Combination of Crizotinib and Osimertinib in T790M+EGFR-Mutant Non-Small Cell Lung Cancer with Emerging MET Amplification Post-Osimertinib Progression in a 10-Year Survivor: A Case Report

被引：6

作者：

Blasi, Miriam ^{[1
]}

Kazdal, Daniel ^{[2
,3
]}

Thomas, Michael ^{[1
,3
]}

Christopoulos, Petros ^{[1
,3
]}

Kriegsmann, Mark ^{[2
,3
]}

Brandt, Regine ^{[2
]}

Volckmar, Anna-Lena ^{[2
]}

Kirchner, Martina ^{[2
]}

Heussel, Claus Peter ^{[3
,4
]}

Stenzinger, Albrecht ^{[2
,3
]}

Kuon, Jonas ^{[1
,3
]}

机构：

[1] Heidelberg Univ, Dept Thorac Oncol, Thoraxklin, Rontgenstr 1, DE-69126 Heidelberg, Germany

[2] Univ Hosp Heidelberg, Inst Pathol, Heidelberg, Germany

[3] German Ctr Lung Res DZL, Translat Lung Res Ctr TLRC Heidelberg, Heidelberg, Germany

[4] Heidelberg Univ, Thoraxklin, Diagnost & Intervent Radiol Nucl Med, Heidelberg, Germany

来源：

CASE REPORTS IN ONCOLOGY | 2021年 / 14卷 / 01期

关键词：

Non-small cell lung cancer; EGFR mutation; MET amplification; Targeted therapy; RESISTANCE; PATIENT; INHIBITORS; GEFITINIB; MECHANISM; AZD9291;

D O I：

10.1159/000513904

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Tyrosine kinase inhibitors (TKIs) represent the standard treatment for patients with non-small cell lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) mutations. The duration of the response is, however, limited in time owing to the development of resistance mechanisms to both first- and second-generation agents such as MET oncogene amplification. This report describes the successful results obtained with the combination of the third-generation TKI osimertinib with the multitargeted TKI and MET inhibitor crizotinib in a patient with EGFR-mutant NSCLC with emerging MET amplification with a tolerable toxicity profile.

引用

页码：477 / 482

页数：6

共 15 条

[1] MET amplification leads to gefitinib resistance in lung cancer by activating ERBB3 signaling [J].

Engelman, Jeffrey A. ;

Zejnullahu, Kreshnik ;

Mitsudomi, Tetsuya ;

Song, Youngchul ;

Hyland, Courtney ;

Park, Joon Oh ;

Lindeman, Neal ;

Gale, Christopher-Michael ;

Zhao, Xiaojun ;

Christensen, James ;

Kosaka, Takayuki ;

Holmes, Alison J. ;

Rogers, Andrew M. ;

Cappuzzo, Federico ;

Mok, Tony ;

Lee, Charles ;

Johnson, Bruce E. ;

Cantley, Lewis C. ;

Janne, Pasi A. .

SCIENCE, 2007, 316 (5827) :1039-1043

[2] EGFR mutations as a prognostic and predictive marker in non-small-cell lung cancer [J].

Fang, Shu ;

Wang, Zhehai .

DRUG DESIGN DEVELOPMENT AND THERAPY, 2014, 8 :1595-1611

[3] AZD9291 in EGFR Inhibitor-Resistant Non-Small-Cell Lung Cancer [J].

Jaenne, Pasi A. ;

Yang, James Chih-Hsin ;

Kim, Dong-Wan ;

Planchard, David ;

Ohe, Yuichiro ;

Ramalingam, Suresh S. ;

Ahn, Myung-Ju ;

Kim, Sang-We ;

Su, Wu-Chou ;

Horn, Leora ;

Haggstrom, Daniel ;

Felip, Enriqueta ;

Kim, Joo-Hang ;

Frewer, Paul ;

Cantarini, Mireille ;

Brown, Kathryn H. ;

Dickinson, Paul A. ;

Ghiorghiu, Serban ;

Ranson, Malcolm .

NEW ENGLAND JOURNAL OF MEDICINE, 2015, 372 (18) :1689-1699

[4] Combined Use of Crizotinib and Gefitinib in Advanced Lung Adenocarcinoma With Leptomeningeal Metastases Harboring MET Amplification After the Development of Gefitinib Resistance: A Case Report and Literature Review [J].

Li, Yalun ;

Zhang, Rui ;

Zhou, Yongzhao ;

Song, Juan ;

Luo, Wenxin ;

Tian, Panwen ;

Li, Weimin .

CLINICAL LUNG CANCER, 2019, 20 (03) :E251-E255

[5] Third-generation epidermal growth factor receptor-tyrosine kinase inhibitors in T790M-positive non-small cell lung cancer: review on emerged mechanisms of resistance [J].

Minari, Roberta ;

Bordi, Paola ;

Tiseo, Marcello .

TRANSLATIONAL LUNG CANCER RESEARCH, 2016, 5 (06) :695-708

[6] Oncogene swap as a novel mechanism of acquired resistance to epidermal growth factor receptor-tyrosine kinase inhibitor in lung cancer [J].

Mizuuchi, Hiroshi ;

Suda, Kenichi ;

Murakami, Isao ;

Sakai, Kazuko ;

Sato, Katsuaki ;

Kobayashi, Yoshihisa ;

Shimoji, Masaki ;

Chiba, Masato ;

Sesumi, Yuichi ;

Tomizawa, Kenji ;

Takemoto, Toshiki ;

Sekido, Yoshitaka ;

Nishio, Kazuto ;

Mitsudomi, Tetsuya .

CANCER SCIENCE, 2016, 107 (04) :461-468

[7] Mechanisms of resistance to EGFR-targeted drugs: lung cancer [J].

Morgillo, Floriana ;

Della Corte, Carminia Maria ;

Fasano, Morena ;

Ciardiello, Fortunato .

ESMO OPEN, 2016, 1 (03)

[8] High MET amplification level as a resistance mechanism to osimertinib (AZD9291) in a patient that symptomatically responded to crizotinib treatment post-osimertinib progression [J].

Ou, Sai-Hong Ignatius ;

Agarwal, Nikita ;

Ali, Siraj M. .

LUNG CANCER, 2016, 98 :59-61

[9] SAVANNAH: A Phase II trial of osimertinib plus savolitinib for patients (pts) with EGFR-mutant, MET driven (MET plus ), locally advanced or metastatic non small cell lung cancer (NSCLC), following disease progression on osimertinib. [J].

Oxnard, Geoffrey R. ;

Cantarini, Mireille ;

Frewer, Paul ;

Hawkins, George ;

Peters, Jane ;

Howarth, Paul ;

Ahmed, Ghada F. ;

Sahota, Tarjinder ;

Hartmaier, Ryan ;

Li-Sucholeiki, Xiaocheng ;

Ahn, Myung-Ju .

JOURNAL OF CLINICAL ONCOLOGY, 2019, 37 (15)

[10] TATTON Phase Ib expansion cohort: Osimertinib plus savolitinib for patients (pts) with EGFR-mutant, MET-amplified NSCLC after progression on prior third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) [J].

Sequist, Lecia V. ;

Lee, Jong Seok ;

Han, Ji-Youn ;

Su, Wu-Chou ;

Yang, James Chih-Hsin ;

Yu, Helena ;

Ottesen, Lone H. ;

Verheijen, Remy B. ;

Mellemgaard, Anders ;

Wessen, Jonathan ;

Oxnard, Geoffrey ;

Cho, Byoung Chul .

CANCER RESEARCH, 2019, 79 (13)

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