Background

Radiation therapy (RT) is a key anti-cancer treatment that involves using ionizing radiation to kill tumor cells. However, this therapy can lead to short- and long-term adverse effects due to radiation exposure of surrounding normal tissue. The type of DNA damage inflicted by radiation therapy determines its effectiveness. High levels of genotoxic damage can lead to cell cycle arrest, senescence, and cell death, but many tumors can cope with this damage by activating protective mechanisms. Intrinsic and acquired radioresistance are major causes of tumor recurrence, and understanding these mechanisms is crucial for cancer therapy. The mechanisms behind radioresistance involve processes like hypoxia response, cell proliferation, DNA repair, apoptosis inhibition, and autophagy.

Conclusion

Here we briefly review the role of genetic and epigenetic factors involved in the modulation of DNA repair and DNA damage response that promote radioresistance. In addition, leveraging our recent results on the effects of low dose rate (LDR) of ionizing radiation on Drosophila melanogaster we discuss how this model organism can be instrumental in the identification of conserved factors involved in the tumor resistance to RT.

中文翻译：

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肿瘤放射抗性中的 DNA 修复：来自果蝇遗传学的见解

背景

放射治疗 (RT) 是一种关键的抗癌治疗方法，涉及使用电离辐射杀死肿瘤细胞。然而，由于周围正常组织受到辐射，这种疗法可能会导致短期和长期的不良反应。放射治疗造成的 DNA 损伤类型决定了其有效性。高水平的基因毒性损伤可导致细胞周期停滞、衰老和细胞死亡，但许多肿瘤可以通过激活保护机制来应对这种损伤。内在和获得性放射抗性是肿瘤复发的主要原因，了解这些机制对于癌症治疗至关重要。放射抗性背后的机制涉及缺氧反应、细胞增殖、DNA 修复、细胞凋亡抑制和自噬等过程。

结论

在这里，我们简要回顾一下遗传和表观遗传因素在促进放射抗性的 DNA 修复和 DNA 损伤反应调节中的作用。此外，利用我们最近关于电离辐射低剂量率 (LDR) 对果蝇影响的结果，我们讨论了这种模型生物如何有助于识别与肿瘤对 RT 耐药性相关的保守因子。