کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3908462 | 1251177 | 2013 | 6 صفحه PDF | دانلود رایگان |
PurposeTo investigate the genomic signaling that defines sensitive lymphocytes to radiation and if such molecular profiles are consistent with clinical toxicity; trying to disclose the radiobiology mechanisms behind these cellular processes.Patients and methodsTwelve consecutive patients suffering from locally advanced breast cancer and treated with high-dose hyperfractionated radiotherapy were recruited. Initial DNA damage was measured by pulsed-field gel electrophoresis and radiation-induced apoptosis was measured by flow cytometry. Gene expression was assessed by DNA microarray.ResultsThirty-four constitutive genes segregated patients with lower DNA-double strand break from those patients with higher DNA-double strand break (p < 0.01). Forty-two genes segregated patients according to radiation-induced apoptosis (p < 0.01). We found common canonical pathways and common biological processes significantly regulated between both set of genes.ConclusionWe introduced new data in the field of molecular genomics regarding to the relation established between radiation toxicity and these predictive factors to radiation injury.
Journal: The Breast - Volume 22, Issue 1, February 2013, Pages 28–33