相关浓度下,TMZ 无法达到这种效果,并且与 MGMT 无关。我们的研究结果确立了 NEO212 作为一种优越的放射增敏剂,并且是新诊断的 GB 患者的 TMZ 的潜在更好替代物,无论其 MGMT 状态如何。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbf8/7470340/a8ce2773ef77/pone.0238238.g001.jpg

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