ALK-rearrangements and testing methods in non-small cell lung cancer: A review

Genes and Cancer

Volumn 5, Issue 1-2, 2015, Pages 1-14

  Shackelford, Rodney E ^a   Vora, Moiz ^a   Mayhall, Kim ^b   Cotelingam, James ^a  

^a LOUISIANA STATE UNIVERSITY   (United States)

^b TULANE UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Anaplastic lymphoma kinase; Crizotinib; Non small cell lung cancer; Pulmonary adenocarcinoma

Indexed keywords

ANAPLASTIC LYMPHOMA TYROSINE KINASE; BRIGATINIB; CERITINIB; CRIZOTINIB; HEAT SHOCK PROTEIN 90; JANUS KINASE; MAMMALIAN TARGET OF RAPAMYCIN; MICROTUBULE ASSOCIATED PROTEIN; MIDKINE; PLEIOTROPHIN; PROTEIN TYROSINE KINASE; UNCLASSIFIED DRUG; ANAPLASTIC LYMPHOMA KINASE; DOCETAXEL; GANETESPIB; HYBRID PROTEIN; PEMETREXED;

ANAPLASTIC LYMPHOMA TYROSINE KINASE GENE; CHROMOSOME TRANSLOCATION; DIARRHEA; FATIGUE; FLUORESCENCE IN SITU HYBRIDIZATION; GENE; GENE AMPLIFICATION; GENE EXPRESSION; GENE MUTATION; GENE REARRANGEMENT; HUMAN; IMMUNOHISTOCHEMISTRY; NAUSEA; NEOPLASM; NEXT GENERATION SEQUENCING; NON SMALL CELL LUNG CANCER; NONHODGKIN LYMPHOMA; OVARY CANCER; PHASE 1 CLINICAL TRIAL (TOPIC); PHASE 2 CLINICAL TRIAL (TOPIC); PLASMA CELL GRANULOMA; PRIORITY JOURNAL; REVERSE TRANSCRIPTION POLYMERASE CHAIN REACTION; REVIEW; SIGNAL TRANSDUCTION; VOMITING; ARTICLE; MULTIMODALITY CANCER THERAPY; PROGRESSION FREE SURVIVAL; PROTEIN EXPRESSION; PROTEIN FOLDING; TUMOR REGRESSION;

EID: 84924358819     PISSN: 19476019     EISSN: 19476027     Source Type: Journal    
DOI: None     Document Type: Review

References (159)

1. Ferlay J, Shin HR, Bray F, Forman D, Mathers C, Parkin DM. Estimates of worldwide burden of cancer in 2008: GLOBOCAN 2008. Int J Cancer. 2010;127:2893-917.
2. Ettinger DS, Akerley W, Bepler G, et al. NCCN Non-Small Cell Lung Cancer Panel Members. Non-small cell lung cancer. J Natl Compr Canc Netw. 2010;8:740-801.
3. Hsiao SH, Chung CL, Lee CM, et al. Suitability of Computed Tomography-Guided Biopsy Specimens for Subtyping and Genotyping of Non-Small-Cell Lung Cancer. Clin Lung Cancer. 2013:S1525-7304(13)00130-7.
4. Alberg AJ, Brock MV, Ford JG, Samet JM, Spivack SD. Epidemiology of lung cancer: Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2013;143(5 Suppl):e1S-29S.
5. SEER Cancer Statistics Review, 1973-2008. Washington DC: US National Institutes of Health. National Cancer Institute.
6. Vogelstein B, Papadopoulos N, Velculescu VE, Zhou S, Diaz LA Jr, Kinzler KW. Cancer genome landscapes. Science. 2013;339:1546-58.
7. Govindan R, Ding L, Griffith M, Subramanian J, et al. Genomic landscape of non-small cell lung cancer in smokers and never-smokers. Cell. 2012;150:1121-34.
8. Soda M, Choi YL, Enomoto M, Takada S, et al. Identification of the transforming EML4-ALK fusion gene in non-small-cell lung cancer. Nature. 2007;448:561-6.
9. Rikova K, Guo A, Zeng Q, et al. Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell. 2007;131:1190-203.
10. Samuels Y, Wang Z, Bardelli A, et al. High frequency of mutations of the PIK3CA gene in human cancers. Science 2004;304:554.
11. Heinmoller P, Gross C, Beyser K, et al. HER2 status in nonsmall cell lung cancer: results from patient screening for enrollment to a phase II study of herceptin. Clin Cancer Res 2003; 9:5238-43.
12. Stephens P, Hunter C, Bignell G, et al. Lung cancer: intragenic ERBB2 kinase mutations in tumours. Nature 2004; 431: 525-26.
13. Ding L, Getz G, Wheeler DA, et al. Somatic mutations affect key pathways in lung adenocarcinoma. Nature 2008;455:1069-75.
14. Malanga D, Scrima M, De Marco C, et al. Activating E17K mutation in the gene encoding the protein kinase AKT1 in a subset of squamous cell carcinoma of the lung. Cell Cycle 2008;7:665-69.
15. Davies H, Bignell GR, Cox C, et al. Mutations of the BRAF gene in human cancer. Nature 2002;417:949-54.
16. Sasaki H, Kawano O, Endo K, et al. Uncommon V599E BRAF mutations in Japanese patients with lung cancer. J Surg Res 2006;133:203-06.
17. Naoki K, Chen TH, Richards WG, Sugarbaker DJ, Meyerson M. Missense mutations of the BRAF gene in human lung adenocarcinoma. Cancer Res 2002;62:7001-03.
18. Marks JL, Gong Y, Chitale D, et al. Novel MEK1 mutation identified by mutational analysis of epidermal growth factor receptor signaling pathway genes in lung adenocarcinoma. Cancer Res 2008;68:5524-28.
19. Onozato R, Kosaka T, Kuwano H, Sekido Y, Yatabe Y, Mitsudomi T. Activation of MET by gene amplifi cation or by splice mutations deleting the juxtamembrane domain in primary resected lung cancers. J Thorac Oncol 2009;4:5-11.
20. Cappuzzo F, Marchetti A, Skokan M, et al. Increased MET gene copy number negatively aff ects survival of surgically resected non-small-cell lung cancer patients. J Clin Oncol 2009;27:1667-74.
21. Beau-Faller M, Ruppert AM, Voegeli AC, et al. MET gene copy number in non-small cell lung cancer: molecular analysis in a targeted tyrosine kinase inhibitor naive cohort. J Thorac Oncol 2008;3:331-39.
22. Cancer Genome Atlas Research Network. Comprehensive genomic characterization of squamous cell lung cancers. Nature. 2012;489:519-25.
23. Forbes SA, Bindal N, Bamford S, Cole C, Kok CY, Beare D, et al. COSMIC: mining complete cancer genomes in the Catalogue of Somatic Mutations in Cancer. Nucleic Acids Res 2011;39:D945-50. P
24. Kohno T, Takahashi M, Manda R, Yokota J. Inactivation of the PTEN/MMAC1/TEP1 gene in human lung cancers. Genes Chromosomes Cancer 1998;22152-6.
25. Marsit CJ, Zheng S, Aldape K, et al. PTEN expression in non-small-cell lung cancer: evaluating its relation to tumor characteristics, allelic loss, and epigenetic alteration. Hum Pathol 2005;36768-76.
26. Soria JC, Lee HY, Lee JI, et al. Lack of PTEN expression in non-small cell lung cancer could be related to promoter methylation. Clin Cancer Res 2002;81178-84.
27. Jin G, Kim MJ, Jeon HS, et al. PTEN mutations and relationship to EGFR, ERBB2, KRAS, and TP53 mutations in non-small cell lung cancers. Lung Cancer 2010;69:279-83.
28. Bass AJ, Watanabe H, Mermel CH, et al. SOX2 is an amplified lineage-survival oncogene in lung and esophageal squamous cell carcinomas. Nat Genet 2009;41:1238-42.
29. Dutt A, Ramos AH, Hammerman PS, et al. Inhibitorsensitive FGFR1 amplification in human non-small cell lung cancer. PLoS ONE 2011;6:e20351.
30. Hammerman PS, Sos ML, Ramos AH, et al. Mutations in the DDR2 kinase gene identify a novel therapeutic target in squamous cell lung cancer. Cancer Discov 2011;1:78-89.
31. Matsumoto S, Iwakawa R, Takahashi K, et al. Prevalence and specificity of LKB1 genetic alterations in lung cancers. Oncogene 2007;26:5911-8.
32. Hussenet T, Dali S, Exinger J, et al. SOX2 is an oncogene activated by recurrent 3q26.3 amplifications in human lung squamous cell carcinomas. PLoS ONE 2010;5:e8960.
33. Weiss J, Sos ML, Seidel D, Peifer M, Zander T, Heuckmann JM, et al. Frequent and focal FGFR1 amplification associates with therapeutically tractable FGFR1 dependency in squamous cell lung cancer. Sci Transl Med 2010;2:62ra93.
34. Bass AJ, Watanabe H, Mermel CH, et al. SOX2 is an amplified lineage-survival oncogene in lung and esophageal squamous cell carcinomas. Nat Genet 2009;41:1238-42.
35. Hammerman PS, Hayes DN, Wilkerson MD, et al. Comprehensive genomic characterization of squamous cell lung cancers. Nature 2012;489:519-525.
36. Rikova K, Guo A, Zeng Q, et al. Global survey of phosphotyrosine signaling identifies oncogenic kinases in lung cancer. Cell 2007;131:1190-203.
37. Takeuchi K, Soda M, Togashi Y, et al. RET, ROS1 and ALK fusions in lung cancer. Nat Med 2012;18:378-81. http://clincancerres.aacrjournals.org/external-ref?access_num=10.1038/nm.2658&link_type=DOI
38. Planchard D. Identification of driver mutations in lung cancer: first step in personalized cancer. Target Oncol. 2013;8:3-14.
39. Köhler J, Schuler M. Afatinib, Erlotinib and Gefitinib in the First-Line Therapy of EGFR Mutation-Positive Lung Adenocarcinoma: A Review. Onkologie. 2013;36:510-8.
40. Ohashi K, Sequist LV, Arcila ME, et al. Lung cancers with acquired resistance to EGFR inhibitors occasionally harbor BRAF gene mutations but lack mutations in KRAS, NRAS, or MEK1. Proc Natl Acad Sci U S A. 2012;109:E2127-33.
41. Burgeiro A, Mollinedo F, Oliveira PJ. Ipilimumab and vemurafenib: two different routes for targeting melanoma. Curr Cancer Drug Targets. 2013;13:879-94.
42. Zimmermann G, Papke B, Ismail S, et al. Small molecule inhibition of the KRAS-PDEδ interaction impairs oncogenic KRAS signalling. Nature. 2013;497:638-42.
43. Maemondo M, Inoue A, Kobayashi K, Sugawara S, Oizumi S, Isobe H, Gemma A, Harada M, Yoshizawa H, Kinoshita I, et al. North-East Japan Study Group. Gefitinib or chemotherapy for non-small-cell lung cancer with mutated EGFR. N Engl J Med. 2010;362:2380-8.
44. Shaw AT, Kim DW, Nakagawa K, Seto T, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med. 2013;368:2385-94.
45. Shepherd FA, Rodrigues Pereira J, Ciuleanu T, Tan EH, Hirsh V, Thongprasert S, Campos D, Maoleekoonpiroj S, Smylie M, et al. National Cancer Institute of Canada Clinical Trials Group. Erlotinib in previously treated nonsmall-cell lung cancer. N Engl J Med. 2005;353:123-32.
46. Jänne PA, Gurubhagavatula S, Yeap BY, et al. Outcomes of patients with advanced non-small cell lung cancer treated with gefitinib (ZD1839, “Iressa”) on an expanded access study. Lung Cancer. 2004;44:221-30.
47. Jackman DM, Miller VA, Cioffredi LA, et al. Impact of epidermal growth factor receptor and KRAS mutations on clinical outcomes in previously untreated non-small cell lung cancer patients: Results of an online tumor registry of clinical trials. Clin Cancer Res. 2009;15:5267-5273.
48. West H, Lilenbaum R, Harpole D, et al. Molecular analysisbased treatment strategies for the management of non-small cell lung cancer. J Thorac Oncol. 2009;4:s1029-s39.
49. Lindeman NI, Cagle PT, Beasley MB, et al. Molecular testing guideline for selection of lung cancer patients for EGFR and ALK tyrosine kinase inhibitors: guideline from the College of American Pathologists, International Association for the Study of Lung Cancer, and Association for Molecular Pathology. J Mol Diagn. 2013;15:415-53.
50. Hallberg B, Palmer RH. Mechanistic insight into ALK receptor tyrosine kinase in human cancer biology. Nat Rev Cancer 2013;13:685-700.
51. Bilsland, J. G. et al. Behavioral and neurochemical alterations in mice deficient in anaplastic lymphoma kinase suggest therapeutic potential for psychiatric indications. Neuropsychopharmacology 2008;33:685-700.
52. Hurley SP, Clary D, Copie V, Lefcort F. Anaplastic lymphoma kinase is dynamically expressed on subsets of motor neurons and in the peripheral nervous system. J. Comp. Neurol. 2006:495;202-12.
53. Vernersson, E. et al. Characterization of the expression of the ALK receptor tyrosine kinase in mice. Gene Expr. Patterns 2006:6;448-61.
54. Weiss, J. B. et al. Anaplastic lymphoma kinase and leukocyte tyrosine kinase: functions and genetic interactions in learning, memory and adult neurogenesis. Pharmacol. Biochem. Behav. 2012:100;566-74.
55. Iwahara, T. et al. Molecular characterization of ALK, a receptor tyrosine kinase expressed specifically in the nervous system. Oncogene 1997:14;439-49.
56. Ning H, Mitsui H, Wang CQ, Suárez-Fariñas M, et al. Identification of anaplastic lymphoma kinase as a potential therapeutic target in Basal Cell Carcinoma. Oncotarget. 2013 in press.
57. Weiss JB, Xue C, Benice T, Xue L, Morris SW, Raber J. Anaplastic lymphoma kinase and leukocyte tyrosine kinase: functions and genetic interactions in learning, memory and adult neurogenesis. Pharmacol Biochem Behav. 2012;100:566-74.
58. Reiner DJ, Ailion M, Thomas JH, Meyer BJ. C. elegans anaplastic lymphoma kinase ortholog SCD-2 controls dauer formation by modulating TGF-beta signaling. Curr Biol. 2008;18:1101-9.
59. Ishihara T, Iino Y, Mohri A, et al. HEN-1, a secretory protein with an LDL receptor motif, regulates sensory integration and learning in Caenorhabditis elegans. Cell. 2002;109:639-49.
60. Stoica GE, Kuo A, Aigner I, et al. Identification of anaplastic lymphoma kinase as a receptor for the growth factor pleiotrophin. J. Biol. Chem. 2001:276;16772-9.
61. Stoica GE, Kuo A, Powers C, et al. Midkine binds to anaplastic lymphoma kinase (ALK) and acts as a growth factor for different cell types. J. Biol. Chem. 2002:277;35990-8.
62. Mathivet TL, Mazot P, Vigny M. In contrast to agonist monoclonal antibodies, both C-terminal truncated form and full length form of Pleiotrophin failed to activate vertebrate ALK (anaplastic lymphoma kinase)? Cell Signal. 2007;19:2434-43.
63. Moog-Lutz CL, Degoutin J, Gouzi JY, et al. Activation and inhibition of anaplastic lymphoma kinase receptor tyrosine kinase by monoclonal antibodies and absence of agonist activity of pleiotrophin. J Biol Chem. 2005;280:26039-48.
64. Mourali JL, Bénard A, Lourenço FC, et al. Anaplastic lymphoma kinase is a dependence receptor whose proapoptotic functions are activated by caspase cleavage. Mol Cell Biol. 2006;26:6209-22.
65. Motegi AL, Fujimoto J, Kotani M, Sakuraba H, Yamamoto T. ALK receptor tyrosine kinase promotes cell growth and neurite outgrowth. J Cell Sci. 2004;117:3319-29.
66. Morris SW, Kirstein MN, Valentine MB, Dittmer KG, Shapiro DN, Saltman DL, Look AT. Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non- Hodgkin’s lymphoma. Science. 1994;263:1281-4.
67. Delsol G, Ralfkiaer E, Stein H, Wright D, Jaffe ES. Anaplastic large cell lymphoma: primary systemic (T/null cell type). In: Jaffe ES, Harris NL, Stein H, eds. World Health Organization (WHO) Classification of Tumours: Pathology and Genetics of Tumours of Haematopoietic and Lymphoid Tissues. Lyon, France: IARC Press; 2001:230-5.
68. Stein H, Foss HD, Durkop H, et al. CD30(+) anaplastic large cell lymphoma: a review of its histopathologic, genetic, and clinical features. Blood. 2000;96:3681-95.
69. Pulford K, Lamant L, Espinos E, et al. The emerging normal and disease-related roles of anaplastic lymphoma kinase. Cell Mol Life Sci. 2004;61:2939-53.
70. Heuckmann JM, Balke-Want H, Malchers F, et al. Differential protein stability and ALK inhibitor sensitivity of EML4-ALK fusion variants. Clin Cancer Res. 2012;18:4682-90.
71. Takeuchi K, Choi YL, Togashi Y, et al. KIF5BALK, a novel fusion oncokinase identified by an immunohistochemistry-based diagnostic system for ALKpositive lung cancer. Clin Cancer Res. 2009;15:3143-9.
72. Lin E, Li L, Guan Y, Soriano R, et al. Exon array profiling detects EML4-ALK fusion in breast, colorectal, and nonsmall cell lung cancers. Mol Cancer Res. 2009;7:1466-76.
73. Robertson FM, Petricoin Iii EF, Van Laere SJ, et al. Presence of anaplastic lymphoma kinase in inflammatory breast cancer. Springerplus. 2013;2:497.
74. Lamant L, Pulford K, Bischof D, et al. Expression of the ALK tyrosine kinase gene in neuroblastoma. Am J Pathol. 2000;156:1711-21.
75. Wang M, Zhou C, Sun Q, Cai R, Li Y, Wang D, Gong L. ALK amplification and protein expression predict inferior prognosis in neuroblastomas. Exp Mol Pathol. 2013;95:124-30.
76. Mossé YP, Laudenslager M, Longo L, et al. Identification of ALK as a major familial neuroblastoma predisposition gene. Nature 2008;455:930-5.
77. Cook JR, Dehner LP, Collins MH, et al. Anaplastic lymphoma kinase (ALK) expression in the inflammatory myofibroblastic tumor: a comparative immunohistochemical study. Am J Surg Pathol 2001;25:1364-71.
78. Gleason BC, Hornick JL. Inflammatory myofibroblastic tumours: where are we now? J Clin Pathol 2008; 61:428-37.
79. Coffin CM, Patel A, Perkins S, Elenitoba-Johnson KS, Perlman E, Griffin CA. ALK1 and p80 expression and chromosomal rearrangements involving 2p23 in inflammatory myofibroblastic tumor. Mod Pathol 2001;14:569-76.
80. Gascoyne RD, Lamant L, Martin-Subero JI, et al. ALKpositive diffuse large B-cell lymphoma is associated with Clathrin-ALK rearrangements: report of 6 cases. Blood 2003;102:2568-73.
81. Laurent C, Do C, Gascoyne RD, Lamant L, et al. Anaplastic lymphoma kinase-positive diffuse large B-cell lymphoma: a rare clinicopathologic entity with poor prognosis. J Clin Oncol 2009;27:4211-6.
82. Powers C, Aigner A, Stoica GE, McDonnell K, and Wellstein A. Pleiotrophin signaling through anaplastic lymphoma kinase is rate-limiting for glioblastoma growth. J Biol Chem 2002;277:14153-8.
83. Grzelinski M, Steinberg F, Martens T, Czubayko F, Lamszus K, Aigner A. Enhanced antitumorigenic effects in glioblastoma ondouble targeting of pleiotrophin and its receptor ALK. Neoplasia 2009;11:145-56
84. Debelenko LV, Raimondi SC, Daw N, et al. Renal cell carcinoma with novel VCL-ALK fusion: new representative of ALK-associated tumor spectrum. Mod Pathol 2011;24:430-42.
85. Mariño-Enríquez A, Ou WB, Weldon CB, Fletcher JA, Pérez-Atayde AR. ALK rearrangement in sickle cell trait-associated renal medullary carcinoma. Genes Chromosomes Cancer 2011;50:146-53.
86. Sukov WR, Hodge JC, Lohse CM, et al. ALK alterations in adult renal cell carcinoma: frequency, clinicopathologic features and outcome in a large series of consecutively treated patients. Mod Pathol 2012;25:1516-25.
87. Sugawara E, Togashi Y, Kuroda N, et al. Identification of anaplastic lymphoma kinase fusions in renal cancer: large-scale immunohistochemical screening by the intercalated antibody-enhanced polymer method. Cancer 2012;118:4427-36.
88. Du XL, Hu H, Lin DC, Xia SH, et al. Proteomic profiling of proteins dysregulted in Chinese esophageal squamous cell carcinoma. J Mol Med. 2007;85:863-75.
89. Dirks WG, Fahnrich S, Lis Y, et al. Expression and functional analysis of the anaplastic lymphoma kinase (ALK) gene in tumor cell lines. Int J Cancer 2002;100:49-56.
90. Li XQ, Hisaoka M, Shi DR, et al. Expression of anaplastic lymphoma kinase in soft tissue tumors an immunohistochemical and molecular study of 249 cases. Hum Pathol 2004;35:711-21.
91. Ren H, Tan ZP, Zhu X, et al. Identification of anaplastic lymphoma kinase as a potential therapeutic target in ovarian cancer. Cancer Res. 2012;72:3312-23.
92. Murugan AK, Xing M. Anaplastic thyroid cancers harbor novel oncogenic mutations of the ALK gene. Cancer Res. 2011;71:4403-11.
93. Niu HT, Zhou QM, Wang F, et al. Identification of anaplastic lymphoma kinase break points and oncogenic mutation profiles in acral/mucosal melanomas. Pigment Cell Melanoma Res. 2013;26:646-53.
94. Pillay K, Govender D, Chetty R. ALK protein expression in rhabdomyosarcomas. Histopathology. 2002;41:461-7.
95. Corao DA, Biegel JA, Coffin CM, et al. ALK expression in rhabdomyosarcomas: correlation with histologic subtype and fusion status. Pediatr Dev Pathol. 2009;12:275-83.
96. Bonvini P, Zin A, Alaggio R, Pawel B, Bisogno G, Rosolen A. High ALK mRNA expression has a negative prognostic significance in rhabdomyosarcoma. Br J Cancer. 2013, in press.
97. Wang WY, Gu L, Liu WP, Li GD, Liu HJ, Ma ZG. ALKpositive extramedullary plasmacytoma with expression of the CLTC-ALK fusion transcript. Pathol Res Pract 2011;207:587-91.
98. Sasaki T, Rodig SJ, Chirieac LR, Jänne PA. The biology and treatment of EML4-ALK non-small cell lung cancer. Eur J Cancer. 2010;46:1773-80.
99. Doebele RCL, Pilling AB, Aisner DL, et al. Mechanisms of resistance to crizotinib in patients with ALK gene rearranged non-small cell lung cancer. Clin Cancer Res. 2012;18:1472-82.
100. Schönherr C, Ruuth K, Eriksson T, et al. The neuroblastoma ALK(I1250T) mutation is a kinase-dead RTK in vitro and in vivo. Transl Oncol. 2011;4:258-65.
101. Rodig SJ, Mino-Kenudson M, Dacic S, et al. Unique clinicopathologic features characterize ALK-rearranged lung adenocarcinoma in the western population. Clin Cancer Res. 2009;15:5216-23.
102. Li Y, Pan Y, Wang R, Sun Y, et al. ALK-rearranged lung cancer in Chinese: a comprehensive assessment of clinicopathology, IHC, FISH and RT-PCR. PLoS One. 2013;8:e69016.
103. Shaw AT, Yeap BY, Mino-Kenudson M, et al. Clinical features and outcome of patients with non-small-cell lung cancer who harbor EML4-ALK. J Clin Oncol. 2009;27:4247-53.
104. Inamura K, Takeuchi K, Togashi Y, et al. EML4-ALK fusion is linked to histological characteristics in a subset of lung cancers. J Thorac Oncol. 2008;3:13-17.
105. Shaozhang Z, Xiaomei L, Aiping Z, et al. Detection of EML4-ALK fusion genes in non-small cell lung cancer patients with clinical features associated with EGFR mutations. Genes Chromosomes Cancer. 2012;51:925-32.
106. Jemal, A. Clegg LX, Ward E, et al. Annual report to the nation on the status of cancer, 1975-2001, with a special feature regarding survival. Cancer 2004;101;3-27.
107. Shaw, AT. et al. Impact of crizotinib on survival in patients with advanced, ALK-positive NSCLC compared with historical controls. J. Clin. Oncol. 2001, 29, Abstr. 7507.
108. Kim H, Xu X, Yoo SB, et al. Discordance between anaplastic lymphoma kinase status in primary non-smallcell lung cancers and their corresponding metastases. Histopathology. 2013;62:305-14.
109. Doebele RC, Lu X, Sumey C, et al. Oncogene status predicts patterns of metastatic spread in treatment-naive nonsmall cell lung cancer. Cancer. 2012;118:4502-11.
110. Lira ME, Kim TM, Huang D, et al. Multiplexed gene expression and fusion transcript analysis to detect ALK fusions in lung cancer. J Mol Diagn. 2013:15:51-61.
111. http://www.abbott.com/news-media/press-releases/2011-aug26.htm
112. Wu YC, Chang IC, Wang CL, et al. Comparison of IHC, FISH and RT-PCR methods for detection of ALK rearrangements in 312 non-small cell lung cancer patients in Taiwan. PLoS One. 2013;8:e70839.
113. Lamant L, Meggetto F, al Saati T, et al. High incidence of the t(2;5)(p23;q35) translocation in anaplastic large cell lymphoma and its lack of detection in Hodgkin’s disease. Comparison of cytogenetic analysis, reverse transcriptasepolymerase chain reaction, and P-80 immunostaining. Blood 1996;87:284-91.
114. Pulford K, Lamant L, Morris SW, et al. Detection of anaplastic lymphoma kinase (ALK) and nucleolar protein nucleophosmin (NPM)-ALK proteins in normal and neoplastic cells with the monoclonal antibody ALK1. Blood 1997;89:1394-04.
115. Mino-Kenudson M, Chirieac LR, Law K, et al. A novel, highly sensitive antibody allows for the routine detection of ALK-rearranged lung adenocarcinomas by standard immunohistochemistry. Clin Cancer Res. 2010;16:1561-71.
116. Thunnissen E, Bubendorf L, Dietel M, et al. EML4-ALK testing in non-small cell carcinomas of the lung: a review with recommendations. Virchows Arch. 2012;461:245-57.
117. Paik JH, Choe G, Kim H, Choe JY, et al. Screening of anaplastic lymphoma kinase rearrangement by immunohistochemistry in non-small cell lung cancer: correlation with fluorescence in situ hybridization. J Thorac Oncol. 2011;6:466-72.
118. Zhang YG, Jin ML, Li L, et al. Evaluation of ALK rearrangement in Chinese non-small cell lung cancer using FISH, immunohistochemistry, and real-time quantitative RT- PCR on paraffin-embedded tissues. PLoS One. 2013;8:e64821.
119. Wang R, Pan Y, Li C, Hu H, et al. The use of quantitative real-time reverse transcriptase PCR for 5’ and 3’ portions of ALK transcripts to detect ALK rearrangements in lung cancers. Clin Cancer Res. 2012;18:4725-32.
120. Geiss GK, Bumgarner RE, Birditt B, et al. Direct multiplexed measurement of gene expression with colorcoded probe pairs. Nat Biotechnol. 2008;26:317-25.
121. Peled N, Palmer G, Hirsch FR, et al. Next-generation sequencing identifies and immunohistochemistry confirms a novel crizotinib-sensitive ALK rearrangement in a patient with metastatic non-small-cell lung cancer. J Thorac Oncol. 2012;7:e14-6.
122. Christensen JG, Zou HY, Arango ME, et al. Cytoreductive antitumor activity of PF-2341066, a novel inhibitor of anaplastic lymphoma kinase and c-Met, in experimental models of anaplastic large-cell lymphoma. Mol Cancer Ther. 2007;6:3314-22.
123. Cui J. et al. Structure based drug design of crizotinib (PF-02341066), a potent and selective dual inhibitor of mesenchymal-epithelial transition factor (c-MET) kinase and anaplastic lymphoma kinase (ALK). Journal of medicinal chemistry 2011;54: 6342-63.
124. Zou HY, et al. An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. Cancer Res 2007;67:4408-17.
125. Li C, Alvey C, Bello A, et al. Pharmacokinetics (PK) of crizotinib (PF-02341066) in patients with advanced nonsmall cell lung cancer (NSCLC) and other solid tumors. J Clin Oncol. 2011;29:e13065.
126. Kwak EL, Camidge DR, Clark J, et al. Clinical activity observed in a phase I dose escalation trial of an oral c-met and ALK inhibitor, PF-02341066. J Clin Oncol 27:15s, 2009 (suppl; abstr 3509).
127. Kwak EL, Bang YJ, Camidge DR, et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med. 2010;363:1693-703.
128. Shaw AT, Kim DW, Nakagawa K, et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N Engl J Med. 2013;368:2385-94.
129. http://www.accessdata.fda.gov/scripts/cder/drugsatfda/index.cfm?fuseaction=Search.DrugDetails
130. Malik SM, Maher VE, Bijwaard KE, et al. U.S. Food and Drug Administration Approval: Crizotinib for Treatment of Advanced or Metastatic Non-small Cell Lung Cancer that Is Anaplastic Lymphoma Kinase Positive. Clin Cancer Res. 2014, in press.
131. http://www.valuebasedcancer.com/article/crizotinibsuperior-chemotherapy-extends-median-survival-first-headhead-trial
132. Lis Y, Roberts MH, Kamble S, J Guo J, Raisch DW. Comparisons of Food and Drug Administration and European Medicines Agency risk management implementation for recent pharmaceutical approvals: report of the International Society for Pharmacoeconomics and outcomes research risk benefit management working group. Value Health. 2012;15:1108-18.
133. Katayama RL, Shaw AT, Khan TM, et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung Cancers. Sci Transl Med. 2012;4:120ra17.
134. Choi YL, Soda M, Yamashita Y, et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. N Engl J Med. 2010;363:1734-9.
135. Sun HY1, Ji FQ. A molecular dynamics investigation on the crizotinib resistance mechanism of C1156Y mutation in ALK. Biochem Biophys Res Commun. 2012;423:319-24.
136. Sasaki T, Koivunen J, Ogino A, et al. A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors. Cancer Res. 2011;71:6051-60.
137. Ji C, Zhang L, Cheng Y, Patel R, et al. Induction of autophagy contributes to crizotinib resistance in ALKpositive lung cancer. Cancer Biol Ther. 2014;15, in press.
138. Gettinger S, Weiss GJ, Salgia R, et al. A first in human dose finding study of the ALK/EGFR inhibitor AP26113 in patients with advanced malignanices. Ann Oncol 2012;(Suppl 9):ix152-74.
139. Shaw AT, Camidge DR, Felip E, et al. Results of the first human phase I study of the ALK inhibitor LKD378 in advanced solid tumors. Ann Oncol 2012;(Suppl 9):ix152-74.
140. Seto T, Kiura K, Nishio M, Nakagawa K, et al. CH5424802 (RO5424802) for patients with ALK-rearranged advanced non-small-cell lung cancer (AF-001JP study): a single-arm, open-label, phase 1-2 study. Lancet Oncol. 2013;14:590-8.
141. Marsilje THL, Pei W, Chen B, et al. Synthesis, structureactivity relationships, and in vivo efficacy of the novel potent and selective anaplastic lymphoma kinase (ALK) inhibitor 5-chloro-N2-(2-isopropoxy-5-methyl-4-(piperidin- 4-yl)phenyl)-N4-(2-(isopropylsulfonyl)phenyl)pyrimidine- 2,4-diamine (LDK378) currently in phase 1 and phase 2 clinical trials. J Med Chem. 2013;56:5675-90.
142. Kinoshita KL, Asoh K, Furuichi N, et al. Design and synthesis of a highly selective, orally active and potent anaplastic lymphoma kinase inhibitor (CH5424802). Bioorg Med Chem. 2012;20:1271-80.
143. Sakamoto H, Tsukaguchi T, Hiroshima S, et al. CH5424802, a selective ALK inhibitor capable of blocking the resistant gatekeeper mutant. Cancer Cell. 2011;19:679-90.
144. Lazzari C, Spitaleri G, Catania C, et al. Targeting ALK in patients with advanced Non Small Cell Lung Cancer: Biology, diagnostic and therapeutic options. Crit Rev Oncol Hematol. 2014;89:358-365.
145. Zhang S, Wang F, Keats J, et al. AP26113, a potent ALK inhibitor, overcomes mutations in EML4-ALK that confer resistance to PF-02341066 (PF1066). Cancer Research:2010;70(aupple 1; abstr. LB-298).
146. http://clinicaltrials.gov/show/NCT01685060
147. Zdzalik D, Dymek B, Grygielewicz P, et al. Activating mutations in ALK kinase domain confer resistance to structurally unrelated ALK inhibitors in NPM-ALKpositive anaplastic large-cell lymphoma. J Cancer Res Clin Oncol. 2014, in press.
148. Garcia-Carbonero R, Carnero A, Paz-Ares L. Inhibition of HSP90 molecular chaperones: moving into the clinic. Lancet Oncol 2013;14:e358-e369.
149. Mahalingam D, Swords R, Carew JS, et al. Targeting HSP90 for cancer therapy. Br J Cancer 2009; 100:1523-9
150. Neckers L, Workman P. Hsp90 molecular chaperone inhibitors: are we there yet? Clin Cancer Res. 2012;18:64-76.
151. Normant E, Paez G, West KA, 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.
152. Ying W, Du Z, Sun L, et al. Ganetespib, a unique triazolone-containing Hsp90 inhibitor, exhibits potent antitumor activity and a superior safety profile for cancer therapy. Mol Cancer Ther 2012; 11:475-84.
153. Sequist LV, Gettinger S, Senzer NN, et al. Activity of IPI- 504, a novel heat-shock protein 90 inhibitor, in patients with molecularly defined nonsmall-cell lung cancer. J Clin Oncol 2010; 28:4953-60.
154. Socinski MA, Goldman J, El-Hariry I, et al. A multicenter phase II study of ganetespib monotherapy in patients with genotypically defined advanced non-small-cell lung cancer. Clin Cancer Res 2013; 19:30680-77.
155. Felip E, Carcereny E, Barlesi F, et al. Phase II activity of the Hsp90 inhibitor AUY922 in patients with ALK rearranged (ALK+) or EGFR mutated advanced non small cell lung cancer (NSCLC). Ann Oncol 2012;(Suppl. 9):ix152-74.
156. Ying J, Guo L, Qiu T, Shan L, Ling Y, Liu X, Lu N. Diagnostic value of a novel fully automated immunochemistry assay for detection of ALK rearrangement in primary lung adenocarcinoma. Ann Oncol. 2013;24:2589-93.
157. Morey ML, Fernández-Marmiesse A, Castiñeiras D, et al. glimpse into past, present, and future DNA sequencing. Mol Genet Metab. 2013;110:3-24.
158. Broekman F, Giovannetti E, Peters GJ. Tyrosine kinase inhibitors: Multi-targeted or single-targeted? World J Clin Oncol. 2011;2: 80-93.
159. Looyenga BD, Cherni I, MacKeigan, JP, Weiss GJ. Tailoring Tyrosine Kinase Inhibitors to Fit the Lung Cancer Genome. Transl Oncol. 2011;4:59-70.