作者: T. A. D. Smith , R. W. Cheyne
DOI: 10.1080/09674845.2011.11730344
关键词:
摘要: Cetuximab, an anti-HER1 (EGFR) antibody, is currently under trial for the treatment of breast cancer. HER1 expression not necessarily a predictor response to cetuximab as mutant components pathways activated by which include PI3K/Akt can lead resistance. Techniques that monitor events downstream are more likely provide accurate measure efficacy treatment. Glucose metabolism has been shown be strongly influenced state activation PI3K/Akt. Here, association between [18F]-FDG incorporation in cancer cells during investigated. The study also reviews development medical imaging probes target sensitivity three tumour cell lines, SKBr3, MDA-MB-453 and MDA-MB-468, expressing at low high levels, determined using MTT assay over six-day period clonogenic carried out after seven- 10-day exposures. Incorporation FDG treated with growth inhibitory doses were 4 hand two, four six days transport (rate uptake non-metabolisable analogue [3H]o-methyl-D-glucose), hexokinase activity lactate production measured on days. IC50, dose MDA-MB-468 IC10 (maximum achievable inhibition) MDA-MB-543 SKBr3 2.6, 5 148 microg/mL, respectively. was found decreased MDA-MB468 IC20, Lactate increased responding cetuximab. level modulated sensitive due modulation HK activity.