The CLIP1-LTK fusion is an oncogenic driver in non-small-cell lung cancer.
Adenocarcinoma of Lung
/ drug therapy
Aminopyridines
/ pharmacology
Animals
Carcinoma, Non-Small-Cell Lung
/ drug therapy
Cell Line, Tumor
Cell Transformation, Neoplastic
/ drug effects
Chromosomes, Human, Pair 12
/ genetics
Chromosomes, Human, Pair 15
/ genetics
Humans
Lactams
/ pharmacology
Lung Neoplasms
/ drug therapy
Mice
Mice, Nude
Microtubule-Associated Proteins
/ genetics
Neoplasm Proteins
/ genetics
Oncogene Proteins, Fusion
/ genetics
Pyrazoles
/ pharmacology
Receptor Protein-Tyrosine Kinases
/ genetics
Xenograft Model Antitumor Assays
Journal
Nature
ISSN: 1476-4687
Titre abrégé: Nature
Pays: England
ID NLM: 0410462
Informations de publication
Date de publication:
12 2021
12 2021
Historique:
received:
27
05
2021
accepted:
13
10
2021
pubmed:
26
11
2021
medline:
1
3
2022
entrez:
25
11
2021
Statut:
ppublish
Résumé
Lung cancer is one of the most aggressive tumour types. Targeted therapies stratified by oncogenic drivers have substantially improved therapeutic outcomes in patients with non-small-cell lung cancer (NSCLC)
Identifiants
pubmed: 34819663
doi: 10.1038/s41586-021-04135-5
pii: 10.1038/s41586-021-04135-5
pmc: PMC8687755
mid: NIHMS1760523
doi:
Substances chimiques
Aminopyridines
0
Lactams
0
Microtubule-Associated Proteins
0
Neoplasm Proteins
0
Oncogene Proteins, Fusion
0
Pyrazoles
0
cytoplasmic linker protein 170
148349-95-5
LTK protein, human
EC 2.7.10.1
Receptor Protein-Tyrosine Kinases
EC 2.7.10.1
lorlatinib
OSP71S83EU
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
319-323Subventions
Organisme : NCI NIH HHS
ID : R01 CA240257
Pays : United States
Commentaires et corrections
Type : CommentIn
Type : CommentIn
Informations de copyright
© 2021. The Author(s), under exclusive licence to Springer Nature Limited.
Références
Konig, D., Savic Prince, S. & Rothschild, S. I. Targeted therapy in advanced and metastatic non-small cell lung cancer. An update on treatment of the most important actionable oncogenic driver alterations. Cancers 13, 713 (2021).
doi: 10.3390/cancers13040804
Saito, M. et al. Gene aberrations for precision medicine against lung adenocarcinoma. Cancer Sci. 107, 713–720 (2016).
doi: 10.1111/cas.12941
The Cancer Genome Atlas Research Network. Comprehensive molecular profiling of lung adenocarcinoma. Nature 511, 543–550 (2014).
doi: 10.1038/nature13385
Fernandez-Cuesta, L. et al. CD74–NRG1 fusions in lung adenocarcinoma. Cancer Discov. 4, 415–422 (2014).
doi: 10.1158/2159-8290.CD-13-0633
Non-small cell lung cancer version 4.2021 National Comprehensive Cancer Network https://www.nccn.org/professionals/physician_gls/pdf/nscl.pdf (2021).
Roll, J. D. & Reuther, G. W. ALK-activating homologous mutations in LTK induce cellular transformation. PLoS ONE 7, e31733 (2012).
doi: 10.1371/journal.pone.0031733
Scheel, J. et al. Purification and analysis of authentic CLIP-170 and recombinant fragments. J. Biol. Chem. 274, 25883–25891 (1999).
doi: 10.1074/jbc.274.36.25883
Grigoryan, G. & Keating, A. E. Structural specificity in coiled-coil interactions. Curr. Opin. Struct. Biol. 18, 477–483 (2008).
doi: 10.1016/j.sbi.2008.04.008
Varmus, H. E. The molecular genetics of cellular oncogenes. Annu. Rev. Genet. 18, 553–612 (1984).
doi: 10.1146/annurev.ge.18.120184.003005
Warmuth, M., Kim, S., Gu, X. J., Xia, G. & Adrián, F. Ba/F3 cells and their use in kinase drug discovery. Curr. Opin. Oncol. 19, 55–60 (2007).
doi: 10.1097/CCO.0b013e328011a25f
Soda, M. et al. Identification of the transforming EML4–ALK fusion gene in non-small-cell lung cancer. Nature 448, 561–566 (2007).
doi: 10.1038/nature05945
Greulich, H. et al. Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants. PLoS Med. 2, e313 (2005).
doi: 10.1371/journal.pmed.0020313
Kobayashi, S. et al. An alternative inhibitor overcomes resistance caused by a mutation of the epidermal growth factor receptor. Cancer Res. 65, 7096–7101 (2005).
doi: 10.1158/0008-5472.CAN-05-1346
Yasuda, H. et al. Structural, biochemical, and clinical characterization of epidermal growth factor receptor (EGFR) exon 20 insertion mutations in lung cancer. Sci. Transl. Med. 5, 216ra177 (2013).
doi: 10.1126/scitranslmed.3007205
Zou, H. Y. et al. PF-06463922, an ALK/ROS1 inhibitor, overcomes resistance to first and second generation ALK inhibitors in preclinical models. Cancer Cell 28, 70–81 (2015).
doi: 10.1016/j.ccell.2015.05.010
Yamada, S. et al. Expression of a chimeric CSF1R–LTK mediates ligand-dependent neurite outgrowth. Neuroreport 19, 1733–1738 (2008).
doi: 10.1097/WNR.0b013e3283186bf8
Bruno, R. & Fontanini, G. Next generation sequencing for gene fusion analysis in lung cancer: a literature review. Diagnostics 10, 521 (2020).
doi: 10.3390/diagnostics10080521
Kohno, T. et al. Beyond ALK–RET, ROS1 and other oncogene fusions in lung cancer. Transl. Lung Cancer Res. 4, 156–164 (2015).
pubmed: 25870798
pmcid: 4384213
The Cancer Genome Atlas Research Network. Integrated genomic characterization of papillary thyroid carcinoma. Cell 159, 676–690 (2014).
doi: 10.1016/j.cell.2014.09.050
Yoshihara, K. et al. The landscape and therapeutic relevance of cancer-associated transcript fusions. Oncogene 34, 4845–4854 (2015).
doi: 10.1038/onc.2014.406
Muller-Tidow, C. et al. High-throughput analysis of genome-wide receptor tyrosine kinase expression in human cancers identifies potential novel drug targets. Clin. Cancer Res. 10, 1241–1249 (2004).
doi: 10.1158/1078-0432.CCR-0954-03
Carvalho, P., Gupta, M. L., Jr., Hoyt, M. A. & Pellman, D. Cell cycle control of kinesin-mediated transport of Bik1 (CLIP-170) regulates microtubule stability and dynein activation. Dev. Cell 6, 815–829 (2004).
doi: 10.1016/j.devcel.2004.05.001
Drilon, A. et al. Cabozantinib in patients with advanced RET-rearranged non-small-cell lung cancer: an open-label, single-centre, phase 2, single-arm trial. Lancet Oncol. 17, 1653–1660 (2016).
doi: 10.1016/S1470-2045(16)30562-9
Kuroda, N. et al. ALK rearranged renal cell carcinoma (ALK-RCC): a multi-institutional study of twelve cases with identification of novel partner genes CLIP1, KIF5B and KIAA1217. Mod. Pathol. 33, 2564–2579 (2020).
doi: 10.1038/s41379-020-0578-0
Pinsolle, J. et al. A rare fusion of CLIP1 and ALK in a case of non-small-cell lung cancer with neuroendocrine features. Clin. Lung Cancer 20, e535–e540 (2019).
doi: 10.1016/j.cllc.2019.05.001
Yeh, I. et al. Clinical, histopathologic, and genomic features of Spitz tumors with ALK fusions. Am. J. Surg. Pathol. 39, 581–591 (2015).
doi: 10.1097/PAS.0000000000000387
Gainor, J. F. et al. Molecular mechanisms of resistance to first- and second-generation ALK inhibitors in ALK-rearranged lung cancer. Cancer Discov. 6, 1118–1133 (2016).
doi: 10.1158/2159-8290.CD-16-0596
Haas, B. J. et al. Accuracy assessment of fusion transcript detection via read-mapping and de novo fusion transcript assembly-based methods. Genome Biol. 20, 213 (2019).
doi: 10.1186/s13059-019-1842-9
Pear, W. S. et al. Efficient and rapid induction of a chronic myelogenous leukemia-like myeloproliferative disease in mice receiving P210 bcr/abl-transduced bone marrow. Blood 92, 3780–3792 (1998).
doi: 10.1182/blood.V92.10.3780
Borowicz, S. et al. The soft agar colony formation assay. J. Vis. Exp. (92), e51998 (2014).
Tomayko, M. M. & Reynolds, C. P. Determination of subcutaneous tumor size in athymic (nude) mice. Cancer Chemother. Pharmacol. 24, 148–154 (1989).
doi: 10.1007/BF00300234