Clinical Practice Points
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What is already known about this subject?
- •Rearranged during transfection (RET) gene fusion are unfrequent (1%-2%) but validated as target mutations in non-small cell lung cancer (NSCLC).
- •Selpercatinib and, pralsetinib have been authorized by the US-FDA in second line or more in NSCLC RET+.
- •The predominant independent mechanism of resistance to RET tyrosine kinase inhibitors (TKI) is the MET amplification but data to overcome MET resistance concern only selpercatinib resistance.
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What are the new findings and how might they impact on clinical practice in the foreseeable future?
- •We report here the first case of a patient who developed a MET amplification as an initial mechanism of acquired resistance to pralsetinib for an advanced KIF5B-RET driven lung adenocarcinoma, successfully treated with a combination of pralsetinib and crizotinib then capmatinib due to an isolated cerebral progression.
- •An isolated progression under crizotinib should raise suspicion of poor penetration through the blood-brain barrier and motivate the switch by an anti-MET with better cerebral penetration like capmatinib.
- •Early evaluation by 18FDG/CT might be a compelling method to justifying the pursuit or not of combination TKI without being predictive of the duration of response.
Keywords
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References
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Article info
Publication history
Published online: August 19, 2022
Accepted:
August 13,
2022
Received in revised form:
August 11,
2022
Received:
July 9,
2022
Identification
Copyright
© 2022 Elsevier Inc. All rights reserved.