Revisiting DNA damage repair, p53-mediated apoptosis and cisplatin sensitivity in germ cell tumors
Revisiting DNA damage repair, p53-mediated apoptosis and cisplatin sensitivity in germ cell tumors
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DOI：
10.1387/ijdb.130135mb
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发表时间：
2013-01-01
影响因子：
0.7
通讯作者：
Barchi, Marco
中科院分区：
文献类型：
--
作者：
Cavallo, Francesca;Feldman, Darren R.;Barchi, Marco
睾丸生殖细胞肿瘤（TGCT），即睾丸生殖细胞瘤和非睾丸生殖细胞瘤，占男性所有肿瘤的1%至3%。它们是年轻白色男性中最常见的癌症，并且对基于顺铂的化疗的反应性是独特的。出于这个原因，TGCT被认为是治愈疾病的模型。然而，到目前为止，这种对DNA损伤剂的特殊反应性背后的分子机制仍不清楚。一个超敏的凋亡反应，以及在修复顺铂诱导的DNA损伤的能力降低可能会解释这种行为。在这篇综述中，建立在最近的研究结果p53诱导的细胞凋亡和DNA修复机制的TGCTs，我们将讨论的分子基础，驱动肿瘤顺铂的敏感性，强调新的治疗方法，提出最终限制肿瘤复发，并针对TGCTs是无反应的标准治疗。
Testicular germ cell tumors (TGCTs), ie, seminomas and nonseminomas, account for 1% to 3% of all neoplasms in men. They are the most common cancer in young white males and are unique in their responsiveness to cisplatin-based chemotherapy. For this reason, TGCTs are considered a model for curative disease. However, up to now, the molecular mechanisms behind this exceptional responsiveness to DNA-damaging agents have remained unclear. A hypersensitive apoptotic response, as well as a reduction in the proficiency to repair cisplatin-induced DNA damage might account for this behavior. In this review, building on recent findings of p53-induced apoptosis and DNA-repair mechanisms in TGCTs, we will discuss the molecular bases that drive tumor sensitivity to cisplatin, emphasizing the new therapeutic approaches proposed to eventually constrain tumor recurrence, and target TGCTs which are unresponsive to standard therapies.