Small-Cell Lung Cancer Transformation as a Mechanism of Resistance to Pralsetinib in RET- Rearranged Lung Adenocarcinoma: A Case Report

被引:19
作者
Gazeu, Alexia [1 ]
Aubert, Mylena [2 ]
Pissaloux, Daniel [1 ,3 ]
Lantuejoul, Sylvie [1 ,3 ,4 ]
Perol, Maurice [2 ]
Ikhlef, Nadia [1 ]
Bouhamama, Amine [5 ]
Franceschi, Tatiana [1 ]
Swalduz, Aurelie [2 ,3 ]
机构
[1] Ctr Leon Berard, Dept Biopathol, Lyon, France
[2] Ctr Leon Berard, Dept Med Oncol, 28 Rue Laennec, F-69008 Lyon, France
[3] Univ Claude Bernard Lyon 1, Univ Lyon, INSERM U1052, CNRS UMR5286,Ctr Leon Berard,Canc Res Ctr Lyon, Lyon, France
[4] Grenoble Alpes Univ, Grenoble, France
[5] Ctr Leon Berard, Dept Radiol, Lyon, France
关键词
RET-fusion; small-cell lung carcinoma; Histological transformation; Resistance; Pralsetinib; TYROSINE KINASE INHIBITORS; CARCINOMAS;
D O I
10.1016/j.cllc.2022.10.005
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:72 / 75
页数:4
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