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1TBX3基因在不同分子亚型乳腺癌中的表达及临床意义显示文摘目的研究TBX3基因在不同分子亚型的乳腺癌中的表达情况。方法采用免疫组化方法,检测乳腺癌、乳腺良性肿瘤和癌旁组织标本中TBX3的表达。结果乳腺癌中TBX3表达率明显高于良性肿瘤和癌旁组织(分别为75.49%、45.55%、30.00%,P均<0.05);中晚期乳腺癌TBX3阳性表达率明显高于早期乳腺癌(Ⅰ、Ⅱ、Ⅲ期乳腺癌其阳性表达率分别为64.44%、90.32%、85.00%,P<0.05);ER阳性者TBX3表达率高于ER阴性者(分别为82.86%、59.38%,P<0.05);Ki-67高表达者TBX3表达率高于低表达者(分别为86.79%、63.27%,P<0.05);Basal-like型TBX3阳性表达率最低(36.36%);luminal A型、luminal B型、Her-2阳性型分别为82.50%、81.82%、72.22%。结论 TBX3基因可能是乳腺癌的基因靶点;TBX3可作为luminal型乳腺癌恶性标志物之一。黄燕 丁罡 陈峰 陆云姝 张明 梁洪享 吴克瑾 2014实用癌症杂志2014,29,10:2
2Mechanism of DNA damage tolerance显示文摘DNA damage may compromise genome integrity and lead to cell death. Cells have evolved a variety of processes to respond to DNA damage including damage repair and tolerance mechanisms, as well as damage checkpoints. The DNA damage tolerance(DDT) pathway promotes the bypass of single-stranded DNA lesions encountered by DNA polymerases during DNA replication. This prevents the stalling of DNA replication. Two mechanistically distinct DDT branches have been characterized. One is translesion synthesis(TLS) in which a replicative DNA polymerase is temporarily replaced by a specialized TLS polymerase that has the ability to replicate across DNA lesions. TLS is mechanistically simple and straightforward, but it is intrinsically error-prone. The other is the error-free template switching(TS) mechanism in which the stalled nascent strand switches from the damaged template to the undamaged newly synthesized sister strand for extension past the lesion. Error-free TS is a complex but preferable process for bypassing DNA lesions. However, our current understanding of this pathway is sketchy. An increasing number of factors are being found to participate or regulate this important mechanism, which is the focus of this editorial.Xin Bi 2015World Journal of Biological Chemistry2015,6,3:0
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