索托拉西作为胰腺癌的四线治疗:病例报告与文献综述

Rhode Island medical journal (2013) Pub Date : 2024-07-01
Ifeanyi David Onukogu, Georgio Medawar, Yashvin Onkarappa Mangala, Ritesh Rathore
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引用次数: 0

摘要

胰腺外分泌癌的分子发病机制涉及 K-RAS、TP53、CDKN2A 和 SMAD4 突变。KRAS 致癌基因导致肿瘤细胞增殖持续活跃,90% 的不可切除或转移性胰腺腺癌都存在这种基因突变。其中,K-RAS 基因的 G12C 变异占突变的 1-2%。一名 65 岁的妇女最初被诊断为 T3N0M0 胰腺腺癌,接受了六周期 mFOLFIRINOX 新辅助化疗,随后接受了 Whipple 手术。她的病理分期为 T4N2。随后,她接受了 mFOLFIRINOX 辅助化疗,但不幸的是,经过多线化疗,她的病情出现了进展。通过下一代序列(NGS)面板进行的分子分析发现了 KRAS G12C 突变。基于这种突变状态,她开始服用索托拉西布(Sotorasib),并在疾病进展前获得了持续约11个月的临床应答。我们的 KRAS G12C 突变胰腺癌患者在标示外使用索托拉西布作为四线治疗,疗效显著,耐受性也相对较好。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sotorasib as Fourth-Line Treatment in Pancreatic Cancer: A Case Report and Literature Review.

The molecular pathogenesis of exocrine pancreatic cancer involves mutations K-RAS, TP53, CDKN2A, and SMAD4. The KRAS oncogene leads to constitutively active tumor cell proliferation and is present in 90% of unresectable or metastatic pancreatic adenocarcinomas. Of these, the G12C variant of K-RAS genes accounts for 1-2% of mutations. A 65-year-old woman initially diagnosed with T3N0M0 pancreatic adenocarcinoma, underwent six cycles of neoadjuvant chemotherapy with mFOLFIRINOX followed by Whipple procedure. Her pathological stage was T4N2. She then received adjuvant mFOLFIRINOX but unfortunately her disease progressed through multiple lines of chemotherapy. Molecular analysis by Next Generation Sequence(NGS) panel revealed KRAS G12C mutation. Based on this mutational status, she was started on Sotorasib to which she had clinical response lasting for about 11 months prior to disease progression. Off-label use of Sotorasib as fourth-line treatment in our patient with KRAS G12C mutated pancreatic cancer was efficacious and relatively well tolerated.

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