Department of Radiation Oncology, Rogel Cancer Center, University of Michigan Medical School, 1301 Catherine Street, Ann Arbor, MI, 48109, USA.
Department of Pediatrics, Division of Pediatric Hematology-Oncology, University of Michigan Medical School, Ann Arbor, MI 48109, USA.
Neoplasia. 2023 Mar;37:100881. doi: 10.1016/j.neo.2023.100881. Epub 2023 Jan 30.
Diffuse intrinsic pontine glioma (DIPG) is a rare but highly lethal pediatric and adolescent tumor located in the pons of the brainstem. DIPGs harbor unique and specific pathological and molecular alterations, such as the hallmark lysine 27-to-methionine (H3K27M) mutation in histone H3, which lead to global changes in the epigenetic landscape and drive tumorigenesis. While fractionated radiotherapy, the current standard of care, improves symptoms and delays tumor progression, DIPGs inevitably recur, and despite extensive efforts chemotherapy-driven radiosensitization strategies have failed to improve survival. Advances in our understanding of the role of epigenetics in the cellular response to radiation-induced DNA damage, however, offer new opportunities to develop combinational therapeutic strategies selective for DIPGs expressing H3K27M. In this review, we provide an overview of preclinical studies that explore potential radiosensitization strategies targeting the unique epigenetic landscape of H3K27M mutant DIPG. We further discuss opportunities to selectively radiosensitize DIPG through strategic inhibition of the radiation-induced DNA damage response. Finally, we discuss the potential for using radiation to induce anti-tumor immune responses that may be potentiated in DIPG by radiosensitizing-therapeutic strategies.
弥漫性内在脑桥神经胶质瘤(DIPG)是一种罕见但高度致命的儿科和青少年肿瘤,位于脑干的脑桥中。DIPGs 具有独特而特定的病理和分子改变,例如组蛋白 H3 中的标志性赖氨酸 27 到蛋氨酸(H3K27M)突变,这导致表观遗传景观的全局变化,并驱动肿瘤发生。虽然分次放疗是目前的标准治疗方法,可以改善症状并延缓肿瘤进展,但 DIPGs 不可避免地会复发,尽管进行了广泛的努力,以化疗为基础的放射增敏策略未能提高生存率。然而,我们对表观遗传学在细胞对辐射诱导的 DNA 损伤的反应中的作用的理解的进步,为开发针对表达 H3K27M 的 DIPG 的组合治疗策略提供了新的机会。在这篇综述中,我们提供了对探索针对 H3K27M 突变 DIPG 独特表观遗传景观的潜在放射增敏策略的临床前研究的概述。我们进一步讨论了通过有策略地抑制辐射诱导的 DNA 损伤反应来选择性放射增敏 DIPG 的机会。最后,我们讨论了利用辐射诱导抗肿瘤免疫反应的潜力,这种反应可能通过放射增敏治疗策略在 DIPG 中得到增强。