Acquired resistance to the ALK inhibitor crizotinib in the absence of an ALK mutation

Journal of Thoracic Oncology

Volumn 7, Issue 3, 2012, Pages 623-625

  Costa, Daniel B ^a   Kobayashi, Susumu ^a  

^a HARVARD MEDICAL SCHOOL   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

COMPLEMENTARY DNA; CRIZOTINIB; PROTEIN TYROSINE KINASE;

ADULT; ARTICLE; CANCER STAGING; CASE REPORT; DRUG SUBSTITUTION; GENE MUTATION; HUMAN; HUMAN TISSUE; LIVER METASTASIS; LUNG ADENOCARCINOMA; LUNG NON SMALL CELL CANCER; MALE; NUCLEOTIDE SEQUENCE; PRIORITY JOURNAL;

EID: 84857836570     PISSN: 15560864     EISSN: 15561380     Source Type: Journal    
DOI: 10.1097/JTO.0b013e318241daab     Document Type: Article

References (5)

1. Kwak EL, Bang YJ, Camidge DR, et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N Engl J Med 2010;363: 1693-1703.
2. Sasaki T, Okuda K, Zheng W, et al. The neuroblastoma-associated F1174L ALK mutation causes resistance to an ALK kinase inhibitor in ALK-translocated cancers. Cancer Res 2010;70:10038-10043.
3. 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;71:6051-6060.
4. 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; 363:1734-1739.
5. Costa DB, Kobayashi S, Pandya SS, et al. CSF concentration of the anaplastic lymphoma kinase inhibitor crizotinib. J Clin Oncol 2011;29: e443-e445.