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肺癌中弥漫性肺内转移的影像学特征与表皮生长因子受体抑制剂的预后不良相关。

Imaging Pattern of Diffuse Intrapulmonary Metastases in Lung Cancer Was Associated with Poor Prognosis to Epidermal Growth Factor Receptor Inhibitors.

作者信息

Fu Yang, Tang Yuan, Zheng Yue, Chen Yue-Yun, Hong Ye, Wang Pei-Pei, Li Qing, Liu Ting, Ding Zhen-Yu

机构信息

Department of Biotherapy, Cancer Center, West China Hospital, West China Medical School, State Key Laboratory of Biotherapy, Sichuan University, Chengdu, People's Republic of China.

Department of Pathology, West China Hospital, West China Medical School, Sichuan University, Chengdu, People's Republic of China.

出版信息

Cancer Manag Res. 2020 Nov 17;12:11761-11772. doi: 10.2147/CMAR.S261983. eCollection 2020.

DOI:10.2147/CMAR.S261983
PMID:33235504
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7680171/
Abstract

BACKGROUND

Epidermal growth factor receptor (EGFR) mutations are more frequently seen in miliary intrapulmonary metastases than EGFR wild-type non-small cell lung cancer (NSCLC). Also, small-scale retrospective studies showed that patients harboring EGFR mutation with miliary pulmonary metastases had a worse prognosis. This study aimed to explore the impact of imaging patterns on the outcomes of EGFR tyrosine kinase inhibitor (TKI) treatment.

METHODS

A cohort of treatment-naive NSCLC patients harboring EGFR mutation with intrapulmonary metastases who were prescribed with TKI were enrolled. The demographic feature, clinical outcome, and CT imaging of each patient were reviewed and analyzed.

RESULTS

A cohort of 174 patients were enrolled. Five intrapulmonary patterns of imaging were recognized: solid nodular, ground-glass nodular, miliary, multiple uniform nodular, and not otherwise specified. Among them, miliary and multiple uniform nodular patterns had similar poor prognosis, and, therefore, were combined as diffuse group. A worse PFS (9.0 mon, 95% CI: 8.0-10.0 mon) was observed compared with the rest (non-diffuse group, 13.3 mon, 95% CI: 10.2-16.4 mon, p<0.001, HR=0.49). The objective response rates (ORR) between the two groups were 76.8% and 84.1%, respectively, with no significant difference (p = 0.474). The OS of the diffuse and the non-diffuse group were 25.6 mon (95% CI 21.9-29.3 mon) and 35.0 mon (95% CI: 27.5-42.5, p = 0.01, HR= 0.59). Organs like bone (p=0.167), liver (p=0.513), and adrenal gland (p=0.375) were involved in similar frequencies in both groups. However, brain (p=0.070) and leptomeningeal (p=0.078) metastases were less common in the non-diffuse group with marginally statistical significance. The 2 groups contained similar missense mutations, and gene amplification was more common in the non-diffuse group.

CONCLUSION

Patients with diffuse intrapulmonary metastases had inferior outcomes after TKI treatment. More aggressive treatments might be warranted for these patients.

摘要

背景

与表皮生长因子受体(EGFR)野生型非小细胞肺癌(NSCLC)相比,EGFR突变在粟粒性肺内转移中更常见。此外,小规模回顾性研究表明,携带EGFR突变且有粟粒性肺转移的患者预后较差。本研究旨在探讨影像学表现对EGFR酪氨酸激酶抑制剂(TKI)治疗效果的影响。

方法

纳入一组初治的携带EGFR突变且有肺内转移并接受TKI治疗的NSCLC患者。对每位患者的人口统计学特征、临床结局和CT影像进行回顾和分析。

结果

共纳入174例患者。识别出五种肺内影像表现类型:实性结节、磨玻璃结节、粟粒状、多发均匀结节以及未另行说明的类型。其中,粟粒状和多发均匀结节型预后相似,因此合并为弥漫型组。与其余组(非弥漫型组,13.3个月,95%CI:10.2 - 16.4个月,p<0.001,HR = 0.49)相比,弥漫型组的无进展生存期更差(9.0个月,95%CI:8.0 - 10.0个月)。两组的客观缓解率(ORR)分别为76.8%和84.1%,无显著差异(p = 0.474)。弥漫型组和非弥漫型组的总生存期分别为25.6个月(95%CI 21.9 - 29.3个月)和35.0个月(95%CI:27.5 - 42.5,p = 0.01,HR = 0.59)。两组中骨(p = 0.167)、肝(p = 0.513)和肾上腺(p = 0.375)等器官受累频率相似。然而,非弥漫型组脑转移(p = 0.070)和软脑膜转移(p = 0.078)较少见,具有边缘统计学意义。两组的错义突变相似,基因扩增在非弥漫型组更常见。

结论

弥漫性肺内转移患者接受TKI治疗后的结局较差。可能需要对这些患者采取更积极的治疗措施。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/5c29e6baa32d/CMAR-12-11761-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/653bbaca58b0/CMAR-12-11761-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/db9289f2ba7b/CMAR-12-11761-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/fd0c71389e79/CMAR-12-11761-g0003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/3a5506774068/CMAR-12-11761-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/dc5170c441e2/CMAR-12-11761-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/5c29e6baa32d/CMAR-12-11761-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/653bbaca58b0/CMAR-12-11761-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/db9289f2ba7b/CMAR-12-11761-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/fd0c71389e79/CMAR-12-11761-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/c7e6521885d3/CMAR-12-11761-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/3a5506774068/CMAR-12-11761-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/dc5170c441e2/CMAR-12-11761-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/570a/7680171/5c29e6baa32d/CMAR-12-11761-g0007.jpg

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