Aggressive pulmonary adenocarcinoma with new FGFR translocation and cMET mutation not responsive to crizotinib and nintedanib treatment: a case report
Status PubMed-not-MEDLINE Jazyk angličtina Země Čína Médium print
Typ dokumentu kazuistiky, časopisecké články
PubMed
35117560
PubMed Central
PMC8797612
DOI
10.21037/tcr.2019.12.85
PII: tcr-09-03-2082
Knihovny.cz E-zdroje
- Klíčová slova
- Fibroblast growth factor receptor (FGFR), cMET, case report, crizotinib, nintedanib,
- Publikační typ
- časopisecké články MeSH
- kazuistiky MeSH
The onset of routine use of the next generation sequencing (NGS) leads to discovery of new mutations in non-small cell lung cancer (NSCLC). In addition, comprehension of therapeutic potential of these genetic alterations in clinical practice is needed and required. Both, rare mutations and the therapeutic considerations they prompt, are dealt with in our case report describing a new fusion mutation of the fibroblast growth factor receptor (FGFR). Our case report describes a 45-year Caucasian female, non-smoker, with the tyrosine-protein kinase Met (cMET) skip 14 mutation and a newly described fibroblast growth factor receptor-cholinergic receptor, nicotinic, alpha 6 (FGFR-CHNRA6) fusion. The tumor in this patient showed aggressive growth and was resistant to all treatment modalities administered (including combination chemotherapy with bevacizumab, pemetrexed and nintedanib), with the exception of very short efficacy of crizotinib. The patient died 5 months after diagnosis. According to the published literature, a theoretical future solution could be to administer multidimensional targeted therapy simultaneously.
Bioptic laboratory Pilsen Czech Republic
Department of Imaging Methods Charles University Faculty of Medicine in Pilsen Pilsen Czech Republic
Department of Pathology Charles University Faculty of Medicine in Pilsen Pilsen Czech Republic
Zobrazit více v PubMed
Siegfried JM, Farooqui M, Rothenberger NJ, et al. Interaction between the estrogen receptor and fibroblast growth factor receptor pathways in non-small cell lung cancer. Oncotarget 2017;8:24063-76. 10.18632/oncotarget.16030 PubMed DOI PMC
Tiseo M, Gelsomino F, Alfieri R, et al. FGFR as potential target in the treatment of squamous non small cell lung cancer. Cancer Treat Rev 2015;41:527-39. 10.1016/j.ctrv.2015.04.011 PubMed DOI
Qin A, Johnson A, Ross JS, et al. Detection of Known and Novel FGFR Fusions in Non-Small Cell Lung Cancer by Comprehensive Genomic Profiling. J Thorac Oncol 2019;14:54-62. 10.1016/j.jtho.2018.09.014 PubMed DOI
Wang R, Wang L, Li Y, et al. FGFR1/3 tyrosine kinase fusions define a unique molecular subtype of non-small cell lung cancer. Clin Cancer Res 2014;20:4107-14. 10.1158/1078-0432.CCR-14-0284 PubMed DOI
Vuong HG, Ho ATN, Altibi AMA, et al. Clinicopathological implications of MET exon 14 mutations in non-small cell lung cancer - A systematic review and meta-analysis. Lung Cancer 2018;123:76-82. 10.1016/j.lungcan.2018.07.006 PubMed DOI
Semrad TJ, Mack PC. Fibroblast growth factor signaling in non-small-cell lung cancer. Clin Lung Cancer 2012;13:90-5. 10.1016/j.cllc.2011.08.001 PubMed DOI
Hibi M, Kaneda H, Tanizaki J, et al. FGFR gene alterations in lung squamous cell carcinoma are potential targets for the multikinase inhibitor nintedanib. Cancer Sci 2016;107:1667-76. 10.1111/cas.13071 PubMed DOI PMC
Wang Y, Peng X, Zhu L, et al. Genetic variants of CHRNA5-A3 and CHRNB3-A6 predict survival of patients with advanced non-small cell lung cancer. Oncotarget 2016;7:26436-43. PubMed PMC
Ebihara M, Ohba H, Ohno SI, et al. Genomic organization and promoter analysis of the human nicotinic acetylcholine receptor alpha6 subunit (CHNRA6) gene: Alu and other elements direct transcriptional repression. Gene 2002;298:101-8. 10.1016/S0378-1119(02)00925-3 PubMed DOI
Guddo F, Fontanini G, Reina C, et al. The expression of basic fibroblast growth factor (bFGF) in tumor-associated stromal cells and vessels is inversely correlated with non-small cell lung cancer progression. Hum Pathol 1999;30:788-94. 10.1016/S0046-8177(99)90139-9 PubMed DOI
Donnem T, Al-Shibli K, Al-Saad S, et al. Prognostic impact of fibroblast growth factor 2 in non-small cell lung cancer: coexpression with VEGFR-3 and PDGF-B predicts poor survival. J Thorac Oncol 2009;4:578-85. 10.1097/JTO.0b013e31819f2e38 PubMed DOI
Rak J, Filmus J, Kerbel RS. Reciprocal paracrine interactions between tumour cells and endothelial cells: the 'angiogenesis progression' hypothesis. Eur J Cancer 1996;32A:2438-50. 10.1016/S0959-8049(96)00396-6 PubMed DOI
Kim B, Wang S, Lee JM, et al. Synthetic lethal screening reveals FGFR as one of the combinatorial targets to overcome resistance to Met-targeted therapy. Oncogene 2015;34:1083-93. 10.1038/onc.2014.51 PubMed DOI PMC
Kim SM, Kim H, Yun MR, et al. Activation of the Met kinase confers acquired drug resistance in FGFR-targeted lung cancer therapy. Oncogenesis 2016;5:e241. 10.1038/oncsis.2016.48 PubMed DOI PMC
Beau-Faller M, Gaub MP, Schneider A, et al. Allelic imbalance at loci containing FGFR, FGF, c-Met and HGF candidate genes in non-small cell lung cancer sub-types, implication for progression. Eur J Cancer 2003;39:2538-47. 10.1016/S0959-8049(03)00623-3 PubMed DOI
Reungwetwattana T, Liang Y, Zhu V, et al. The race to target MET exon 14 skipping alterations in non-small cell lung cancer: The Why, the How, the Who, the Unknown, and the Inevitable. Lung Cancer 2017;103:27-37. 10.1016/j.lungcan.2016.11.011 PubMed DOI
Hilberg F, Tontsch-Grunt U, Baum A, et al. Triple Angiokinase Inhibitor Nintedanib Directly Inhibits Tumor Cell Growth and Induces Tumor Shrinkage via Blocking Oncogenic Receptor Tyrosine Kinases. J Pharmacol Exp Ther 2018;364:494-503. 10.1124/jpet.117.244129 PubMed DOI PMC
Bronte G, Passiglia F, Galvano A, et al. Nintedanib in NSCLC: evidence to date and place in therapy. Ther Adv Med Oncol 2016;8:188-97. 10.1177/1758834016630976 PubMed DOI PMC