Neil W. Gibson

TL;DR: It is shown that wild-type EGFR-containing human NSCLC lines show a range of sensitivities to EGFR inhibition dependent on the degree to which they have undergone an epithelial to mesenchymal transition (EMT), suggesting that EMT may be a general biological switch rendering non-small cell lung tumors sensitive or insensitive to EG FR inhibition.

TL;DR: The 3-methyl analogue, 8-carbamoyl-3-methylimidazo[5,1-d]-1,2,3,5-tetrazin-4(3H)-one (CCRG 81045), was investigated further and found to possess good activity, when administered i.p. or p.o. to mice bearing the L1210 leukemia.

TL;DR: Findings suggest that EGFR somatic mutations directly influence both erlotinib sensitivity and cellular transformation, and cells harboring these mutant receptors form tumors in immunocompromised mice.

TL;DR: The ideas that reductive activation of MMC by DTD may be important in the cytotoxicity of M MC and that polymerase chain reaction may be a useful technique for quantitating the relative expression of genes in human tumors are supported.

TL;DR: This work sought to determine if rapamycin, an inhibitor of mTOR, could enhance erlotinib sensitivity for cell lines derived from a variety of tissue types (non–small-cell lung, pancreatic, colon, and breast).