A wealth of data indicates that certain genetic abnormalities can target sp
ecific cytotoxic drugs and intervene at an early step as a mechanism of I r
esistance in the treatment of non-small-cell lung cancer. Therefore prescri
bing certain combinations of cytotoxic anticancer agents to a vast majority
of these patients is futile. Genetic abnormalities have been found to be u
seful surrogate markers for response, particularly in colorectal cancer: th
ymidylate synthase mRNA and ERCC1 mRNA levels. In addition, beta -tubulin m
utations may also confer paclitaxel resistance inpatients. An important tar
get to be explored for gemcitabine resistance is the assessment of a partic
ular region in chromosome 11p15.5 wherein lies the I ribonucleotide reducta
se gene that could affect gemcitabine metabolism. Shedding light on this ge
netic framework, several proposed customized chemotherapy studies could hel
p validate the relevance of these markers.