Parshad R, Price F M, Bohr V A, Cowans K H, Zujewski J A, Sanford K K
Department of Pathology, Howard University College of Medicine, Washington, DC 20059, USA.
Br J Cancer. 1996 Jul;74(1):1-5. doi: 10.1038/bjc.1996.307.
Women with breast cancer and a family history of breast cancer and some with sporadic breast cancer are deficient in the repair of radiation-induced DNA damage compared with normal donors with no family history of breast cancer. DNA repair was measured indirectly by quantifying chromatid breaks in phytohaemagglutinin (PHA)-stimulated blood lymphocytes after either X-irradiation or UV-C exposure, with or without post treatment with the DNA repair inhibitor, 1-beta-D-arabinofuranosylcytosine (ara-C). We have correlated chromatid breaks with unrepaired DNA strand breaks using responses to X-irradiation of cells from xeroderma pigmentosum patients with well-characterised DNA repair defects or responses of repair-deficient mutant Chinese hamster ovary (CHO) cells with or without transfected human DNA repair genes. Deficient DNA repair appears to be a predisposing factor in familial breast cancer and in some sporadic breast cancers.
与无乳腺癌家族史的正常供体相比，患有乳腺癌且有乳腺癌家族史的女性以及一些散发性乳腺癌患者在修复辐射诱导的DNA损伤方面存在缺陷。通过对经植物血凝素（PHA）刺激的血液淋巴细胞在X射线照射或紫外线C照射后（无论是否使用DNA修复抑制剂1-β-D-阿拉伯呋喃糖基胞嘧啶（ara-C）进行后处理）的染色单体断裂进行定量，间接测量DNA修复情况。我们利用对具有明确DNA修复缺陷的着色性干皮病患者细胞的X射线照射反应，或对有或无转染人DNA修复基因的修复缺陷型中国仓鼠卵巢（CHO）细胞的反应，将染色单体断裂与未修复的DNA链断裂相关联。DNA修复缺陷似乎是家族性乳腺癌和一些散发性乳腺癌的一个易感因素。
