Recently, several groups have explored responsiveness to chemotherapy using mRNA microarrays. While these studies consistently identified different gene profiles correlating to responsiveness to different regimens, the predictive value was too low for clinical application. Moreover, the results did not add to our understanding of the biological mechanisms causing drug resistance. In contrast, studies exploring different forms of cancer have started to reveal specific gene alterations, in particular affecting pathways of DNA damage repair or apoptosis in relation to drug resistance. Thus, our primary aim is to explore potential gene disturbances based on functional hypotheses.