This brings to mind the idea that perhaps it is a synergistic action of docetaxel and bavituximab which could explain a bigger effect in the second-line trial. It would be a lot easier to figure out if the first-line trial also used docetaxel. This paper explored the immunomodulatory aspects of docetaxel. A Novel Chemoimmunomodulating Property of Docetaxel: Suppression of Myeloid-Derived Suppressor Cells in Tumor Bearers Krithika N. Kodumudi, Karrune Woan, Danielle L. Gilvary, et al. FREE: http://clincancerres.aacrjournals.org/content/16/18/4583.full.pdf+html From the Discussion .... These studies show the novel finding that docetaxel directly modulates MDSC signaling and therefore phenotype and function (i.e., cytokine) in vitro. Moreover, as evidenced by the MDSC splenic leukocyte coculture, MDSCs may be able to influence polarization of T cells as well. The in vivo circumstances may be more complex, but it can be inferred that docetaxel can directly induce an M1-like polarization of MDSCs and contribute to an overall shift toward M1/Th1 antitumor responses. However, it does not rule out the possibility of paracrine contribution of T cells and other leukocytes. Until now, in vivo docetaxel treatment is thought to reduce tumor burden through direct cytotoxicity (41); however, in this study, we show an indirect immunomodulatory mechanism as well. As previously mentioned, MDSC accumulation has been correlated directly with tumor burden (8). Thus, there may be synergism between multiple mechanisms of action of docetaxel (i.e., direct cytotoxicity to tumors and a specific subset of MDSCs and indirect antitumor responses via immunomodulation).