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ALK融合阳性转移性肺癌中基线肝转移的预后影响:一项回顾性研究

Prognostic Impact of Baseline Liver Metastasis in ALK Fusion-Positive Metastatic Lung Cancer: A Retrospective Review.

作者信息

Khaddar Satvik, Kapoor Akhil, Noronha Vanita, Patil Vijay M, Menon Nandini, Mahajan Abhishek, Janu Amit, Kumar Rajiv, Purandare Nilendu, Prabhash Kumar

机构信息

Department of Medical Oncology, Tata Memorial Hospital, Homi Bhabha National Institute, Mumbai, Maharashtra, India.

Department of Medical Oncology, Homi Bhabha Cancer Hospital, Varanasi, Uttar Pradesh, India.

出版信息

South Asian J Cancer. 2022 Mar 22;11(3):243-248. doi: 10.1055/s-0042-1742596. eCollection 2022 Jul.

DOI:10.1055/s-0042-1742596
PMID:36588605
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9803546/
Abstract

Akhil Kapoor  The prognosis of anaplastic lymphoma kinase (ALK) fusion-positive metastatic non-small cell lung cancer (mNSCLC) patients has improved drastically since the introduction of targeted therapies. Apart from age, performance status, and type of driver mutation in a mNSCLC, prognosis also depends on baseline metastatic sites number as well as location with liver metastases being a poor prognostic factor. However, the clinical and prognostic association of baseline liver metastases in ALK fusion-positive mNSCLC is not well known.  We performed a retrospective analysis of ALK fusion-positive mNSCLC patients to assess prognostic impact of liver metastases. Records were obtained from lung cancer audit database and electronic medical records. Patients were started on either chemotherapy, ALK-directed tyrosine kinase inhibitors, or given best supportive care as per the clinical scenario. Radiological response was assessed every 2 to 3 months or earlier at clinical suspicion of progressive disease. Adverse events were evaluated as per Common Terminology Criteria for Adverse Events v4.02.  A total of 441 patients were screened, out of which 76 had baseline liver metastases. Median age was 49 years with 64.5% males. Median progression-free survival (mPFS) was 14.2 months (95% confidence interval [CI] 8.9-19.4) in patients with baseline liver metastases. In patients who received first-line ALK inhibitor therapy versus who received first-line chemotherapy, mPFS was significantly better in the ALK-directed therapy subgroup, 15.3 months (95% CI 11.7-18.9) versus 5.9 months (95% CI 2.7-9.1), respectively (hazard ratio [HR] 0.3 [95% CI 0.17-0.54];  < 0.001). Median overall survival (mOS) was 27.6 months (95% CI 17.4-37.7) in patients with baseline liver metastases which was not statistically significant from patients without baseline liver metastases which was 32.3 months (95% CI 28.8-35.7) (HR 1.32 [95% CI 0.91-1.9];  = 0.22). Use of ALK-directed therapy in patients with baseline liver metastases resulted in better OS, mOS not reached versus 15.7 months (95% CI 2.7-28.8) in the chemotherapy group (HR 0.33 [95% CI 0.16-0.67];  < 0.001).  In patients with ALK fusion-positive mNSCLC, baseline liver metastases was not found to be an independent prognostic factor. However, the use of ALK-directed therapy resulted in a significantly better PFS and OS as compared with chemotherapy in patients with baseline liver metastases. This underscores the importance of the use of ALK-directed therapy whenever feasible in this group of patients.

摘要

阿希尔·卡普尔  自靶向治疗引入以来,间变性淋巴瘤激酶(ALK)融合阳性转移性非小细胞肺癌(mNSCLC)患者的预后有了显著改善。除了年龄、体能状态和mNSCLC中的驱动基因突变类型外,预后还取决于基线转移部位的数量以及位置,肝转移是一个不良预后因素。然而,ALK融合阳性mNSCLC中基线肝转移的临床和预后关联尚不清楚。  我们对ALK融合阳性mNSCLC患者进行了回顾性分析,以评估肝转移的预后影响。记录来自肺癌审计数据库和电子病历。根据临床情况,患者开始接受化疗、ALK靶向酪氨酸激酶抑制剂治疗或给予最佳支持治疗。每2至3个月评估一次放射学反应,或在临床怀疑疾病进展时更早评估。根据不良事件通用术语标准v4.02评估不良事件。  共筛查了441例患者,其中76例有基线肝转移。中位年龄为49岁,男性占64.5%。有基线肝转移的患者中位无进展生存期(mPFS)为14.2个月(95%置信区间[CI]8.9 - 19.4)。在接受一线ALK抑制剂治疗的患者与接受一线化疗的患者中,ALK靶向治疗亚组的mPFS明显更好,分别为15.3个月(95%CI 11.7 - 18.9)和5.9个月(95%CI 2.7 - 9.1)(风险比[HR]0.3[95%CI 0.17 - 0.54];P < 0.001)。有基线肝转移的患者中位总生存期(mOS)为27.6个月(95%CI 17.4 - 37.7),与无基线肝转移的患者(mOS为32.3个月,95%CI 28.8 - 35.7)相比无统计学差异(HR 1.32[95%CI 0.91 - 1.9];P = 0.22)。在有基线肝转移的患者中使用ALK靶向治疗可使OS更好,mOS未达到,而化疗组为15.7个月(95%CI 2.7 - 28.8)(HR 0.33[95%CI 0.16 - 0.67];P < 0.00

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/81d433b3f926/10-1055-s-0042-1742596-i2180592-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/58e9cfff8390/10-1055-s-0042-1742596-i2180592-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/94bbd8646876/10-1055-s-0042-1742596-i2180592-1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/2c48473deb26/10-1055-s-0042-1742596-i2180592-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/81d433b3f926/10-1055-s-0042-1742596-i2180592-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/58e9cfff8390/10-1055-s-0042-1742596-i2180592-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/94bbd8646876/10-1055-s-0042-1742596-i2180592-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/e6c34c40086a/10-1055-s-0042-1742596-i2180592-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/2c48473deb26/10-1055-s-0042-1742596-i2180592-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4e8e/9803546/81d433b3f926/10-1055-s-0042-1742596-i2180592-4.jpg

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