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阿来替尼作为间变性淋巴瘤激酶阳性晚期非小细胞肺癌患者从克唑替尼诱导的间质性肺疾病恢复后的一种治疗选择。

Alectinib as a treatment option following recovery from crizotinib-induced interstitial lung disease in patients with anaplastic lymphoma kinase-positive advanced non-small-cell lung cancer.

作者信息

Nukaga Shigenari, Naoki Katsuhiko, Kamo Tetsuro, Masuzawa Keita, Yasuda Hiroyuki, Soejima Kenzo, Betsuyaku Tomoko

机构信息

Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo 160-8582, Japan.

Division of Pulmonary Medicine, Department of Medicine, Keio University School of Medicine, Tokyo 160-8582, Japan; Cancer Center, Keio University School of Medicine, Tokyo 160-8582, Japan.

出版信息

Mol Clin Oncol. 2016 Jun;4(6):1085-1087. doi: 10.3892/mco.2016.838. Epub 2016 Mar 30.

DOI:10.3892/mco.2016.838
PMID:27284449
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4888013/
Abstract

Crizotinib is a tyrosine kinase inhibitor that displays antitumor activity against anaplastic lymphoma kinase ()-positive advanced non-small-cell lung cancer. However, crizotinib-associated interstitial lung disease (ILD) has been reported as an infrequent, but potentially fatal complication. We herein describe the case of a 63-year-old male patient with -rearranged advanced lung adenocarcinoma. Chest computed tomography (CT) revealed extensive bilateral ground-glass opacity and airspace consolidation with traction bronchiectasis on day 27 of crizotinib therapy. No signs of infection or left heart failure were identified and we considered the lesions to be consistent with crizotinib-induced ILD. Following corticosteroid treatment and discontinuation of crizotinib, CT revealed improvement of ILD, but also showed regrowth of the tumor. Alectinib, a novel alternative ALK inhibitor, was initiated, and has been successfully continued, with neither disease progression nor recurrence of ILD. The present case indicates that alectinib may be considered as an alternative agent in cases of crizotinib-induced ILD, irrespective of the pattern of ILD, i.e., a diffuse alveolar damage (DAD) or non-DAD pattern, with careful observation.

摘要

克唑替尼是一种酪氨酸激酶抑制剂,对间变性淋巴瘤激酶(ALK)阳性的晚期非小细胞肺癌具有抗肿瘤活性。然而,克唑替尼相关的间质性肺疾病(ILD)已被报道为一种罕见但可能致命的并发症。我们在此描述了一例63岁的男性患者,患有ALK重排的晚期肺腺癌。在克唑替尼治疗的第27天,胸部计算机断层扫描(CT)显示双侧广泛的磨玻璃影和实变影,并伴有牵拉性支气管扩张。未发现感染或左心衰竭的迹象,我们认为这些病变与克唑替尼诱导的ILD相符。在接受皮质类固醇治疗并停用克唑替尼后,CT显示ILD有所改善,但肿瘤也出现了复发。阿来替尼是一种新型的ALK抑制剂,开始使用后已成功持续使用,既没有疾病进展也没有ILD复发。本病例表明,无论ILD的模式是弥漫性肺泡损伤(DAD)还是非DAD模式,在仔细观察的情况下,阿来替尼可被视为克唑替尼诱导的ILD病例的替代药物。

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本文引用的文献

1
Crizotinib Associated with Ground-Glass Opacity Predominant Pattern Interstitial Lung Disease: A Retrospective Observational Cohort Study with a Systematic Literature Review.克唑替尼相关磨玻璃影型为主的间质性肺疾病:一项回顾性观察队列研究及系统文献复习。
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2
Safety and activity of alectinib against systemic disease and brain metastases in patients with crizotinib-resistant ALK-rearranged non-small-cell lung cancer (AF-002JG): results from the dose-finding portion of a phase 1/2 study.克唑替尼耐药的间变性淋巴瘤激酶(ALK)重排非小细胞肺癌(NSCLC)患者中艾乐替尼针对全身疾病和脑转移的安全性和活性:一项 1/2 期研究剂量探索部分的结果。
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Successful crizotinib retreatment after crizotinib-induced interstitial lung disease.克唑替尼诱发间质性肺病后成功再次使用克唑替尼治疗。
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Crizotinib versus chemotherapy in advanced ALK-positive lung cancer.克唑替尼与化疗用于治疗晚期 ALK 阳性肺癌。
N Engl J Med. 2013 Jun 20;368(25):2385-94. doi: 10.1056/NEJMoa1214886. Epub 2013 Jun 1.
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CH5424802 (RO5424802) for patients with ALK-rearranged advanced non-small-cell lung cancer (AF-001JP study): a single-arm, open-label, phase 1-2 study.克唑替尼(RO5424802)治疗间变性淋巴瘤激酶(ALK)重排的晚期非小细胞肺癌患者(AF-001JP 研究):一项单臂、开放标签、1 期和 2 期研究。
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Severe acute interstitial lung disease after crizotinib therapy in a patient with EML4-ALK-positive non-small-cell lung cancer.一名EML4-ALK阳性非小细胞肺癌患者接受克唑替尼治疗后发生严重急性间质性肺病。
J Clin Oncol. 2013 Jan 1;31(1):e15-7. doi: 10.1200/JCO.2012.43.3730. Epub 2012 Nov 19.
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ROS1 rearrangements define a unique molecular class of lung cancers.ROS1 重排定义了一类独特的肺癌分子亚型。
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Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma.PF-2341066(一种间变性淋巴瘤激酶和c-Met的新型抑制剂)在间变性大细胞淋巴瘤实验模型中的减瘤抗肿瘤活性。
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