Abstract
The majority of resistance to Rearranged during transfection (RET)-specific tyrosine kinase inhibitors (TKI) described in RET-rearranged non-small cell lung cancer (NSCLC) patients are driven by RET-independent mechanisms. We provide the first case report of a RET-rearranged lung adenocarcinoma (LUAD) transformation into small-cell lung cancer
(SCLC) as a mechanism of acquired resistance to pralsetinib. A 43-year-old patient
presented with a RET-rearranged LUAD revealed by pleural effusion. After 14 months of response to pralsetinib,
biopsy of a progressive pleural lesion found a phenotypic transformation into SCLC.
Molecular analysis identified the same RET fusion and TP53 mutation in both primary adenocarcinoma and recurrence as SCLC. The patient achieved
partial response after switch to carboplatin and etoposide chemotherapy and presented
with progression disease after 6 months. Histological transformation could be a mechanism
of resistance to RET-TKIs and rebiopsy should be considered to adapt subsequent treatment.
Keywords
Abbreviations:
LUAD (lung adenocarcinoma), SCLC (small cell lung carcinoma), CT (computed tomography), MRI (magnetic resonance imaging), ALK (anaplasic lymphoma kinase), PFS (progression free survival), Rearranged during transfection (RET)To read this article in full you will need to make a payment
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Article info
Publication history
Published online: November 01, 2022
Accepted:
October 24,
2022
Received in revised form:
October 18,
2022
Received:
June 28,
2022
Identification
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© 2022 Elsevier Inc. All rights reserved.