A Novel c-Mesenchymal-Epithelial Transition Factor Intergenic Fusion Response to Crizotinib in a Chinese Patient With Lung Adenocarcinoma: A Case Report

被引:2
作者
Liang, Hongge [1 ]
Zhou, Dexun [1 ]
Dai, Lin [2 ]
Zhang, Moqin [1 ]
Gao, Zhancheng [1 ]
Mu, Xinlin [1 ]
机构
[1] Peking Univ, Dept Resp & Crit Care Med, Peoples Hosp, Beijing, Peoples R China
[2] Peking Univ, Dept Pathol, Peoples Hosp, Beijing, Peoples R China
来源
FRONTIERS IN ONCOLOGY | 2021年 / 11卷
关键词
lung adenocarcinoma; MET intergenic fusion; crizotinib; partial response; interstitial lung disease; ANTITUMOR-ACTIVITY; MET; REARRANGEMENT;
D O I
10.3389/fonc.2021.727662
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Background The c-mesenchymal-epithelial transition factor (C-MET) is an oncogene encoding a tyrosine kinase receptor that plays an important role in tumor growth and metastasis. The National Comprehensive Cancer Network (NCCN) guidelines have approved carbatinib/crizotinib for advanced non-small cell lung cancer (NSCLC) patients with MET exon 14 skipping. Methods In June 2020, the Department of Respiratory and Critical Care Medicine of Peking University People's Hospital admitted a 72-year-old male patient with lung adenocarcinoma (LADC) with a history of interstitial lung disease secondary to antineutrophil cytoplasmic antibody-associated vasculitis. Genetic examination by next-generation sequencing showed an intergenic fusion of MET, and crizotinib was administered on August 14, 2020. Follow-up showed that tumor volume was significantly reduced. However, crizotinib was discontinued in November 2020 because of the patient's worsening interstitial lung disease, and CT scans showed continued partial response (PR) for 5 months. In April 2021, right lower lobe mass progressed, and disease progression was considered. Conclusion This was the first case of a patient with LADC with MET intergenic fusion who significantly benefited from crizotinib. Even after crizotinib was discontinued for 5 months, the patient continued exhibiting PR, suggesting that MET intergenic fusion may have carcinogenic activity in LADC and was sensitive to crizotinib.
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共 15 条
  • [1] KIF5B-MET Gene Rearrangement with Robust Antitumor Activity in Response to Crizotinib in Lung Adenocarcinoma
    Cho, Jang Ho
    Ku, Bo Mi
    Sun, Jong-Mu
    Lee, Se-Hoon
    Ahn, Jin Seok
    Park, Keunchil
    Ahn, Myung-Ju
    [J]. JOURNAL OF THORACIC ONCOLOGY, 2018, 13 (03) : E29 - E31
  • [2] Structure Based Drug Design of Crizotinib (PF-02341066), a Potent and Selective Dual Inhibitor of Mesenchymal-Epithelial Transition Factor (c-MET) Kinase and Anaplastic Lymphoma Kinase (ALK)
    Cui, J. Jean
    Tran-Dube, Michelle
    Shen, Hong
    Nambu, Mitchell
    Kung, Pei-Pei
    Pairish, Mason
    Jia, Lei
    Meng, Jerry
    Funk, Lee
    Botrous, Iriny
    McTigue, Michele
    Grodsky, Neil
    Ryan, Kevin
    Padrique, Ellen
    Alton, Gordon
    Timofeevski, Sergei
    Yamazaki, Shinji
    Li, Quhua
    Zou, Helen
    Christensen, James
    Mroczkowski, Barbara
    Bender, Steve
    Kania, Robert S.
    Edwards, Martin P.
    [J]. JOURNAL OF MEDICINAL CHEMISTRY, 2011, 54 (18) : 6342 - 6363
  • [3] Dramatic Response to Crizotinib in a Patient With Lung Cancer Positive for an HLA-DRB1-MET Gene Fusion
    Davies, Kurtis D.
    Ng, Terry L.
    Estrada-Bernal, Adriana
    Le, Anh T.
    Ennever, Peter R.
    Camidge, D. Ross
    Doebele, Robert C.
    Aisner, Dara L.
    [J]. JCO PRECISION ONCOLOGY, 2017, 1 : 1 - 6
  • [4] Antitumor activity of crizotinib in lung cancers harboring a MET exon 14 alteration
    Drilon, Alexander
    Clark, Jeffrey W.
    Weiss, Jared
    Ou, Sai-Hong Ignatius
    Camidge, D. Ross
    Solomon, Benjamin J.
    Otterson, Gregory A.
    Villaruz, Liza C.
    Riely, Gregory J.
    Heist, Rebecca S.
    Awad, Mark M.
    Shapiro, Geoffrey I.
    Satouchi, Miyako
    Hida, Toyoaki
    Hayashi, Hidetoshi
    Murphy, Danielle A.
    Wang, Sherry C.
    Li, Sherry
    Usari, Tiziana
    Wilner, Keith D.
    Paik, Paul K.
    [J]. NATURE MEDICINE, 2020, 26 (01) : 47 - +
  • [5] Targeting MET in Lung Cancer: Will Expectations Finally Be MET?
    Drilon, Alexander
    Cappuzzo, Federico
    Ignatius, Sai-Hong
    Camidge, D. Ross
    [J]. JOURNAL OF THORACIC ONCOLOGY, 2017, 12 (01) : 15 - 26
  • [6] Prognostic and predictive value of MET deregulation in non-small cell lung cancer
    Finocchiaro, Giovanna
    Toschi, Luca
    Gianoncelli, Letizia
    Baretti, Marina
    Santoro, Armando
    [J]. ANNALS OF TRANSLATIONAL MEDICINE, 2015, 3 (06)
  • [7] The Met tyrosine kinase receptor in development and cancer
    Gentile, Alessandra
    Trusolino, Livio
    Comoglio, Paolo M.
    [J]. CANCER AND METASTASIS REVIEWS, 2008, 27 (01) : 85 - 94
  • [8] Phosphoproteomic analysis identifies activated MET-axis PI3K/AKT and MAPK/ERK in lapatinib-resistant cancer cell line
    Lee, Yong Yook
    Kim, Hwang-Phill
    Kang, Min Jueng
    Cho, Byoung-Kyu
    Han, Sae-Won
    Kim, Tae-You
    Yi, Eugene C.
    [J]. EXPERIMENTAL AND MOLECULAR MEDICINE, 2013, 45 : e64 - e64
  • [9] MET Oncogene in Non-Small Cell Lung Cancer: Mechanism of MET Dysregulation and Agents Targeting the HGF/c-Met Axis
    Liang, Hongge
    Wang, Mengzhao
    [J]. ONCOTARGETS AND THERAPY, 2020, 13 : 2491 - 2510
  • [10] Hepatocyte growth factor/MET in cancer progression and biomarker discovery
    Matsumoto, Kunio
    Umitsu, Masataka
    De Silva, Dinuka M.
    Roy, Arpita
    Bottaro, Donald P.
    [J]. CANCER SCIENCE, 2017, 108 (03): : 296 - 307