PDF(Pubmed)
Abstract：
PARP inhibitors have recently emerged as a maintenance treatment option for metastatic pancreatic cancer patients with germline BRCA mutations. However, the possibility of PARP-inhibitor use as a standalone-targeted therapy for patients with various homologous repair pathway alterations remains mostly undetermined. Here we report a clinical case of a 56-year-old woman with pancreatic ductal adenocarcinoma harboring a somatic PALB2 mutation. Following disease progression after 10 cycles of FOLFIRINOX chemotherapy and two cycles of second-line gemcitabine, she was switched to talazoparib and achieved a complete clinical response after 25 months of treatment. The patient remains alive without clinical or radiological signs of disease progression three years after the start of talazoparib with no targeted therapy-related toxicities. This case highlights the role of broad molecular profiling as a window of opportunity to achieve a durable response for selected pancreatic cancer patients while pinpointing our gaps in understanding the whole picture of management of these patients since a new puzzle element represented by PARP inhibitors was introduced to clinical practice.
摘要：
PARP抑制剂最近已成为具有种系BRCA突变的转移性胰腺癌患者的维持治疗选择。然而,对于有各种同源修复途径改变的患者,使用PARP抑制剂作为独立靶向治疗的可能性大部分仍未确定.在这里，我们报告了一名56岁的胰腺导管腺癌患者的临床病例，该患者具有体细胞PALB2突变。10个周期的FOLFIRINOX化疗和2个周期的二线吉西他滨治疗后疾病进展，在治疗25个月后,她转用了他唑帕尼,并获得了完全的临床缓解.患者在开始使用他唑帕尼三年后仍活着，没有疾病进展的临床或放射学迹象，没有靶向治疗相关的毒性。这个案例强调了广泛的分子谱分析作为一个机会窗口的作用，为选定的胰腺癌患者实现持久的反应，同时指出了我们在理解这些患者的整体管理方面的差距，因为PARP抑制剂代表的一种新的难题元素被引入临床实践。
