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首页> 外文期刊>Radiotherapy and oncology: Journal of the European Society for Therapeutic Radiology and Oncology >Residual DNA and chromosomal damage in ex vivo irradiated blood lymphocytes correlated with late normal tissue response to breast radiotherapy.
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Residual DNA and chromosomal damage in ex vivo irradiated blood lymphocytes correlated with late normal tissue response to breast radiotherapy.

机译：离体辐射血液淋巴细胞中的残留DNA和染色体损伤与晚期正常组织对乳腺放射治疗的反应有关。

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摘要

PURPOSE: To test the association of DNA double-strand break (DSB) repair and chromosomal radiosensitivity in ex vivo irradiated blood lymphocytes with late-onset normal tissue responses following breast radiotherapy. METHODS: Breast cancer patients with minimal (controls) or marked late radiotherapy changes (cases) were retrospectively selected. DSB were quantified by gammaH2AX/53BP1 immunofluorescence microscopy 0.5 and 24 h after exposure of unstimulated blood lymphocytes to 0.5 and 4 Gy X-rays, respectively. Chromosomal aberrations were scored in blood lymphocyte metaphases after 6 Gy X-rays. RESULTS: Despite similar foci levels at 0.5 h in cases (n=7) and controls (n=7), foci levels 24 h after 4 Gy irradiation differed significantly between them (foci per cell were 12.8 in cases versus 10.2 in controls, p=0.004). Increased chromosomal radiosensitivity was also observed in cases (aberrations per cell were 5.84 in cases versus 3.79 in controls, p=0.001) with exchange and deletion type aberrations contributing equally to the difference between cases and controls. Residual foci correlated with formation of deletions (Spearman's R=0.589, p=0.027) but not exchanges (R=0.367, p=0.197) in blood lymphocytes from the same patients. CONCLUSIONS: Higher levels of exchange type aberrations observed among radiosensitive breast cancer patients suggest a role for DSB misrepair, in addition to residual damage, as determinants of late normal tissue damage. Correlation of residual foci levels with deletion type aberration yields in the same cohort confirms their mechanistic linkage.
机译：目的：测试离体辐射血液淋巴细胞中DNA双链断裂（DSB）修复和染色体放射敏感性与乳腺癌放疗后迟发性正常组织反应的关系。方法：回顾性选择乳腺癌患者（对照）或晚期放疗变化明显（病例）。在未刺激的血液淋巴细胞分别暴露于0.5和4 Gy X射线后0.5和24小时，通过gammaH2AX / 53BP1免疫荧光显微镜对DSB进行定量。 6 Gy X射线后，在血液淋巴细胞中期对染色体畸变进行评分。结果：尽管病例（n = 7）和对照组（n = 7）在0.5 h处的病灶水平相似，但4 Gy照射后24 h的病灶水平之间却有显着差异（病例中每个细胞的病灶为12.8，对照组为10.2，p = 0.004）。在病例中也观察到了染色体放射敏感性的增加（病例中每个细胞的畸变为5.84，对照组为3.79，p = 0.001），而交换和缺失型畸变同样地导致了病例与对照之间的差异。残留病灶与同一患者血液淋巴细胞中的缺失形成相关（Spearman R = 0.589，p = 0.027），但与交换不相关（R = 0.367，p = 0.197）。结论：放射敏感性乳腺癌患者中观察到的更高水平的交换型像差表明，DSB失修是造成残余正常组织损伤的重要因素，此外还有残余损伤。在同一队列中，残留病灶水平与缺失型畸变的相关性证实了它们的机制联系。

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