 Overall, these genes efficiently cluster tumors into 3 groups: CR, PR, and NR. We have selected 2337 genes from these data for further analysis. As expected, the majority of these genes show heterogeneous expression patterns independent of treatment response, but six large gene clusters approximately 180 genes appear to predict likelihood of response to Taxotere therapy. Consistent with an apoptosis-induction mode of action for taxanes, responsive tumors appear to have higher expression of stress-related proteins, such as mitochondrial proteins involved in apoptosis cytochromes, proteasome subunits, and higher levels of motility-related microfilament proteins actin, myosin, and tropomyosin. Non-responders patterns are more complex but show elevated levels of some microtubule proteins presumed to be targets of Taxotere therapy tubulins, tubulin-interacting proteins and elevated levels of inflammatory-response genes. Surprisingly, non-responders also showed elevated proliferation KI67 and oncogene ABL1, MYC and JUNB expression levels. This molecular portrait of Taxotere resistance differs from the expected profiles of general chemoresistance. Quantitative RT-PCR and immunohistochemistry studies to confirm these differential gene patterns of expression are in progress for all 40 patients. 