关键词: BRCA Homologous recombination deficiency Mismatch repair deficiency NRG1 fusions NTRK fusions PALB2 PARP inhibitor Pancreatic adenocarcinoma

Mesh : Humans Pancreatic Neoplasms / drug therapy genetics Poly(ADP-ribose) Polymerase Inhibitors / therapeutic use pharmacology Adenocarcinoma / drug therapy genetics Proto-Oncogene Proteins p21(ras) / genetics Carcinoma, Pancreatic Ductal / drug therapy genetics Pancreatic Neoplasms

来  源:   DOI:10.1016/j.hoc.2022.07.007

Abstract:
Pancreatic ductal adenocarcinoma (PDAC) has a poor prognosis, with a mere ∼10% of patients in the United States surviving 5 years from the time of diagnosis. Until recently, the treatment for advanced PDAC differed little based on patient or tumor characteristics. However, recent breakthroughs have identified subgroups of patients who benefit from novel, biomarker-driven therapies. We review the data and role for PARP inhibitors and for other biomarker-directed therapies, including for patients with NTRK fusions, NRG1 fusions, mismatch repair deficiency, and KRAS p.G12C mutations.
摘要:
胰腺导管腺癌(PDAC)预后差,美国只有10%的患者从诊断之日起存活5年。直到最近,根据患者或肿瘤特征,晚期PDAC的治疗差异不大.然而,最近的突破已经确定了受益于新的患者亚组,生物标志物驱动的疗法。我们回顾了PARP抑制剂和其他生物标志物导向疗法的数据和作用。包括NTRK融合患者,NRG1融合,错配修复缺陷,和KRASp.G12C突变。
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