Imatinib in melanoma: A selective treatment option based on KIT mutation status? [16]

Journal of Clinical Oncology

Volumn 25, Issue 7, 2007, Pages

  Becker, Jürgen C ^a   Bröcker, Eva B ^a   Schadendorf, Dirk ^b   Ugurel, Selma ^b  

^a UNIVERSITY OF WÜRZBURG   (Germany)

^b UNIVERSITY OF HEIDELBERG   (Germany)

Author keywords

[No Author keywords available]

Indexed keywords

IMATINIB; STEM CELL FACTOR; ANTINEOPLASTIC AGENT; PIPERAZINE DERIVATIVE; PYRIMIDINE DERIVATIVE; STEM CELL FACTOR RECEPTOR;

CLINICAL TRIAL; DRUG EFFICACY; GENE EXPRESSION; GENE FREQUENCY; GENE MUTATION; HUMAN; LETTER; MELANOMA; METASTASIS; MUTATION RATE; OUTCOME ASSESSMENT; PRIORITY JOURNAL; TREATMENT RESPONSE; GENETICS; MUTATION; NOTE;

ANTINEOPLASTIC AGENTS; HUMANS; MELANOMA; MUTATION; PIPERAZINES; PROTO-ONCOGENE PROTEINS C-KIT; PYRIMIDINES;

EID: 33947515933     PISSN: 0732183X     EISSN: None     Source Type: Journal    
DOI: 10.1200/JCO.2006.08.9664     Document Type: Letter

References (5)

1. Curtin JA, Busam K, Pinkel D, et al: Somatic activation of KIT in distinct subtypes of melanoma. J Clin Oncol 24:4340-4346, 2006
2. Curtin JA, Fridlyand J, Kageshita T, et al: Distinct sets of genetic alterations in melanoma. N Engl J Med 353:2135-2147, 2005
3. Frost MJ, Ferrao PT, Hughes TP, et al: Juxtamembrane mutant V560GKit is more sensitive to imatinib (STI571) compared with wild-type c-kit whereas the kinase domain mutant D816VKit is resistant. Mol Cancer Ther 1:1115-1124, 2002
4. Ugurel S, Hildenbrand R, Zimpfer A, et al: Lack of clinical efficacy of imatinib in metastatic melanoma. Br J Cancer 92:1398-1405, 2005
5. Wyman K, Atkins MB, Prieto V, et al: Multicenter phase II trial of high-dose imatinib mesylate in metastatic melanoma: Significant toxicity with no clinical efficacy. Cancer 106:2005-2011, 2006