Research Highlights: Mechanisms of resistance to crizotinib in patients with ALK gene rearranged non-small-cell lung cancer

Pharmacogenomics

Volumn 15, Issue 2, 2014, Pages 133-135

  Tibaldi, Carmelo ^a  

^a Department of Oncology   (Italy)

Author keywords

[No Author keywords available]

Indexed keywords

CRIZOTINIB; EPIDERMAL GROWTH FACTOR RECEPTOR; EPIDERMAL GROWTH FACTOR RECEPTOR KINASE INHIBITOR; ERLOTINIB; GEFITINIB; IMATINIB;

ALK GENE; AMINO ACID SUBSTITUTION; DRUG BINDING; DRUG RESPONSE; EGFR GENE; GENE MUTATION; GENE REARRANGEMENT; HUMAN; KRAS GENE; LUNG NON SMALL CELL CANCER; NONHUMAN; NOTE; ONCOGENE; PROTEIN DOMAIN;

EID: 84893071319     PISSN: 14622416     EISSN: 17448042     Source Type: Journal    
DOI: 10.2217/pgs.13.236     Document Type: Note

References (6)

1. Kwak EL, Bang YJ, Camidge DR et al. Anaplastic lymphoma kinase inhibition in non-small-cell lung cancer. N. Engl. J. Med. 363(18), 1693-1703 (2010).
2. Shaw AT, Kim DW, Nakagawa K et al. Crizotinib versus chemotherapy in advanced ALK-positive lung cancer. N. Engl. J. Med. 368(25), 2385-2394 (2013).
3. Choi YL, Soda M, Yamashita Y et al. EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors. N. Engl. J. Med. 363(18), 1734-1739 (2010).
4. Doebele RC, 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. 18(5), 1472-1482 (2012).
5. Katayama R, Shaw AT, Khan TM et al. Mechanisms of acquired crizotinib resistance in ALK-rearranged lung cancers. Sci. Transl. Med. 4(120), 120ra17 (2012).
6. Matsuoka H, Kurata T, Okamoto I et al. Clinical response to crizotinib re-treatment after acquisition of drug resistance. J. Clin. Oncol. 31(19), e322-e323 (2013).