Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer

J Weiss; ML Sos; D Seidel; M Peifer; T Zander; JM Heuckmann; RT Ullrich; R Menon; S Maier; A Soltermann; H Moch; P Wagener; F Fischer; S Heynck; M Koker; J Schöttle; F Leenders; F Gabler; I Dabow; S Querings; LC Heukamp; H Balke-Want; S Ansén; D Rauh; I Baessmann; J Altmüller; Z Wainer; M Conron; G Wright; P Russell; B Solomon; E Brambilla; C Brambilla; P Lorimier; S Sollberg; OT Brustugun; W Engel-Riedel; C Ludwig; I Petersen; J Sänger; J Clement; H Groen; W Timens; H Sietsma; E Thunnissen; E Smit; D Heideman; F Cappuzzo; C Ligorio; S Damiani; M Hallek; R Beroukhim; W Pao; B Klebl; M Baumann; R Buettner; K Ernestus; E Stoelben; J Wolf; P Nürnberg; S Perner; RK Thomas

Journal article

Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer

J Weiss, ML Sos, D Seidel, M Peifer, T Zander, JM Heuckmann, RT Ullrich, R Menon, S Maier, A Soltermann, H Moch, P Wagener, F Fischer, S Heynck, M Koker, J Schöttle, F Leenders, F Gabler, I Dabow, S Querings Show all

Science Translational Medicine | Published : 2010

DOI: 10.1126/scitranslmed.3001451

Abstract

Lung cancer remains one of the leading causes of cancer-related death in developed countries. Although lung adenocarcinomas with EGFR mutations or EML4-ALK fusions respond to treatment by epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK) inhibition, respectively, squamous cell lung cancer currently lacks therapeutically exploitable genetic alterations.We conducted a systematic search in a set of 232 lung cancer specimens for genetic alterations that were therapeutically amenable and then performed high-resolution gene copy number analyses. We identified frequent and focal fibroblast growth factor receptor 1 (FGFR1) amplification in squamous cell lung cancer (n = 15..

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University of Melbourne Researchers

Zoe Wainer Author

Matthew Conron Author

Gavin Wright Author

Grants

Awarded by National Cancer Institute

Funding Acknowledgements

This work was supported by the Deutsche Krebshilfe (grant 107954 to R. K. T.); the German Ministry of Science and Education (BMBF) as part of the NGFNplus program (grants 01GS08100 to R. K. T. and 01GS08101 to J. Wolf and P.N.); the Max Planck Society (M.I.F.A.NEUR8061 to R. K. T.); the Deutsche Forschungsgemeinschaft (DFG) through SFB (TP6 to R. K. T. and R. T. U.; TP5 to L. C. H. and R. Buettner); the Ministry for Innovation, Science, Research and Technology of the State of Nordrhein-Westfalen (MIWT, 4000-12 09 to R. K. T. and B. K.); and an anonymous foundation to R. K. T. E. B. and C. B. were supported by the PNES INCA grant 2008. B. S. was supported by the International Association for the Study of Lung Cancer Young Investigator Award. W. P. was supported by a grant from the NIH National Cancer Institute. Z.W. was supported by the Royal Australasian College of Surgeons and a Raelene Boyle Scholarship. G. W. was supported by the Australasian Society of Cardiac and Thoracic Surgeons Foundation Grant, Peter MacCallum Foundation Grant, and a private research donation from family and friends of former patients. R.K.T. receives consulting and lecture fees from Sequenom, Sanofi-Aventis, Merck, Roche, Infinity, Boehringer, AstraZeneca, and ATLAS Biolabs, as well as research support from Novartis and AstraZeneca. J. Wolf is a member of advisory boards of Roche, AstraZeneca, Novartis, Amgen, Bayer, and Merck and has received lecture fees from Roche, AstraZeneca, and Merck. R. Beroukhim receives consulting fees for Novartis Institutes for BioMedical Research. W. P. receives consulting fees from Molecular MD, AstraZeneca, BMS, and Symphony Evolution. H. G. received research support from Eli Lilly, Roche, and Boehringer Ingelheim through the University Medical Center Groningen. The other authors declare that they have no competing interests. Accession numbers: All raw data are publicly available (GEO; GSE25016).