Differential protein stability and ALK inhibitor sensitivity of EML4-ALK fusion variants

Clinical Cancer Research

Volumn 18, Issue 17, 2012, Pages 4682-4690

  Heuckmann, Johannes M ^a,b   Balke Want, Hyatt ^a,b   Malchers, Florian ^a,b   Peifer, Martin ^a,b   Sos, Martin L ^a,b,e   Koker, Mirjam ^a,b   Meder, Lydia ^a   Lovly, Christine M ^c   Heukamp, Lukas C ^a   Pao, William ^c   Küppers, Ralf ^d   Thomas, Roman K ^a,b  

^a UNIVERSITY OF COLOGNE   (Germany)

^b MAX PLANCK INSTITUTE FOR NEUROLOGICAL RESEARCH   (Germany)

^c VANDERBILT UNIVERSITY SCHOOL OF MEDICINE   (United States)

^d UNIVERSITY OF DUISBURG ESSEN   (Germany)

^e UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CRIZOTINIB; HEAT SHOCK PROTEIN 90; HEAT SHOCK PROTEIN 90 INHIBITOR; HYBRID PROTEIN; MICROTUBULE ASSOCIATED PROTEIN 4; PROTEIN TYROSINE KINASE; PROTEIN TYROSINE KINASE ALK; PROTEIN TYROSINE KINASE ALK ECHINODERM MICROTUBULE ASSOCIATED LIKE PROTEIN 4 FUSION PROTEIN; PROTEIN TYROSINE KINASE ALK INHIBITOR; PROTEIN TYROSINE KINASE INHIBITOR; TAE 684; UNCLASSIFIED DRUG;

ARTICLE; CANCER CELL CULTURE; CELLULAR DISTRIBUTION; CONTROLLED STUDY; CORRELATIONAL STUDY; DRUG CYTOTOXICITY; DRUG POTENTIATION; DRUG SENSITIVITY; DRUG TARGETING; EML4 ALK FUSION GENE; ENZYME INHIBITION; FUSION GENE; GENE; GENE CONSTRUCT; GENE DELETION; GENE LOCATION; GENETIC VARIABILITY; HUMAN; HUMAN CELL; KIF5B ALK GENE; NPM1 ALK GENE; PRIORITY JOURNAL; PROTEIN STABILITY;

ADENOCARCINOMA; ANIMALS; APOPTOSIS; CARCINOMA, NON-SMALL-CELL LUNG; CELL LINE, TUMOR; CELL PROLIFERATION; HSP90 HEAT-SHOCK PROTEINS; HUMANS; KINESIN; LUNG NEOPLASMS; MICE; NIH 3T3 CELLS; ONCOGENE PROTEINS, FUSION; PROTEIN KINASE INHIBITORS; PROTEIN STABILITY; PROTEIN-TYROSINE KINASES; PYRAZOLES; PYRIDINES; PYRIMIDINES; RECEPTOR PROTEIN-TYROSINE KINASES; SIGNAL TRANSDUCTION;

EID: 84865776102     PISSN: 10780432     EISSN: 15573265     Source Type: Journal    
DOI: 10.1158/1078-0432.CCR-11-3260     Document Type: Article

References (26)

1. Soda M, Choi YL, Enomoto M, Takada S, Yamashita Y, Ishikawa S, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature 2007;448:561-6.
2. Kwak EL, Bang YJ, Camidge DR, Shaw AT, Solomon B, Maki RG, et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer.N Engl J Med 2010;363:1693-703.
3. Takeuchi K, Choi YL, Soda M, Inamura K, Togashi Y, Hatano S, et al. Multiplex reverse transcription-PCR screening for EML4-ALK fusion transcripts. Clin Cancer Res 2008;14:6618-24.
4. Koivunen JP, Mermel C, Zejnullahu K, Murphy C, Lifshits E,Holmes AJ, et al. EML4-ALK fusion gene and efficacy of an ALK kinase inhibitor in lung cancer. Clin Cancer Res 2008;14:4275-83.
5. Soda M, Takada S, Takeuchi K, Choi YL, Enomoto M, Ueno T, et al. A mouse model for EML4-ALK-positive lung cancer. Proc Natl Acad Sci U S A 2008;105:19893-7.
6. FDA news release, August 26. Silver Spring, MD. U.S. Food and Drug Administration 2011.
7. Morris SW, Kirstein MN, Valentine MB, Dittmer KG, Shapiro DN, Saltman DL, et al. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin's lymphoma. Science 1994;263:1281-4.
8. Takeuchi K, Choi YL, Togashi Y, Soda M, Hatano S, Inamura K, et al. KIF5B-ALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALK-positive lung cancer. Clin Cancer Res 2009;15:3143-9.
9. Choi YL, Soda M, Yamashita Y, Ueno T, Takashima J, Nakajima T, et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. N Engl J Med 2010;363:1734-9.
10. Sasaki T, Rodig SJ, Chirieac LR, Janne PA. The biology and treatment of EML4-ALK non-small cell lung cancer. Eur J Cancer 2010;46:1773-80.
11. Pollmann M, Parwaresch R, Adam-Klages S, Kruse ML, Buck F, Heidebrecht HJ. Human EML4, a novel member of the EMAP family, is essential for microtubule formation. Exp Cell Res 2006;312:3241-51.
12. Sharma SV, Bell DW, Settleman J, Haber DA. Epidermal growth factor receptor mutations in lung cancer. Nat Rev Cancer 2007;7:169-81.
13. Kancha RK, von Bubnoff N, Peschel C, Duyster J. Functional analysis of epidermal growth factor receptor (EGFR) mutations and potential implications for EGFR targeted therapy. Clin Cancer Res 2009;15:460-7.
14. Soria JC, Mok TS, Cappuzzo F, Janne PA. EGFR-mutated oncogene-addicted non-small cell lung cancer: current trends and future prospects. Cancer Treat Rev 2012;38:416-30.
15. Yuza Y, Glatt KA, Jiang J, Greulich H, Minami Y, Woo MS, et al. Allele-dependent variation in the relative cellular potency of distinct EGFR inhibitors. Cancer Biol Ther 2007;6:661-7.
16. Greulich H, Chen TH, Feng W, Janne PA, Alvarez JV, Zappaterra M, et al. Oncogenic transformation by inhibitor-sensitive and -resistant EGFR mutants. PLoS Med 2005;2:e313.
17. SosML, Koker M,Weir BA, Heynck S, Rabinovsky R, Zander T, et al. PTEN loss contributes to erlotinib resistance in EGFR-mutant lung cancer by activation of Akt and EGFR. Cancer Res 2009;69:3256-61.
18. Sos ML, Rode HB, Heynck S, Peifer M, Fischer F, Kluter S, et al. Chemogenomic profiling provides insights into the limited activity of irreversible EGFR Inhibitors in tumor cells expressing the T790M EGFR resistance mutation. Cancer Res 2010;70:868-74.
19. Heuckmann JM, Holzel M, Sos ML, Heynck S, Balke-Want H, Koker M, et al. ALK mutations conferring differential resistance to structurally diverse ALK inhibitors. Clin Cancer Res 2011;17:7394-401.
20. Lovly CM, Heuckmann JM, de Stanchina E, Chen H, Thomas RK, Liang C, et al. Insights into ALK-driven cancers revealed through development of novel ALK tyrosine kinase inhibitors. Cancer Res 2011;71:4920-31.
21. Takezawa K, Okamoto I, Nishio K, Janne PA, Nakagawa K. Role of ERK-BIM and STAT3-survivin signaling pathways in ALK inhibitor-induced apoptosis in EML4-ALK-positive lung cancer. Clin Cancer Res 2011;17:2140-8.
22. Xu C, Min J. Structure and function of WD40 domain proteins. Protein Cell 2011;2:202-14.
23. Normant E, Paez G, West KA, Lim AR, Slocum KL, Tunkey C, et al. The Hsp90 inhibitor IPI-504 rapidly lowers EML4-ALK levels and induces tumor regression in ALK-driven NSCLC models. Oncogene 2011;30:2581-6.
24. Chen Z, Sasaki T, Tan X, Carretero J, Shimamura T, Li D, et al. Inhibition of ALK, PI3K/MEK, and HSP90 in murine lung adenocarcinoma induced by EML4-ALK fusion oncogene. Cancer Res 2010;70:9827-36.
25. Katayama R, Khan TM, Benes C, Lifshits E, Ebi H, Rivera VM, et al. Therapeutic strategies to overcome crizotinib resistance in non-small cell lung cancers harboring the fusion oncogene EML4-ALK. Proc Natl Acad Sci U S A 2011;108:7535-40.
26. Peifer M, Weiss J, Sos ML, Koker M, Heynck S, Netzer C, et al. Analysis of compound synergy in high-throughput cellular screens by population-based lifetime modeling. PLoS One 2010;5:e8919.