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Crizotinib Re-Challenge Overcomes Multiple Resistant Clones in cMET Positive NSCLC Patient

 

Crizotinib Re-Challenge Overcomes Multiple Resistant Clones in cMET Positive NSCLC Patient

Walid Shalata1,2*, Roni Gillis1,2*, Waleed Kian1,2, Michal Goldhirsh1,2, Aharon Yehonatan Cohen1,2, Roxana Denisa Grinberg1,2, Dina Levitas1,2, Lior Soussan Gutman3, Addie Dvir3, Steve Olsen4, Richard B. Lanman4, Laila C. Roisman2 and Nir Peled1,2

1Goldman Medical School, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer Sheva, Israel

2The Legacy Heritage Center and Dr. Larry Norton Institute, Soroka Medical Center, Beer Sheva, Israel

3Oncotest-Teva / GUARDANT Health

4Guardant Health, Inc., Redwood City, California, USA 
 
*Corresponding author: Walid Shalata, MD, Resident Physician of Oncology, The Legacy Heritage Oncology Center and Dr. Larry Norton Institute, Soroka Medical Center and Ben-Gurion University, Beer-Sheva, Israel, Tel: +972 (0)542967100; Email: walid.shalata@gmail.com 
 
Received: May 28, 2020; Accepted: June 10, 2020; Published: July 04, 2020 

Citation: Walid S, Roni G, Waleed K, et al. Crizotinib Re-Challenge Overcomes Multiple Resistant Clones in cMET(+) NSCLC Patient. Clin Image Case Rep J. 2020; 2(3): 118.

Abstract

Objectives: Non-Small Cell Lung Carcinomas (NSCLC) presents mesenchymal-epithelial transition factor exon 14 skipping (METex14) mutation in 0.6-7 % of patients. Crizotinib is a Tyrosine Kinase Inhibitor (TKI) that has been approved for the treatment of ALK-rearranged tumors and demonstrated clinical activity in MET(+) NSCLC. Acquired point mutations in the MET gene have been described as mechanisms of resistance to crizotinib. 
 
Materials and Methods: For the evaluation of the MET clones we have used cell-free DNA (cfDNA) NGS test (Guardant360). 
 
Results: In this report, we present a 66-year-old previously healthy non-smoking male who was diagnosed with metastatic adenocarcinoma of the lung with METex14 mutation, PDL-1 expression more than 50 %. The patient developed multiple secondary c-MET resistant clones and responded to re-exposure to crizotinib therapy. 
 
Conclusion: According to this case we suggest that clonal evolution is not necessarily a synonymous with resistant to previous lines (beyond the recent one). Similar phenomenon was previously reported in an ALK fusion case with respond to crizotinib re-exposure, by Shaw et al. The eradication of the emerging clones by crizotinib, as presented in this case, may support this assumption and suggest cautious re-exposure to previous lines in case of emerging resistant. Hypothetically, if this is not the case, we may suggest that crizotinib has changed the microenvironment in a way allowing eradication of the different clones by the activated immune system, however we do not have any support for this assumption. 

Keywords: Targeted therapy; Non-small cell lung carcinoma (NSCLC); c-MET Acquired resistance; Crizotinib 

https://www.literaturepublishers.org/

https://www.literaturepublishers.org/archive/Crizotinib-Re-Challenge-Overcomes-Multiple-Resistant-Clones-in-cMET-Positive-NSCLC-Patient.html

Location: United Kingdom

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